Evaluation of the efficacy of

Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra

(with special reference to Vitiligo)

By

Dr. Satish Kumar Tiwari

As partial fulfillment of post graduation degree M.D.(Ayurveda Vachaspati) Kayachikitsa

Under Rajeev Gandhi University of Health Sciences, Bangalore, Karnataka

Guide Prof. Dr. Ch. Ranga Rao

M.D.(Ayu) (Osm)

Professor and head of the department Post graduation and research center

Kayachikitsa

Co-Guide Dr. Siva Rama Prasad Kethamakka

M.D. (Ayu) (Osm)

Reader in Kayachikitsa Post graduation and research center

Kayachikitsa

D.G. Melmalagi Ayurvedic Medical College Gadag - 582 103

Post graduation and research center Kayachikitsa

1998-2001

J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE,

& POSTGRADUATE AND RESEARCH CENTER, GADAG, 582 103

Certificate

This is to certify that Dr. Satish Kumar Tiwari has worked for his

thesis on the topic entitled “Evaluation of the efficacy of Dhatrayadi Yoga

(Internal) and Avalgujadi lepa (external) along with and without sodhana

(Vamana) in Switra (with special reference to Vitiligo)”.

He has successfully done the work under the guidance of Prof. Dr. Ch.

Ranga Rao M.D. (Ayu) (Osm) and Co-guidance of Dr. Siva Rama Prasad

Kethamakka M.D. (Ayu) (Osm).

This particular study helps in treating the disease Switra (Vitiligo) with

present scientific approaches.

I here with forward this thesis for the evaluation and adjudication.

(Dr. G. B. Patil) Principal

This is to certify that the contents of this thesis entitled “Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)” has

been worked out by Satish Kumar Tiwari, under my supervision with close guidance

and co guidance of Dr. Siva Rama Prasad Kethamakka, M.D. (Ayu) (Osm).

Even though this disease, Switra has been mentioned in Ayurvedic texts, the

etiology, pathogenesis etc., needs further evaluation and research. It is as developed

and explained by Satish Kumar Tiwari is unique and scientific and will definitely help in

elucidation of this disease in Ayurvedic and Modern scientific parlance and further

planning with the management.

This work is applied, scientific and an original contribution in the field of research

in Ayurveda.

I am fully satisfied with the work and recommend the thesis to be put before the

adjudication.

Guide Dr.Ch.Ranga Rao M.D. (Ayu) (Osm)

Professor and head of the department Post graduation and research center

Kayachikitsa D.G.M. Ayurvedic Medical College, Gadag

This is to certify that Satish Kumar Tiwari (M.D. (Ayurveda) Kayachikitsa), has

worked for his thesis on the topic entitled “Evaluation of the efficacy of Dhatrayadi

Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana

(Vamana) in Switra (with special reference to Vitiligo)”.

Clinical trials are done under my supervision and guidance. This thesis makes a

distinct advance on scientific lines in the above subject and the findings are highly

significant at the statistical evaluation and have considerably contributed to the present

knowledge of the subject.

I am fully satisfied with his original work and hereby forward the thesis for the

evaluation of adjudicators.

Co-Guide

Dr. Siva Rama Prasad Kethamakka M.D. (Ayu) (Osm)

Reader in Kayachikitsa Postgraduate and Research Center (Kayachikitsa)

D.G.M. Ayurvedic Medical College, Gadag.

Acknowledgement By the grace of goddess Mata Vaishno Devi it is pleasure to express my full

respect and regard to my parents Sri Mangaleshwar Tiwari and Late Parvathi Devi who

made me mentally strong and capable to face and solve the problems in the life without

any tension and fear. She used to treat human and cattle of the area with compassion

using some of the herbal preparations. She carefully and wisely gave her knowledge to

me in respect of utilization of the folklore medicine in my career.

I am one out of the luckiest people to get Prof. Dr.Ch. Ranga Rao as my Head of

the Department, Kayachikitsa P.G. Wing of the college as a guide. He provided all type

of surveillance and suggestion, which make the guideline to this thesis. His experience

and views allowed me to take new concepts for trial and completion of the thesis in time.

My thanks and respect to his dynamic personality.

I express my complete respect and regard to my co-guide Dr. K. Siva Rama

Prasad, reader in Kayachikitsa and in-charge professor of Kayachikitsa P.G in the

college. He is not only co-guiding this thesis but also his importance in induction of

complete constructive changes in my academic and professional career. He is the real

architect of this research work and allowed me to build a successful research. The entire

hurdle, which came during the time of the trial of medicine, was solved by his valuable

suggestions.

My sincere thanks to Dr. G. B. Patil, principal of D.G.M Ayurvedic medical college

Gadag who provided all types of moral support to full fill my M.D Ayurveda course.

My thanks to Dr. A.K. Panda and Dr. Doddamani, lecturers in P.G. Department of

this college who honestly helped all over to me which was necessary to make a student

to capable in his career.

I am very much thankful to the ex Directors of CCRAS Dr. V. N Pandey, Dr. H.R.

Goel, and Dr. Prem Kishore and present Director Dr. Vellu Chamy who provided me

technical, moral and administrative support for the completion of this course in a

stipulated period. My sincere thanks to Dr. Bikshapathi (Assistant Director RRI

Bangalore) and is my best friend Mr. Janardhanan (Head Clerk RRI Bangalore) for

maximum help and cooperation which was really need full in respect of completion of

M.D. Ayurveda course.

I have a deep respect for three famous physicians of Gadag town. They are Dr.

V.K. Chintamani presidents of K.H Patil hospital, DR.S.R. Naganur (secretary and chief

physician of K.H. Patil hospital) and Dr. S.N. Karur (Retired Major of Indian army) who

allowed me to work in a full-fledged ultra modern hospital a part of my study.

I have a proud on the friend ship of my senior M.D scholars like Dr. Viresh

Kottrushetter, Dr. S.T. Hombal, Dr. Yashoda Mudigoudar and Dr. A.S. Patil. And also I

am thankful to my classmate Dr. C.V. Ragashekar and other junior colleagues Dr. S.N.

Reddy and Dr. Yasmin who helped me during my dissertation compellation.

I express my deep affectionate love to my wife Smt Vishalakshi who cooperates

to me through out my life especially at present in building the academic career. It is a

fact that without her cooperation, moral and cardinal support the completion of the M.D.

course was impossible.

I express my eternal love to my daughter Baby Samskrita for dispelling al the

tension and tiredness with her talk love and respect.

I can never forget the worthy support of my mother in law Smt N. Jayamma, who

provided all types of support, which was necessary to complete the post graduation.

All the above are meaningless if I do not recollect late D. G. Melmalagi who

contributed his entire property to Shivananda math for development of Ayurvedic

Medical College, in Gadag. I am very much thankful to the management and the staff of

this prestigious institute, who extended timely help in the research completion and in

further maintaining this institute at the supernumerary, there by the Government of

Karnataka, RGUHS and CCIM has permitted M.D Ayurveda course to this college

Dr. Satish Kumar Tiwari

Index 1. Introduction 1- 8

♦ Vitiligo looks with ♦ Causes in general ♦ Historical aspect ♦ Kausika-sutra ♦ Other references ♦ Charaka samhita

♦ Astanga Hridaya and Susruta Samhita

♦ Madhava Nidana ♦ Contemplation ♦ Definition of Switra

2. Shareera 9 - 44 ♦ Is VITILIGO a melanin malfunction

or a skin disease? ♦ Synonyms of Twak: ♦ Utpathi of Twak: ♦ Rachana of Twak: ♦ Kriya of Twak: ♦ Varna of Twak: ♦ Chaya and prabha : ♦ Chaya nirupana (panchabhuta

sambandha) ♦ Layers of twak ♦ Charaka ♦ Bhrajaka Pitta and skin colour ♦ "Bhela": ♦ "Vagbhata" observes: ♦ "Arunadutta" observes: ♦ According to modern science ♦ Twak - modern concept ♦ Derivation: (development) ♦ Microscopic anatomy of the skin: ♦ Epidermis ♦ Stratum corneum ♦ Stratum lucidum ♦ Stratum granulosum ♦ Stratum spinosum ♦ Stratum generminatinum: ♦ Dermis ♦ Appendages ♦ Hairs ♦ Sweat glands ♦ Sebaceous glands ♦ Nails ♦ Functions of the skin: ♦ Skin colour: ♦ The physiology of melanin pigment

formation ♦ Introduction

♦ Introductory Definitions ♦ Melanocytes: ♦ Origin of melanocytes: ♦ Melanocytes in Development ♦ Melanocytes - distribution: ♦ Melanocytes are found in selected

body sites. ♦ Distribution within the epidermis ♦ Sub-cellular structure of

melanocytes: ♦ Melanocyte Ultrastructure ♦ General Features ♦ Stage I melanosomes. ♦ Stage II melanosomes. ♦ Stage III melanosomes. ♦ Stage IV melanosomes. ♦ Biochemistry of Melanogenesis ♦ Eumelanin ♦ Pheomelanin ♦ Trichochrome ♦ Oxymelanin ♦ Mixed-type melanins ♦ Neuromelanins ♦ Urinary melanogens ♦ VI. Melanosome Transfer ♦ VII. Regulation of Melanogenesis ♦ Genetics ♦ Hormonal ♦ Cytokines ♦ Biosynthesis: ♦ Dendrites: ♦ Keratinocytes: ♦ Synthesis and "movement" flow of

melanin: ♦ Excretion of melanin: excretion of

melanin is effected by ♦ Movement flow of melanin

3. Nidana 45 – 67 ♦ Nidana from various texts ♦ Charaka ♦ Susruta ♦ Vagbhata ♦ Madhava Nidana ♦ Bhavaprakasakara ♦ Hareeta ♦ Samprapthi ♦ Nidana: ♦ Agni: ♦ Dosha ♦ Srothas ♦ Dushya: ♦ Pathogenesis (sammurchana):

♦ Pradhanya samprapthi: ♦ Bala samprapthi: ♦ Kala samprapthi ♦ Purvarupa: ♦ Rupam ♦ Asadhya lakshana – ♦ Sadhya lakshana ♦ Classification of switra ♦ Samhita ♦ Switra bhedas - various

acharyas ♦ Vyavachedaka nidana ♦ Sadyasadyata

4. CHIKITSA – KARMA 68 - 76

♦ Satwavajaya chikitsa: ♦ Yuktivyapasraya chikitsa ♦ Bahiparimarjanam: ♦ Shastrapranidhanam ♦ Pathyapathya ♦ Ahara ♦ Vihara ♦ Pathyas in kishta ♦ Local treatment ♦ Topical preparation

♦ Tanning, specific effect of UV light

♦ Intralesional infiltration ♦ Chemical tattooing ♦ Surgery ♦ Role of sun light in the

management of Leucoderma ♦ Drugs affecting skin

pigmentation ♦ Trioxsalen ♦ Methoxsalen

5. Drug review 77 – 91 ♦ DHATRYADI YOGA ♦ Method of preparation of

Dhatryadi yoga ♦ Analytical findings of

Dhatryadi yoga and Avalgujadi lepa

♦ Bakuchi - Psoralia cordifolia (seeds)

♦ Amalaki - Emblica officinalis (Fruits)

♦ Khadira – Acacia catechu (Hard wood) ♦ Harital - Arsenic trisulphidum

6. Material and Methods & Case sheet 92 - 101 7. Observations 102 – 121 8. Discussion and conclusion 122 - 136 9. Summary i - xii References and Bibliography

List of Photographs

Photograph-1 11 Structure of the skin –

Synoptic view of cutaneous architecture Photograph-2 12 Structure of the skin –

Melanocytes : Melanosome formation and distribution Photograph-3 16

Structure of the skin – An view of the loose connective tissue of the papillary dermis

Photograph-4 18 Structure of the skin - The vascular architecture of the Dermis Photograph-5 81 Ingredients of the Dhatryadi Yoga and Avalgujadi lepa - Bakuchi – Psoralia corylifolia Photograph-6 87 Ingredients of the Dhatryadi Yoga and Avalgujadi lepa – Khadira – Acacia catechu Photograph-7 90 Ingredients of the Dhatryadi Yoga and Avalgujadi lepa – Amalaki – Emblica officinalis Photograph-8 91 Ingredients of the Dhatryadi Yoga and Avalgujadi lepa – Harital – Arsenic Trisulphidum Photograph-9 91A Preparation of the Dhatryadi Yoga and Avalgujadi lepa Photograph-10 124 Patient showing the improvement periodically Photograph-11 126 Patient showing the improvement periodically Photograph-12 128 Patient showing the improvement periodically Photograph-13 135 Patient showing the improvement periodically

Page Number

List of Charts

1. Chart number – 1A 102 Demography Sodhana therapy

2. Chart number – 1B 103

Demography Shamana therapy 3. Chart number – 2A 104

Complaints (Sodhana Group) 4. Chart number – 2A1 105

Complaints (Sodhana Group)

5. Chart number – 2B 106

Complaints (Shamana Group)

6. Chart number – 2B2 107

Complaints (Shamana Group) 7. Chart number – 3A 108

Hetu (Sodhana Group) 8. Chart number – 3B 109

Hetu (Shamana Group) 9. Chart number – 4A 110

Ahara & Vihara (Sodhana Group) 10. Chart number – 4B 111

Ahara & Vihara (Shamana Group) 11. Chart number – 5A 112

Poorvaroopa (Sodhana Group)

Page Number

12. Chart number – 5B 113

Poorvaroopa (Shamana Group) 13. Chart number – 6A 114

Sadhya-asadhyata of Sodhana Group 14. Chart number – 6B 115

Sadhya-asadhyata Shamana group 15. Chart number – 7A 116

Sodhana therapy Assessment 16. Chart number – 7B 117

Shamana therapy Assessment 17. Chart number – 8A 118

Statistical Assessment before treatment 18. Chart number – 8B 119

Statistical Assessment after treatment 19. Chart number – 8C 120

Statistical Assessment Individual study of group "A" 20. Chart number – 8D 121

Statistical Assessment Individual study of group "B"

List of Graphs

Graph No 1: 129

Showing sex ratio of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Graph No 2: 130 Showing Age Incidence of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Graph No 3: 131 Religion distribution of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Graph No 4: 132 Economical status distribution of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Graph No 5: 133 Occupation distribution of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Graph No 6: 134 Diet distribution of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Graph No 7: 135 Showing the Result of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Page Number

Vitiligo is a common chronic and progressive skin disease characterized by

the lack of melanin pigments producing skin patches with sharp and often hyper

pigmented edges. This disease affects approximately 1% of the worldwide

population. The etiopathogenesis of Vitiligo is still unknown to date, even though the

multi-factorial character of its clinical expression is quite clear. There are three

classical pathogenetic theories: an immunologic theory, a neurologic theory and a

self-destruction hypothesis. Possible hereditary factors and psychosomatic issues

should undoubtedly be taken into account as well. The clinical expression of the

disease also varies between individual patients, according to personal

characteristics, and between patches, according to the partial or total lack of

pigments. The prognosis of this skin disease is thoroughly benign, even though the

psychological and social implications following up the aesthetic modifications due to

the appearance of patches may be very serious and disabling.

Since the etiological cause of Vitiligo may not be removed, medicine may only

act on symptoms by means of therapies aimed at restoring the lost colour uniformity.

However it is not always easy to suggest to a patient a treatment being effective, long

lasting and free of side effects at the same time. The most widely used therapy in the

last thirty years was the PUVA therapy (UVA+trimethylpsoralen), with results ranging

from 25% to 50%. This therapy requires a careful assessment of the patient's general

conditions and clinical picture, as well as the identification of the correct drug dose to

be administered and patient monitoring throughout the treatment period.

2

As a border organ, the skin is crucial for the body's homeostasis, to which it

contributes through a number of particles specialized in receiving stimuli and

forwarding them to the central organs of the nervous system. Along with these, there

is a special family of receptors, the melanocytes, whose task is to react to the light

stimulus by synthesizing a special protein, melanin, constituting the most important

skin-protection factor. Evaluation of the role of immunogenetic factors and trace

elements (copper) in pathogenesis of Vitiligo provided the basis for the improvement

of its photochemotherapy by using Cupir and T-activin. This yielded an opportunity

for a better management of this dermatosis. Results of the study suggest indications

for the use of T-activin (immunomodulator) and Cupir (copper-containing product) in

the treatment of Vitiligo.

Vitiligo looks with

• White patches of skin usually on exposed areas of the body- can

occur symmetrically.

• Hair may go gray in patches.

Usually this disorder occurs before the age of 20. It can come and go or lay

dormant for year. It is usually stress related. The onset of the loss of pigmentation

varies in different people, one person may lose all their pigmentation, while another

may only have a few spots of lost colour.

Vitiligo is not dangerous, but it is sometimes linked with other diseases or

disorders such as thyroid problems, pernicious anaemia, Addison's disease

(decreased adrenal gland function), and alopecia areata (hair loss in patches).

3

Causes in general

It is not known what causes Vitiligo, although it is suspected that it is

hereditary. Emotional stress may the onset of Vitiligo. In essence what happens in

the body is that the cells stop producing melanin which gives the skin and hair its

colour. There are several possibilities one is that this is an autoimmune disease in

which the cells attack their own cells, perceiving them as foreign. The problem can

cause distress and embarrassment and can affect people’s self esteem.

HISTORICAL ASPECT

'Atharvanaveda' is well known and treasure of knowledge with Ayurveda as

the Upaveda. It focuses tenacious knowledge about Kusta and its other aspects,

which can be well gathered from the eight versions available, with the German

attempt by R. Roth and W.D. Whitney appears to be the oldest publication in the year

1855 and in India by S.P. Pandit in 1898. In the available texts there are 20 - kandas

and 731 suktas. Out of which kandas 1,5,6 and 19 mention the terms under this

study.

S.No Atharvaveda Word appeared

1 Kanda-1, Sukta-23 Swetakushta nasana sukta

2 Kanda-5 kushtatakmanasana

3 Kanda-6 'Kustaushadhi'

4 Kanda-19 Kushta nasana

The term swetha Kusta appears particularly in first khanda and in the whole of

the sukta given under this title sweta Kusta only. The other terms used in the place of

swetha Kusta, Kilasa and Palita are synonymous.

4

The term Kilasa appears in Rigveda (6000 BC approximately) as the name of

a spotted deer. The term hence was used for a person who shows white patches on

the body. The term Kilasa also appears in the other Vedic literature, such as

Vajasaneya-samhita, Kathaka-samhita (Kathopanishad), Taittariya brahamana and

Kaushika sutra. The term Palita indicates the white spot and is well known in the later

literature of Ayurveda as meaning gray hair.

The remedy gives for sweta Kusta in Atharvanaveda chiefly consist of four

plants. Which go under the terms 'Rama, Krishna, Asikni and Rajani. According to

some authors these four terms are synonymous. These plants are identified

botanically as under –

Rama Bringaraja Ecilipta alba Krishna Indravaruni Citrullus colocynthus Asikni Neeli Indigofera tinctoria Rajani Haridra Curcuma longa

It may be noted here that there appears to be no evidence of the knowledge

of Psoraliodes cyamophasia in the available texts of Atharvanaveda.

Kausika-sutra

The next treatise of importance from the study point of view is 'Kausika-sutra'.

This Grihya sutra of Atharvanaveda is believed to be older than Gopatabrahmana.

These Kausika sutras give some more details for the application of the plants,

mentioned in Atharvanaveda. The white spots have to be rubbed by a cow-dung till

they become somewhat pinkish in colour, a paste is to be applied to the affected area

prepared by mixing the plants mentioned. It is strange to note that Kausika-sutra

does not throw any more light on the term's Kilasa, Palita and Kusta and there

appears to be no addition of any more drugs than the four plants mentioned in

Atharvanaveda.

5

Other references

The description of sweta Kusta also found in 'Manusmruthi' and 'Yagnavalkya

smruthi' and which ban the marriage from affected families. In 'Artha sastra' of

kautilya there are descriptions about swetaKusta and syameekaranayoga

(kangutaila) mentioned in the same text.

Charaka Samhita1

Centuries after Kausika-sutra, Charaka Samhita is a benchmark in the history

of Ayurveda. The knowledge regarding Kusta appears very ubiquitously in these

centuries and Charaka treats the clinical conditions of Kusta in all its aspects. One

special chapter appears in Nidana Sthana, which deals with the detailed

classification, Aetiology, signs and symptom. The predominate types of Maha Kusta

(kapala, udumbara, mandala, risyajihwa, pundarika, sidhma and kakanaka)

described in this chapter. A good deal of emphasis has been given on the foods

which gives rise Kusta if used extensively.

The abnormal manners and mental upsets are also mentioned along with

dietetic reasons. Charaka has devoted one whole chapter to the treatment of this

disease in Chikitsa Sthana. In this chapter additional classification of Kusta into two

chief classes viz, Maha Kusta and kshudra Kusta, in addition to 7 Mahakustas and

11 kshudra Kustas are mentioned here.

The term 'Kilasa' appears in Chikitsa chapter, along with Kusta. Preparations

have been described for both conditions. The term Palita however, rarely appears in

Charaka has been indicated as a Rasapradosaja roga.

Chikitsa Sthana of Charaka devotes 7th chapter entirely to the treatment of

Kusta and allied conditions. The mention of 'Bakuchi' is found as an external

6

application in 3 places. The mention of 'Somaraji' as a remedy for Kusta appears in

the Charaka Chikitsa Sthana although the drug appears to be mentioned in sutra

Sthana for other uses.

Astanga Hridaya and Susruta Samhita

Vagbhata mentions all the important terms - Kusta, Switra and Kilasa, but he

mentions Krimi with Kusta and Switra in one and the same chapter. The term Kusta

has been explained as

i´ÉSÉÉ: EÖò´ÉÇÎxiÉ ´Éè´ÉhªÉÇ, ºÉ´ÉÇ EÖò¹hÉÉÊiÉ iÉuù{ÉÖ:

that which destroys all the tissues (Dhatu) of the body. 'Vagbhata' and

'Susruta' are restricted this term to the condition of skin only.

Madhava Nidana

The later authors like 'Madhavakara' and others also followed the same

general classification of seven Mahakustas and 11 kshudra Kustas. Switra is

differentiated from Kusta by almost all - subsequent authors by its being less

destructive to the tissues of the body.

Contemplation

All these facts put together, the term Switra is used separately from Kusta, in

which destruction of tissues does not occur. As Switra is characterized by a change

in the colour of the skin, it can be equated to that of "leucoderma"(vitiligo) in modern

medicine. The term vitiligo was first mentioned by "celcus" a scientist and physician

of 'Rome' in the 2nd century A.D. This term has been derived from a Latin word

"vitilious" interprets with a 'calf' comparing the whiteness of the skin of the calf to the

human skin. The same disease has been described as 'bars' in the holy 'Qhuran' of

7

the 6th century. The 'Unani' physicians like Avicenna, Rhazes, Mohammed,

Azamkhan etc., have suggested that the vitiligo can be transmitted from parents to

progeny.

Almost all the authors of Ayurveda described Switra on the basis of Dosha

like - Vata, Pitta and Kapha. And as well as on the basis of involvement of Dhatu

like- Rakta, Mamsa and Medas - but both classifications take into consideration the

colour of the Switra lesions as -Rakta, tamra and sukla varnas respectively. Some

authors feel these are the three phases in the progress of the disease process.

All authorities of Ayurveda accept the limitation of Switra up to the skin. It is in

the 3rd of the 6th layers according to Charaka and in the 4th of 7th layers of Susruta.

According to Ayurveda, vitiation of Bhrajaka Pitta brings changes in the normal colour

of the skin, in vitiligo, which is something like defective melanin formation.

Definition of Switra

This is an unappealing yet harmless skin disorder characterised by white

patches of skin that have seemingly lost their ability to produce the normal colour of

the skin. The description of Switra is available since vedic literature only. The terms

used in the place of Switra in vedic literature are sweta Kusta, Kilasa and palita. The

term kilasa-its meaning in Rigveda explained as the 'spotted deer'. Hence this term

devotes the impairment of the colour of the skin. The term's palita and sweta Kusta

are also supports the changing of the normal colour of skin into white. The term

Switra is firstly appears in Ayurvedic classes only. The term Switra derives from the

root - "swita varne swita" - that means which gives white colour. So Switra can be

defined as the disease which turns the normal colour of the skin to white.

8

In Amarakosha gurubala prabhodhini the term Switra is defined as

"swetate twaganena Switram" - means by which the colour of skin -

turns into white.

In Sabdhakalpadruma as - "swetate ltihi"

In Vachaspathyam as "swetaKusta bedhe” (davala)

Description in Anjana nidana - Switram tathah sitam"

All the above references from various texts and classics of Ayurveda support the

meaning of the Switra as - colour change of the normal skin to white. The cardinal

symptom of the Vitiligo is localised de pigmented patches. The all above-mentioned

definition gives support to Vitiligo and its cardinal symptom perfectly.

Present study is made under the following headings.

Index

1. Introduction

2. Shareera

3. Nidana

4. Chikitsa - karma

5. Drug review

6. Material and methods

7. Discussion and conclusion

8. Summary

References

Bibliography

9

Within this area are the basic studies of the materials that make up the skin

and its cells, how they are assembled into the structures that we see under the light

and electron microscope. In further how skin cells interact with one another via cell to

cell signalling and attachment, how the skin protects itself from the external

environment has to be studied in detail. And how that protection can be breached in

a controlled manner to apply drugs to treat skin and systemic diseases, we have to

study skin elaborately.

Many skin diseases have an autoimmune basis, some of them specific to the

skin as the primary or exclusive end organ being attacked. Many other skin diseases

are inflammatory without being autoimmune. Studying the skin as an active immune

organ, with a focus on immunocompetent cells that are both resident within skin and

trafficking through skin. Studying gene translation and expression, as well as patho

physiologic studies of how the abnormal gene product results in the Disease State.

A major function of the skin is to prevent water loss from the inside and penetration of

chemicals from the outside. It is not completely clear, however, how this function is

accomplished.

The consequences of ageing on skin occurs as a result of not only chronological

effects but probably more from accumulated environmental damage, much of it from

ultraviolet radiation (UV) radiation from the sun (and artificial sources for those who

frequent tanning salons). These effects are both in the:

10

(1) epidermis, which discolors, dries out (thus changing its resistance to chemical

penetration), and develops skin cancers, precancers, and benign tumors; and

(2) dermis which loses adnexal structures (hair, sebaceous and sweat glands),

thins, and becomes fragile.

Skin stem cells include that necessary for the continued repopulation of the skin

itself as well as those related to skin appendages, hair, nails, and eccrine and

apocrine glands.

Is VITILIGO a melanin malfunction or a skin disease?

After many years of research I have come to the conclusion that Vitiligo is the

outcome of some organs deterioration: pancreas, spleen, liver and kidneys that

accumulate serous residues not eliminated by the organism on time and that are

deposited in our organs responsible for toxic residues elimination, increasing so the

organism free-radicals "toxins".

Abnormally functioning nerve cells may make toxic substances that injure

melanocytes. The body’s immune system may destroy melanocytes. Researchers

think pigment may be destroyed as the body responds to a substance it perceives as

foreign. Pigment-producing cells may self-destruct. While pigment is forming, toxic by

products could be produced and destroy melanocytes.

With a toxic residues overload, the liver function is diminished giving rise to

cephaleas that are common in Vitiligo carriers, as well as bitter taste in the mouth,

thick saliva, greasy sweating all over the body and sporadic abdominal pains. In this

back ground it is essential to study Twak Rachana and Kriya Shareer.

11

Synonyms of Twak:

Twak

Charma

Raktadhara

Asrgdhara

Sparsanedriya etc.,

The term "TWAK" derives from the root "twacha - samvarne" (which cover).

It can be defined as substance of the body, which covers the internal tissues like

rakta, mamsa etc.

Utpathi of Twak2:

The layers of Twak forms in the stages of grabhavastha, as layer of scum

formation on boiling milk. Later in the stages of dhatu parinama, Twak forms as an

upadhatu from prasada paka of Mamsa Dhatu. All the mridu bhavas of garbha were

considered as maternal elements. So twak can be considered as a maternal element

only. Astanga Hridya tells formation of twak is in the sixth month of gestation3.

Rachana of Twak:

According to "Susruta" Twak is composed of seven layers and six layers by

"Charaka". Susruta described the thickness of each layer taking one "vreehi" as

standard for total skin, where as Charaka does not mention the thickness of layers.

The above Acharyas have described the diseases that manifest in each layer. But

they have got difference in opinion of layer, in which the "Switra" occurs. Charaka

considered it as third, while Susruta in the fourth layer.

12

Kriya of Twak:

1. Bhrajaka pitta stana4

2. Sparsanendriya stana

3. Stana for swedagati5

4. Absorptional area of abhyanga, lepa, pariseka6 etc.

In Switra the cardinal symptom is accepted as depigmentation. Thus the

study regarding the factors responsible for 'varna' (pigment) as per Ayurveda is

essential.

Varna of Twak:

"Tejobhuta" is the main factor in formation of Twak varna and among the

Dosha, "Pitta" is said to be responsible for the normal as well as abnormal coloration

of the skin. The specific "Bhrajaka Pitta" is located in Twak.

During the garbhavasta, with the predominance of tejobhuta the colour

formation in foetal skin is accepted as below.

Udaka + akasa bhuta

Prithvi + vayu bhuta

goura varna

krishna varna

Equal combination of Panchabhutas syama varna

"Charaka" described7 prakrita varnas are four in number, those are krisna,

krisna syama, syamavadata and avadata. Beside these are atikrisna and atigoura

who are "ninditas" mentioned in Charaka sutra Sthana.

Chaya and prabha:

These are the factors, which are having close relation with skin colour. Chaya

masks the varna, while prabha brightens the varna chaya can be appreciated from

close vision, while prabha is visible from distance8.

13

Tejobhuta is the basic of all types of prabha. The prabha is classified into

seven, viz. rakta, peeta, sita, syava, harita, pandu and asita9.

Varna in normal is permanent from birth to death, chaya may alter due to

"rishta" (asanna mrityu lakshana), while prabha changes according to the temporary

state of health. The normal colour of the body is the outcome of these three only.

Chaya nirupana (panchabhuta sambandha10)

Type Lakshnas

1 Nabhasi Nirmala, neelavarna, snehayukta, saprabha

2 Vayavi Ruksha, syavavarna, hatahprabha

3 Agneya Visudharakta, deeptabha, darsanapriya

4 Apya Shudha, vaiduryavimala, susnigdha

5 Parthiva Sthira, snigdha, ghana, syama, sweta

LAYERS OF TWAK AND MANIFESTING DISEASES

Susrutha

No Layer Diseases

1 Avabhasini Sidhma padma, kantaka

2 Lohita Tilakalaka, nyacha

3 Sweta Vyanga, ajagalika, mashaka

4 Tamra "kilasa" Kusta

5 Vedhini Kusta, visarpa

6 Rohini Grandhi, apachi,arbuda, galaganda

7 Mamsadhara Bhagandara, arsha, vidradhi

14

Charaka

No Layer Diseases

1 Udakadara -

2 Raktadara -

3 Triteeya Sidhma, "kilasa"

4 Chaturtha Dadru, kista

5 Panchama Alaji, vidradhi

6 Sashta Arsha, bhagandhara

Bhrajaka Pitta and skin colour

Bhrajaka Pitta is stated to be located in the skin and to impart to this structure

its characteristic colour and lustre. It has also been stated that it governs the normal

and abnormal temperature of the body.

'Charaka' has not described this Pitta as a separate entity but he has included

the functions attributed to it among those of Pitta in general. He has stated that the

production of normal and abnormal temperature of the body, as well as the normal

and abnormal colour of the skin due to Pitta11.

'Chakrapani dutta', in his commentary on the above, has stated that the

regulation or otherwise of the body heat and variations in the colour of the body are

the functions of Bhrajaka Pitta which is located in the skin. Susruta12, Bhela and

Vagbhata have, on the other hand, made separate and mention this Pitta, including

the functions ascribed to it.

Bhrajaka Pitta, which is located in the skin is spoken of as Bhrajakagni, in as

much as, it enables the digestion (utilisation) of substances used for "Abhyanga",

15

"parisheka", "avagaha", "lepana" etc. it irradiates the glow of one's natural

complexion. Commenting on above "dashana" observes by Twak is understood the

bahya twak, known as avabhasini, by Abhyanga etc. is meant the dravyas employed

for the kriya (preparation) and karma (action) etc.

"Bhela":

Bhrajaka Pitta is that which is responsible for the manifestation of the specific

characteristic of body, it emphasises its importance, creates different prabhas (hues)

of the head, hands, feet, sides back, abdomen, thighs, face, nails, eyes and hair. It

also brightens them.

"Vagbhata" observes:

Bhrajaka is located in the skin. It is so called because it imparts lustre to the

skin and makes it radiate. Commenting on the above13,

"Arunadutta" observes:

It is known as Bhrajaka because it performs dipana and pachana of

(substances used for) abhyanga, lepa, parisheka etc.

It will be seen from the citations above that,

Bhrajaka belongs to a larger species of substances described in Ayurveda

as Pitta.

It is located in the bahya twak, in its layer known as avabhasini (Dalhana)

Its functions are state to be

The production of normal and abnormal heat of the body (Charaka)

The production of normal and abnormal colour of the skin, as whole , and

parts and structures of the body viz. Hands, feet, sides, back etc., (Bhela)

16

The absorption and digestion of substances used together with oils,

decoctions used for sprinkling over the body etc.(Dalhana & Arunadutta)

It may be stated, in general, that Bhrajaka Pitta may represent the factor or

factors present in the body, which is or are responsible for the colour of the skin and

other structures.

According to modern science

The factors which confer on the skin, its characteristic normal colour, is are

metabolically produced by melanoblasitc cells in the skin by the enzyme "tyrosinase",

to that extent we have a confirmation of the claim of Ayurveda that there exists, in the

layer of the skin, known as avabhasini. A Pitta known as the Bhrajaka, which is

responsible for providing the skin with, which pigments which confers on it its

characteristic normal colour. The same is also true of the colour of other structures of

the body as the hair, eye etc., which, according to 'Bhela', is due to Bhrajaka Pitta.

TWAK - MODERN CONCEPT (ANATOMY PHYSIOLOGY)

Derivation: (development)

The epidermis and its appendages are developed from the ectoderm. The

corium or true skin is of mesodermal origin. About the fifth week of foetal

development, the epidermis consists of two layers of cells, the deeper one

corresponding to the ratemucosum. The subcutaneous fat appears about the fifth

month, and the papillae of the true skin about the sixth month. A considerable

desquamation of epidermis takes place during foetal life, and this desquamated

epidermis mixed with sebacious secretion constitutes the vernix caseosa.

17

The nails are formed at the 3rd month and begin to project from epidermis by

the sixth month. The hairs appear between the third and fourth month in the form of

solid, down growths of the deeper layer of the epidermis. The central cells of the solid

down growth undergo alteration to form the hair, while the peripheral cells are

retained to form the living cells of the hair follicle. About the fifth month of the foetal

life hairs (lanugo) appear first on the head and then on the other parts, they drop

after birth and give place to permanent hairs. The cellular structure of the

sudoriferous and sebaceous glands is formed from the ectoderm where as the

connective tissues and blood vessels are derived from the mesoderm. All the sweat

glands are fully formed at birth, they begin to develop as early as the fourth month.

Microscopic anatomy of the skin:

Structurally the skin consists of two principal parts. The outer, thinner portion,

which is composed, of epithelium, is called epidermis. The epidermis is cemented to

the inner, thicker, connective tissue part called the dermis. Beneath the dermis is a

subcutaneous layer. This layer also called the superficial fascia or hypodermis,

consists of areolar and adipose tissues. Fibres from the dermis extend down into the

superficial fascia and anchor the skin to the subcutaneous layer. The superficial facia

in turn is firmly attached to underlying tissues and organs.

Epidermis

The epidermis consists of 5 layers, which are

1. Stratum corneum

2. Stratum lucidum

3. Stratum granulosum

4. Stratum spinosum (prickle cell layer)

5. Stratum germinatinum

18

Stratum corneum

This layer consists of 25 to 30 rows of flat, dead cells completely filled with

keratin. These cells are continuously shed and replaced. The stratum corneum

serves as an effective barrier against light and heat waves, bacteria, and many

chemicals. The epidermis contains no blood vessels, the nutrition being derived from

the capillaries of the dermis.

Stratum lucidum

This layer is quite pronounced in the thick skin of the palms and soles. It

consists of several rows of clear, flat, dead cells that contain droplets of a substance

called "eleidin". The layer is so named because eleidin is translucent. Eleidin is

formed from keratolyatin and is eventually transformed to keratin.

Stratum granulosum

It is about 3 cell layers thick and lies the stratum granulosum are very

important for keratin synthesis. The precursors of keratin take the shape of granules,

which are present within the cells of the stratum granulosum from which the name

has been derived.

Stratum spinosum

Is several (3to5) cells thick, the individual cells have a prickled appearance is

due to the fact that cytoplasmic processes come out from the individual cells to meet

their fellow cytoplasmic strands of the adjacent cells.

Stratum generminatinum:

The cells of the stratum germinativum continuously produce new cells by

mitotic division. These cells move continuously towards the surface side and on the

way receive a special material, called kertin, ultimately when the superficial most

19

surface is reached, the cells become dead and highly keratinized and constitute the

stratum corneum. Stratum germinativum cells are columnar and stand on the

basement membrane.

Dermis

The bulk of the dermis is made up of collagenous fibers. The superficial

portion of the dermis, makes inroads into the epidermis, and these inroads are called

papillae. These collagenous fibres are responsible for the water holding property of

the skin. The dermal capillaries, especially those of the papillae are responsible for

the nutrition of the epidermis. Dermis also contains nerve fibers and lymphatics.

Histologically, the dermis is often divide into two layers, viz., the papillary or

superficial layer and the reticular or deeper layer.

Appendages

Hairs

The hairs are of three types

Lanugo hair

Vellus hair

Terminal hair

Lanugo hair found in the foetal body including its scalp and eyelids. They

begin to develop at around 3rd month of intrauterine life. A few months after birth

these hairs shed off and are replaced by the vellous hair.

The vellous hair covers all thin skin, so that the vellous is the body hair of all

the infants and children. The terminal hair begins to grow at the age of puberty. They

replace the vellous hairs. Terminal hairs from the scalp hairs body hairs, axillary hairs

and genital hairs of the adult and are coarse and pigmented.

20

Sweat glands

Sweat glands are of two types

Eccrine

Apocrine

Eccrine glands are the common sweat glands, occurring all over the body, but

their population is most dense over the thick skin. An eccrine gland is basically a

simple tubular structure, which at the beginning in the deeper part of the dermis, is

highly coiled like a resting snake. The rest of the duct is straight coursing through the

superficial part of the dermis, then through the epidermis, ultimately opening through

the pore into the exterior. Sweat is synthesised by the coiled portion of the sweat

gland. Apocrine glands are found in the axilla and around the nipple of the breast.

They have apparently, some relationship with reproductive physiology. They begin to

function vigorously with the onset of puberty. Their secretion by it self is not odours,

but bacterial decomposition makes it odorous. To some extent the odours rather

characteristic of an individual.

Sebaceous glands

These glands usually open to the hair follicles but in the face they may open

into the exterior directly. The secretion of these glands is rich in oily substances. This

presents the evaporation of water from the skin and consequently present heat loss

from the body. Sebaceous glands develop from the hair follicles and therefore, they

are not found over the thick skin. The male harmone "dehydropepiandosterone"

(DHEA) stimulates growth of these glands, consequently, the acne develops

maximally at puberty.

21

Nails

Nails are composed of many layers of flattened keratinised cells fused into a

homogenous mass. Arising from epidermis nails glow 0.1 mm perday.

Functions of the skin:

Temperature regulation

Sence perception

Machanical protection

Water balance

In the skin and hair it is probable that melanin serves a protective action

against the harmful effects of sunlight. Prolonged exposure to sunlight stimulates

melanin formation and causes the so-called sun tanning. The function of melanin in

the choroid coat is mainly to convert the eyeball into a perfect dark chamber. Since,

nervous tissue is derived from ectoderm, the melanin in the substantia nigra may

represent the vestigial remnants of the melanin forming properties.

Skin colour:

The colour of skin is due to melanin, a pigment in the epidermis, carotene, a

pigment in the dermis, and blood in the capillaries in the demis.

The amount of melanin varies the skin colour from pale yellow to black. This

pigment is found primarily in the based and spinosum layers. Melanin is synthesized

in cells called melanocytes. The number of melanocytes is about it in allreces,

difference in skin colour is due to the amount of pigment the melanocytes produce

and disperse.

22

The pigment carotene is found in the stratum corneum and fatty areas of the

dermis. Together corotene and melanin account for the yellowish skin. The pink

colour of caucasion skin is due to blood in capillaries in the dermis.

The physiology of melanin pigment formation

Melanocytes are situated In between the keratinocytes of the based layer of

the epidermis.

Introduction

Epidermal melanocytes reside in the epidermal basal layer and synthesize

melanin within specialized organelles called melanosomes. The melanosomes are

taken up by neighboring keratinocytes. Within the keratinocytes, melanin acts as a

chromophore for harmful solar radiation and thereby protects the underlying

structures from the effects of this radiation.

Introductory Definitions14

• melanoblast - precursor to melanocytes and melanophores

• melanocyte - a cell that synthesizes melanosomes

• melanophore - a type of melanocyte that participates with other

chromophores in the rapid color change by intracellular redistribution of

melanosomes in some fish, amphibians, reptiles, and invertabrates.

• secretory melanocytes - distribute their melanosomes into neighboring cells

• continent melanocytes - retain their melanosomes within themselves, not

secretory

• nevocellular melanocyte (nevus cell) - a subtype of epidermal melanocytes

that are continent with their melanosomes

23

Melanocytes:

Melanin pigmentation in the skin in man is a dual process which involve not

duly the production of melanosomes within the melanocyte, termed melanogenesis,

but also the distribution and transfer of these pigment granules to surrounding

epidermal keratinocytes. Each epidermal melanocyte is surrounded by a group of

keratino-cytes with which it maintains functional contact, the whole being an

epidermal unit.

The number of active epidermal melanin units varies considerably in the

different regions of the body. The number of kertinocytes served by each Melanocyte

remains constant. This concept of the epidermal melanin unit is as a structural and

functional unit.

Origin of melanocytes:

It is accepted that the melanocytes are derived from the neural crest. Ultras

structural studies on early human embryos have shown the presence of melanocytes

in the epidermis by the eighth week of gestation and that by the tenth week these

cells contain melanosomes showing early melanisation.

Melanocytes in Development

Melanocytes are derived from melanoblasts in the ectodermal neural crest.

1. By 2 1/2 weeks gestation, melanoblasts migrate into mesenchyme and

differentiate into melanogonia.

2. By 8 weeks gestation, melanocytes are found in the epidermis.

3. By 10 weeks gestation, melanocytes contain melanosomes, first on the

eyelids, lips, and external auditory canal.

24

4. Melanin synthesis begins in the 12th week in the head epidermis, proceeds

cephalocaudally, and is everywhere by the 16th week (Lever).

5. Melanoblast migration seems to depend on the c-kit proto-oncogene which is

expressed on melanocytes, mast cells, germ cells, enteric ganglion

pacemaker cells of the intestine, and bone marrow stem cells15.

6. A 145 kDa membrane spanning receptor protein with homology to tyrosine

kinases, and the white (w) locus in mice.

7. Upon binding its substrate it dimerizes and autophosphorylates and activates

second mesenger pathways.

8. The second messenger pathway leads to increased TRP-1 and gp100/Pml

9. C-kit substrate is stem cell factor (SCF)/steel/melanocyte,mast cell growth

factor (MGF), KIT ligand

10. SCF protects stem cells and mast cells from apoptosis.

11. C-kit also seems to be important for adult melanocyte homeostasis since

soluble SCF injected into adult human skin xenografts on mice results in

increased size, number, dendricity, proliferation (Ki 67+), and activation

(TRP1, pmel17) of melanocytes16.

Melanocytes - distribution:

These melanocytes can be found in the superficial epidermis, hair follicles,

dermis around the blood vessels, peripheral nerves and the sympathetic chain, and

in the living of the coelomic cavity. In the basal layer of the human epidermis there

are about two billion melanocytes.

The differences in colour between Caucasoid, Mongoloid and Negroid skin

are due to the amount of melanin produced. Ultra structural studies indicate that skin

25

colour in the different races is largely determined by the packing distribution and

degradation of melanosomes within the keratinocytes. A reduction in the number of

melanocytes occurs in the skin with advancing age.

A. Melanocytes are found in selected body sites.

1. Melanocytes are found in the epidermis, mucosal epithelium, hair bulb matrix, hair

follicle outer root sheath, hair shaft cortex, uveal tract (choroid, retina, sclera), inner

ear (cochlea, stria vascularis), CNS (leptomeninges, substantia nigra, locus ceruleus,

dorsal root ganglia, cranial ganglia), and mesentery.

2. Melanocytes in the retina migrate from the optic nerve cap vs. optic cup of the

forebrain.

B. Distribution within the epidermis

Total adult epidermal melanocyte population is about 2(109) cells with a

volume of 1-1.5 cm3. There are only minor variations in melanocyte densities

between races17. There are no significant differences in melanocyte densities

between the sexes. There is variation by body site within each individual. This

variation is present at birth, but is less pronounced than in adults. The mean density

is about 1500 melanocytes / mm2. In adults, sun exposed skin (especially the head

and forearms) have approximately twice the melanocyte density as sun protected

skin (except the genitalia). There is an age-related decrease in melanocyte density of

6- 8%/decade in both sun exposed skin (especially the head and forearms) and sun

protected skin (except the genitalia).

The position and distribution of melanocytes is influenced by keratinocytes

since melanocytes are clustered, both basally and suprabasally, when cultured in

26

fetal skin equivalents, Whereas in neonatal skin equivalents they are singly

distributed along the basal layer only18.

Melanocytes undergo mitosis infrequently in unstimulated skin (thymidine

index 0.7% of melanocytes are labelled) relative to keratinocytes (thymidine index

15% of KCs), but are activated to divide in UV-stimulated skin (thymidine index 2.1%

of density in sun-exposed skin over sun-protected skin.

Sub-cellular structure of melanocytes:

1. Melanocyte has comparatively large nucleus.

2. Mitochondria and endoplasmic reticulum surround the nucleus. Mitochondria are

the organelle of the cytoplasm and consist of two sets of membranes - a smooth

continuous outer coat and a convoluted inner membrane arranged in folds.

Mitochondrion is the principal energy source of the cell and contains many

enzymes. Endoplasmic reticulum is a system of fine tubules concerned with

secretion.

3. Slightly away from the nucleus is seen the golgi membrane. By definition golgi

apparatus is a network of fine tubules adjacent to the nucleus of a cell, concerned

with intracellular formation of secretary products.

4. Also within the melonocytes are seen melanin granules. These differ from

melanosomes in being uniformly laden with pigment. Melanin granules also take

enzymatic activity.

1. Appear as clear cells resting on the basement membrane in the basal layer.

2. Small, darkly staining nucleus relative to basal keratinocyte nuclei.

3. Clear cytoplasm is partially the result of shrinkage/retraction (Lever), melanocytes

have fewer attachments

27

4. Vertical sections have a melanocyte: basal keratinocyte ratio 1:10.

5. Epidermal melanocytes are dendritic cells whose dendrites interdigitate among

neighboring keratinocytes within the malpighian (cell cycling) layer. Each

melanocyte provides melanin for keratinocytes within its "epidermal melanin unit".

On average, this consists of 36 neighbouring basal and spinous layer

keratinocytes. In sites where melanocyte density is lower, e.g. sun-protected

areas (except genitalia), their dendrites are longer and they supply more

keratinocytes. The opposite is true in sites where melanocyte density is higher.

6. The direction of melanocyte dendrite growth may be affected by the direction of

UV light since melanocytes overlying BCCs have dendrites oriented sideways,

toward the tumours, possibly because of ultraweak biophotons in the 210-330 nm

UV range emitted by these tumors19.

7. Melanin appears brown with H and E staining.

8. Special stains (Lever)

a. Melanin is argyrophylic. Silver stains, e.g. Fontana-Masson stain melanin.

b. Melanin can be bleached (oxidized) with hydrogen peroxide or potassium

permanganate, distinguishing it from iron.

c. The "dopa reaction" of fresh, unfixed tissue turns melanocytes brown from the

action of tyrosinase on dopa (3,4- dihydroxyphenylalanine).

d. Immunohistochemistry

i. S100+ cytoplasm, not specific

ii. HMB45+ cytoplasm, especially activated melanocytes, melanoma >

junctional components of some nevi > dermal components of some nevi.

28

Melanocyte Ultrastructure

A. General Features

1. No tonofilaments (cytokeratins)

2. Many mitochondria Well developed ER, golgi (for secretory functions), and

melanosomes.

3. Contain fine, cytoplasmic, 100 nm filaments that are apparently involved in

melanosome trafficing.

4. No desmosomes. No specific attachment structures to neighboring keratinocytes.

5. Melanocytes do use N-CAM and CAM-like adhesion molecules.

6. Have modified hemidesmosomes for basement membrane attachment. These

hemidesmosomes appear slightly smaller than those of keratinocytes.

a. Have a cytoplasmic dense plate attached to the inner leaflet of a trilaminar

plasma membrane.

b. Melanocytes have anchoring filaments extending from the outer plasma

membrane to the lamina densa.

c. There are no anchoring fibrils (collagen VII) below the lamina densa under

melanocytes.

d. There is no dense plaque below the lamina densa under melanocytes as

there is under keratinocytes.

e. The basement membrane below melanocytes often appears doubled or

"reduplicated".

1. Melanosomes are specialized spherical or ellipsoidal organelles that are the sites

of melanin synthesis and storage.

30

b. Stage II melanosomes.

i. Found in the cytoplasm. Round or oval, with longitudinally oriented filaments.

• Form by assembly of structural protiens with tyrosinase and post-tyrosinase

regulatory proteins.

• Structural proteins: about 15-16 polypeptides that are insoluble in non-ionic

detergents. One identified as a 94kDA precursor protein that is processed to a

53kDA species; this is probably the same protein precipitated by monoclonal

antibody HMSA-2.

c. Stage III melanosomes.

i. Found in the cytoplasm or dendrite. Round or oval, electron dense, melanin

partially obscures the internal filament network.

ii. Tyrosinase activity becomes positive (Melanization begins at this stage.)

d. Stage IV melanosomes.

i. Found in the cytoplasm or dendrite. Round or oval, electron opaque.

1. Formed by progressive melanization.

2. Eumelanogenesis vs. Pheomelanogenesis

3. Vesiculoglobular bodies (VGB) appear to be key units involved in organization

and melanization of melanosomes

4. VGB,s attach to inner lamellae of eumelanosomes, vs., fuse with each other

to form amorphous matrix of pheomelanosomes.

5. Under genetic control:

• Eumelanogenesis: 1) B gene = Brown = TRP-1 or DHICA oxidase 2) P gene =

pink-eyed dilution = tyrosine transporter

• Pheomelanogenesis: 1) A gene = agouti = MSH receptor antagonist 2) A^^ gene

• Golgi Complex: C gene = albino = tyrosine hydroxylase or DOPA oxidase

31

Biochemistry of Melanogenesis

A. Types of Melanin

1. Eumelanin

a. A stiff, rod-like molecule <10kDa.

b. The lamellar pattern of ellipsoidal melanosomes is due to parallel double helix

polymers of eumelanin and proteins.

2. Pheomelanin

a. UV exposure induces a high rate of decomposition and free radical generation,

particularly superoxide.

b. Has mutagenic properties by the Ames test.

3. Trichochrome

a. Pink pigment extracted from hair by hot sulfuric acid.

b. May not exist in normal skin or hair.

c. Related to pheomelanin in that it contains cysteinyldopas.

d. Has been found in the urine of patients with melanoma.

4. Oxymelanin

a. Reddish or yellow

b. Similar to pheomelanin but have low sulfer content.

c. Probably structural variants of eumelanins arising from postsynthetic

degradation.

5. Mixed-type melanins

a. probably combinations of eumelanin and pheomelanin.

29

a. Melanosomes are membrane bound and contain melanin as well as

approximately 15 types of protein (enzymes, structural proteins,

receptors, etc.).

b. Epidermal melanosomes are synthesized in the cytoplasm and

travel to the ends of dendrites.

1. The melanosome-containing dendrite ends are pinched off and endocytosed

by neighboring keratinocytes within the epidermal melanin unit.

2. There are 4 recognised stages of melanosome development that are

traversed as melanosomes travel from the cytoplasm to end of a dendrite.

a. Stage I melanosomes.

i. Found in the cytoplasm, spherical, 0.3 um, membrane-delineated organelle

containing unoriented filaments.

ii. Formed by the fusion of premelanosomes with "coated vesicles" and

"vesiculoglobular bodies" (aka 40 nm microvesicles).

iii. Premelanosomes are large blebs from the smooth or rough endoplasmic

reticulum that contains unoriented structural protein filaments.

iii. Coated vesicles, are small blebs from the cis golgi apparatus and contain

the enzyme tyrosinase and Lamp proteins.

iv. Vesiculoglobular bodies are small blebs from the golgi apparatus and

contain post-tyrosinase melanogenesis regulatory factors (e.g. DHICA

oxidase aka TRP-1, TRP-2 aka dopachrome tautomerase, and others - see

below).

32

6. Neuromelanins

a. Neuromelanins appear as brown/black cytoplasmic particles in selected CNS

neurons (ganglia, locus ceruleus, substantia nigra -> Parkinson's dz).

b. Accumulates with age until about 60 yo, then declines.

c. Neuromelanins are not affected by oculocutaneous albanism, suggesting that

they are not made by tyrosinase.

d. Ear melanin is affected by OCA which may lead to deafness.

e. May be derived from an aberrant or nonenzymatic oxidative pathway of

dopamine.

7. Urinary melanogens

a. Several melanogenesis intermediates and/or their metabolites are found in the

urine, presumably after secretion by or leakage from melanocytes.

b. Also found in variable amounts in the epidermis and various body fluids.

B. Enzyme Pathways

1. Melanin is formed by the sequential oxidation, both enzymatic and

autooxidation, and progressive polymerization of soluble tyrosine into insoluble

melanin.

2. Tyrosinase

a. A member of the tyrosinase gene family that also includes tyrosinase

related proteins TRP-1, TRP-2, and Pmel 17.

b. Is a marker for melanocytes. Locus is 11q14-21.

c. Catalyzes the rate limiting step in melanogenesis (as well as others).

d. A 67 kDa glycoprotein that has 4 isoforms based on its glycosylation

pattern;

33

i. Isoforms T1 and T2 are soluble.

ii. Isoform T3 accounts for 90% of tyrosinase activity and is

insoluble and bound to ER and golgi membranes.

iii. Isoform T4 is bound to melanosomes.

e. Catalyzes at least 3 reactions;

i. Cresolase or monophenolase activity - hydroxylation of tyrosine

to dopa (dihydroxyphenylalanine).

ii. Catecholase or diphenolase activity -

oxidation of dopa to dopaquinone.

iii. 5,6-dihydroxyindole to indole-5,6-quinone

f. Uses cofactors;

i. Copper (Cu2+), 2 atoms per molecule

ii. dopa - one of its substrates, is required for optimal activity.

2. TRP-1

a. aka DHICA oxidase

b. Contains a single transmembrane domain.

c. Only involved in eumelanogenesis, not pheo.

3. TRP-2

a. aka dopachrome tautomerase

b. Contains a single transmembrane domain.

c. Only involved in eumelanogenesis, not pheo.

4. Pmel 17/gp100

a. A member of the TRP family

b. Contains a single membrane domain

c. May catalyze the conversion of DHICA to melanin

34

5. Lamp Gene Family (lysosome-associated membrane proteins, at least 3

members)

a. Lamp-1

i. Contain a single transmembrane domain and coats the inner

surface of both lysosomes and melanosomes.

ii. Is highly glycosylated with both N- and O-linked

oligosaccharides.

iii. Acts in part as a scavenger of free radicals and other free

radical products generated during melanogenesis.

b. Lamp-2

c. Lamp-3, aka CD63

6. Peroxidase

7. Catalase

8. Glutathione metabolizing enzymes

9. Metal ions; Cu, Zn, Fe

C. Dopaquinone as the switchpoint/branchpoint between eumelanogenesis and

pheomelanogenesis.

1. Seems to depend on cysteine levels and on tyrosinase compartmentalization

into microvesicles/coated vesicles.

2. Under conditions of low intramelanosomal sulfhydryl compunds, e.g. cysteine

and glutathione, dopaquinone is converted to dopachrome and subsequently to

eumelanin.

35

3. When intramelanosomal sulfhydryl concentrations are high, cysteine is

conjugated to dopaquinone, making cysteinyldopas and subsequently

pheomelanins.

a. The same switch can be induced by metal ions; Cu, Zn, Fe.

b. Tyrosinase activity levels are lower during pheomelanogenesis than

eumelanogenesis.

4. Available evidence suggests that tyrosinase is present within the

microvesicles where it converts tyrosine to dopaquinone, which diffuses out of

the microvesicle into the melanoplasm to combine with cysteine to form

cysteinyldopa. Cysteinyldopa does not reenter the microvesicle but instead

forms pheomelanin in the melanoplasm, giving pheomelanosomes their

granular appearence.

D. Post-tyrosinase conversion factors

1. dopachrome conversion factor

a. increases conversion of dopachrome to DHI

b. associated with both soluble and insoluble tyrosinase

2. indole blocking factor

a. inhibits conversion of DHI to melanochrome

b. associated with only soluble tyrosinase

3. indole conversion factor

a. acclerates conversion of DHI to melanochrome

VI. Melanosome Transfer

A. Melanin/melanosome transfer is by "injection" secretion, aka cytocrine.

B. Melanosomes are transported on two systems20:

36

1. actin-based system via myosin V

2. microtubule-based system via kinesin (anterograde movement) or dynein

(retrograde movement).

3. Kinesin and dynein function as chemomechanical motor that converts ATP-

stored energy along the alpha:beta tubulin dimers within microtubules.

C. Dendrite tips are actively pinched off and phagocytosed by keratinocytes.

D. Within the keratinocyte, melanosomes are packaged into secondary lysosomes

containing,

1. single melanosomes if the melanosome is large (>1 um) as in blacks > asians

> American indians > whites.

2. melanosome aggregates if the melanosomes are small (<1 um) as in whites >

American indians > asians > blacks.

E. Secondary lysosomes form "supranuclear caps" over the basal cell and

spinous cell nuclei.

F. Nuclear caps give rise to "central clusters" of secondary lysosomes in

corneocytes (no nuclei).

F. Lysosomal hydrolases act on melanosomes as the host keratinocyte

differentaites through the epidermal layers.

G. Melanin is ultimately shed from the epidermis within corneocytes, after which it

resides on shirts in the form of ring-around-the-collar, or is ingested by house

dust mites.

VII. Regulation of Melanogenesis

A. Melanin is one of 4 basic pigments in the skin; yellow (carotinoids), red

(oxyhemoglobin), blue (deoxyhemoglobin), and brown (melanin).

37

B. There are 2 modes of melanin synthesis

1. Constitutive synthesis refers to the basal, unstimulated rate of

melanogenesis, e.g. that responsible for buttocks skin color.

2. Facultative synthesis refers to the induced or stimulated rate, e.g. following

UV exposure, hormonal stimulation, post-inflammatory, etc.

a. Reversible

b. Melanocytes on exposed surfaces are more responsive to UV-

induced pigmentation.

3. Skin color on most skin surfaces is due to the sum of constitutive and

facultative melanization.

a. UV-induced facultative melanization or tanning

i. Immediate pigment darkening (Meirowsky phenomenon). Best-seen in dark

skinned people, Does not involve new melanin sythesis or melanosome

transfer and can be seen in UV-exposed cadaver skin.

ii. Delayed pigment darkening

b. UV stimulates melanogenesis by: Increase production and

secretion of multiple paracrine factors by keratinocytes (Endothelin-1,

NGF, bFGF, alpha-MSH)

Activation of protein kinase C, leading to activation of tyrosinase.

Formation of photoproducts: repair of these photoproducts results in release of ss-

DNA fragments, which stimulates transcription of tyrosinase.

C. Genetics

There are more than 80 genetic loci that determine skin, eye, and fur colour.

38

D. Hormonal

1. MSH= melanocortin. Early experiments showed that injected alpha-MSH,

beta-MSH, and ACTH bind Melanocortin-1 Receptor, stimulating cAMP

formation, leading to increased melanogenesis. ACTH and beta-lipotropin

(LPH) are currently thought to be the only physiologically relevant pituitary

hormones.

• Alpha-MSH is not made in adult pituitaries because of lack of pituitary

intermediate lobe.

• Beta-MSH; There is little evidence that beta-MSH has any physiologic

function outside the CNS.

• Topical beta-MSH with UVR induce significantly greater pigmentation than

either agent alone (in guinea pigs).

• Estrogens and progesterone; seem to increase pigment during pregnancy,

but pigmentation is not effected by castration or menstrual cycles.

• Estrogens and progesterone interact with UVR to induce increased

melanization without melanocytic proliferation seen in melasma.

• Addison,s ds and Nelson,s ds are associated with elevated ACTH and beta-

LPH

Cytokines

In general increase melanocyte cAMP or decrease DAG.

1. Basic fibroblast growth factor (bFGF), made by keratinocyes, is a melanocyte

mitogen whose levels are increased 6-fold after UVR.

2. Many other candidates not well studied.

3. Other KC-derived factors

39

a. hepatocyte growth factor stimulates melano.

b. Insulin-like growth factor stimulates

c. endothelins, LTC4, LTD4 are mitogenic

d. TGFalpha and LTC4 stimulate migration

e. KCs and melanocytes make a POMC homolog (85%

homologus to pituitary POMC)21

1. KCs make basal and UV-induced or IL-1-induced alpha-MSH and ACTH22.

2. KCs also express an MSH/melanocortin -1 receptor (MC1-R)23.

Biosynthesis:

Melanin, whenever it is found, is formed in the local cells by the enzyme -

tyrosinase of melanase. The mother substance, upon which the enzyme acts, is a

tyrosine derivative (DOPA) believed to be formed in the adrenals.

Staring product of melanogenesis is tyrosine by the action of the enzyme tyrosinase,

tyrosine is converted to DOPA and then DOPA is converted to melanin as follows.

Turisubase DOPA oxidase +cu

Tirosine DOPA melanin

Possibly both the tyrosinase and dopa oxide activities are performed by one single

copper containing aerobic oxidase enzyme.

The whole process may be studied under following steps :

+02

1. Tyrosine DOPA DOPA – Quinone Tyrosinase 2. DOPA Quinone carboxy - 2.3 – dihydro –5,6 – dihydroxindole

2 carboxy –2,3 dihydro indole –5, 6 – quinone Melanin

40

1. Tyrosine is hydroxylated to dihydroxy phenylalanine that is DOPA

2. DOPA is then dehydrogenated to dopaquinone.

3. Dopaquinone is rerranged to form an indole compound 'leucodopa chrome'

4. Leucodopa chrome is decarboxylated and rearranged form 5-6 dihydroxy

indole.

5. 5-6 dihydorxy indole is oxidised to indole 5-6 quinone

6. indole 5-6 quinone gets polymerised and then gets linked to form melano

protien.

Melanin formation in both human and amphibian skin is augmented by the

hormone known as intermedin or melanocyte stimulating hormone (MSH) secreted

by the pars intermedias of the pituitary gland. Adreno corticotropic hormone (ACTH)

secreted by ant piluitary has melanocyte stimulating activity similar to MSH although

to a much lower degree. In addisons disease, ACTH is secreted in a large amount

and these is brownish - black pigmentation of the exposed parts of the skin, e.g.,

hands, feet etc and mucous membrane.

Melatonin, extract from bovine pineal gland, causes concentration of melanin

near the nuclei of melanocyte in frog, and as a result of this the skin becomes palar,

its exact role in human is not known.

"Albinism" - The defect in this congenital disease is lake of enzyme tyrosinase in

the malanocyte cells and so the pigment melanin is not formed, localized failure of

pigment formation might also occur, e.g., the eyes.

41

Dendrites:

These are branched tubular structures arising from the melanocytes. The

terminal ramification of this arborised collection of tubulus tends to form umbrella like

caps over the basal epidermal cells.

Keratinocytes:

Transfer of melanin to keratinocytes is not completely a passive process. It is

held that melanocytes, keratinocytes should be viewed together as an integrated

epidermal melanin unit.

Melanin accumulates as a supraneulear cap or distributed diffusely in the

cytoplasm of the keratinocytes. As the epidermal cells move out wards and

keratinize, the melanin granules progressively disorganise and very little remains in

the stratum corneum.

Synthesis and "movement" flow of melanin:

Melanin synthesis, along with the action of the MSH hormone which raises

the intra-cellular cAMP by increasing tyrosinase build-up, occurs as a consequence

of the latter's oxidative effect on tyrosine, which changes into DOPA and dopakinone

through the catalysing action especially performed by copper ions (Cu++). The

subsequent oxidative polymerization of 5,6-dihydroxyindoles completes the molecule.

When sun or artificial UV-rays strike the skin, they probably interact with the -SH

groups of cell structures by releasing hydrogen ions (H+) and electrons (e-), which

would bring copper to the monovalent state by increasing tyrosinase's activity and

therefore causing more intermediate products to be available to increment melanin

synthesis.

42

1. Ribosome is a tiny cell particulate rich in ribonucleic acid and the starting

site of protein synthesis in the cytoplasm. The first step in the direction is

that the polypeptides (amino acids) are synthesised on these ribosomes

of the endoplasmic reticulum.

2. From ribosomes through the endoplasmic reticulum polypeptides are

transferred to the golgi apparatus.

3. In golgi apparatus these polypeptides acquire a membranous envelope

and form the golgi vesicle. Within the golgi vesicle the tyrosinase is

condensed and oriented in a regular manner to form the pre-melanosome.

The golgi membranes thus justify being called as apparatus.

4. From the melanosomes are formed the melanosomes and these

melanosomes are having tyrosinase activity.

5. From melanosomes melanin granules are formed. Melanin granules are

amorphous and take enzymatic activity. Melanin granules may be viewed

as final product ready for transport.

6. Melanin granules enter dendrites, travel through these tubules and enter

keratinocytes of the basal cell layer.

7. In the keratinocytes of the basal cell, melanin granules either remain as a

supranuclear cap is distributed diffusely.

8. This consumer behaviour of the keratinocyte imparts the completion to the

skin. The visual colour of the skin is caused by this arrangement of the

melanin granules within the keratinocytes. In caucasoids the melanin

granules within the cytoplasm of the keratinocytes are arranged as a

supra nuclear cap. While in Negro skin, they are distributed diffusely.

43

9. From the keratinocytes of the basal cell layer, melanin gets carried to the

stratum corneum, by the progressive differentiation of keratinocytes,

through various layers. This has been compared a conveyor belt like lifting

action.

Excretion of melanin: excretion of melanin is effected by

Desquamation

Ingestion by chromophores

Transfer to lymph nodes

Kidneys and G.I tract

An analogy:

As an analogy melanocytes may be compared to a brick factory

1. Golgi apparatus is the machinery in the factory

2. The golgi vesicle, the premelanosome and the melanosomes are progressive

stages in the manufacture of a brick.

3. The brick powder is the melanin

4. While the melanin granule is a completely formed brick ready for transport

5. Dendrites are the transport vehicle.

6. Keratinocyte is the consumer who may seek these bricks in the store as a supra

nuclear cap or may utilise it peripherally and thus allow it to exhibit more

appreciably.

44

Movement flow of melanin

Ribosome of endoplasmic reticulum

Golgi vesicle

Premelanosome Melanosome

Melanin granules

Dendrites

Keratinicytes of the basal cell layer

Supraneuclear cap diffuse

Migration towards stratum corneum

Desquamation

Dhromatophores ingestion

Transfer to lymph nodes

G. I. tract and kidneys

45

NIDANA

The term "Kusta" in Ayurveda is used in wider sense. Most of the skin

disorders described by modern medical science are explained under the heading of

Kusta in Ayurveda. Ayurveda describes eighteen varieties of Kusta. Switra is not

considered as one out of them, but due to its resemblance to Kusta, it is described

along with kushtas by most of the authors, except Acharya Kasyapa, who includes it

in eighteen kushtas24.

Nidana from various texts

Nidana for Switra mentioned, in compact form various texts are as follows.

Charaka (In Chikitsa seventh chapter,)

Untruthfulness of speech, ingratitude, blaspheme against god, derision of the

elders, Sinful actions, acts of past lives and virudha anna are explained as etiology of

Switra25.

Susruta

Mithyahara - especially guru, virudha, asatmya and ajeernahara,

adhyashana, ahitahara, ahitachras like vyavaya immediately after intake of large

quantity of sneha or after vamana karma, in take of milk along gramya -anupa-

oudaka mamsa, immerse in cold water when body is too hot, suppression of vegas,

especially the vamana, sinful actions and acts of past lives also mentioned in Susruta

Samhita as Nidana26.

Vagbhata

mithyahara especially virudhas, mithyaviharas, papakarmas.

46

Madhava Nidana & Bavaprakasakara

Virudhaharas, drava, snigdha and guru aharas, suppression of natural vegas

especially of vamana, exercise and exposure to heat after the excessive intake of

foods, entering in cold water immediately after afflicted with fear exhaustion and heat,

regular intake of food when the previously taken is not digested, panchakarma

apachara, excessive intake of navanna, dadhi, matsya, mulaka, pishtanna, tila,

kshira, guda etc; vyavaya when food is not properly digested, daytime sleep derision

of teachers and papakarmas will make Switra to develop in the body.

Hareeta

Virudha pana, excessive guru and amla aharas, papodaka, divaswapna,

jagarana, papas and stealing of silver items27.

SAMPRAPTHI

Samprapthi is also called as 'doshadushya sammurchana'. The essential

factors for Samprapthi are Nidana, Dosha and Dushya strength of relation between

these factors decides severity of the disease28.

"Agni" and "Srothas" are the secondary factors in the production of the

disease (samprapthi), with the association of the above mentioned essential factors.

In a particular vyadhi Samprapthi the place of the secondary factors are-between

Nidana and Dosha. The secondary factor is Agni and between Dosha and Dhatu it is

Srothas. State of these secondary factors also has significance in the severity and

duration of a particular disease.

47

Nidana

Agni

Dosha

Srotas

Dushya

Vyadhi

Nidana: Discussed previously, which causes the vitiation of Dosha

Agni: According to all of Ayurvedic classics, mithyaharas regarded as the cardinal

causes among the all nidanas. Which causes the impairment (vikruti) of Agni, which

results in vitiation of Rasa and raktadi dhatu.

Dosha: Tridoshas - said to be involved in Switra

Srothas: Reference regarding the Srothas involved in Switra is not mentioned in any

texts, but the involvement of Srothas in Kusta mentioned in Astanga Hridaya29 as -

The vitiated Doshas moves towards the Rasa raktadi dhatus through

thiryaggatha sisras. The names of these siras or srothases are not mentioned.

Most of the Acharyas accepted the etiological factors for Kusta and Switra are same

as - kushtaikasambhavam switram.

Hence the above-mentioned Srothas involvement in Kusta may be acceptable

to Switra also. The thiragata siras mentioned in this reference should be the

"dhatugata srothases", and in case of Switra they extend only up to medodhatugata

Srothas, spreading of the Dosha starts initially through rasavahi Srothas only.

48

Dushya: Dhatus involved in the pathogenesis of Switra are Rakta, Mamsa and

Medas. Dushti of the Dhatus starts from Twak only and which leads to Rakta, Mamsa

and Medas in the course of the disease.

Pathogenesis (sammurchana):

As a result of indulgence and practice of the etiological factors, the Dosha get

vitiated and occupies the three Dhatus namely Rakta, Mamsa and Meda. As a result

Switra occurs.

The above involvement of tridoshas is termed as "Tridhatudbhava

samshrayam"30. This tridhatudbhava samshrayam leads to a bit of confusion for the

lesion of Switra is manifesting in Twak. The explanation is that, it is only the vitiated

doshas that are dislodged which in turn have got displaced in to the Rakta, Mamsa

and Meda Dhatu. In fact the Dhatus are not yet vitiated at this juncture.

There are different opinions of Brihatrayee in the layer of skin, in which the

Switra manifests. Charaka opinions that it is in third layer - "triteeya sidhma

kilasascha sambhavadhistana"31. While Susruta described in fourth layer - tamra32.

Susruta described seven layers of skin, while Charaka six only. More over the

diseases that are occurring in the first three layers of skin described by Susruta

occurs in the third layer of Charaka. 'Gangadhara' has commented that third and

fourth layer of Susruta are to included in the third layer of Charaka's description. This

makes it clear that it in the third layer where Switra manifests.

Incase of the etiological factors if practiced even at this juncture it invariably

leads to the vitiation of the Rakta, Mamsa and Meda Dhatus. When this is

accompanied with 'srava' it is called Kusta. For the definite factor 'aparisravi' signs of

Switra exists no longer. 'vishwamitra' has also stated that when kilasa having crossed

49

the dermal layers (Twak) invades the deeper tissues (dhatus) should be accounted

as Kusta.

There are some conditions where the Dosha concentrated in one of the three

Dhatus alone33. According to ' Hareetha Samhita', Pitta is the main Dosha in Switra,

which vitiates Rakta and causes Switra Kusta with the help of motive force Vata.

Predominance of vatadi doshas in raktadi dushyas mentioned in Astanga Hridaya34

and other texts35.

Vata pradhanyata in - rakta dhatu

Pitha pradhanyata in - mamsa dhatu

Kapha pradhanyata in - medo dhatu

Sankya samprapthi : Discussed previously.

Vikalpa samprapthi : though it is annipathika vyadhi

Ekadoshaja bhedas are also mentioned as vatika, paithika and kaphaja.

Pradhanya Samprapthi:

In all of the Ayurvedic texts Switra is described as a swatantra roga. But

according to modern concept it may be associated with intestinal parasites,

nutritional deficiencies and liver disorders etc.

Bala Samprapthi:

It varies according to the state of Nidana, dosha and dushya in each case.

Kala Samprapthi

Vyadhi kala is not described.

50

Purvarupa:

Purvarupa is the lakshana or group of lakshanas that indicates the disease to

be manifest. Purvarupa precipitate due to the doshadushya sammurchana in the

sthana samsraya stage. Purvarupa of Switra is not mentioned Ayurvedic texts.

RUPAM

It is the stage of a disease where the signs and symptoms of a manifested

disease exposed clearly. In Switra the general symptom is the appearance of swetha

varna mandalas that is depigment patches or macules.

The lakshanas mentioned in various texts, according to Dosha involved.

Text Dosha Lakshana

Vata Mandala, aruna, parusa, paridwamsi

Pitta Padmapatra varna, daha

S.S

Kapha Swetha, snigdha, bahala, kandu

A.S Vata Rooksha, aruna

A.H B.P Pitta Tamravarna, daha, romadwamsi

M.N Kapha Swetha, ghana, guru, kandu

(S.S - Sushruta samhita, A.H - Ashtaga hridaya, A.S - Astanga sangraha, B.P- Bhava prakasha, M.N - Madhava nidana)

Charaka does not differentiate the particular Dosha lodged in each Dhatu,

even though variability in degree of vitiation is mentioned. Rupa mentioned based on

the Dhatus in which Dosha are lodged36.

Rakta dhatu - rakta varna

Mamsa dhatu - tamra varna

Medo dhatu - sweta varna

51

In Hareeta Samhita rupa of Switra explained according to Sadhaya and

Asadhya bhedas of Switra.

Asadhya lakshana - Eeshad rakta panduta, sarvanga chira, snigdha.

Sadhya lakshana - peetachavi, pandu, ruksha,

Clinical features in various texts

S.No Lakshana C.S S.S A.H B.P M.N H.S

1 Sweta varna + + + + + +

2 Rakta varna + + + + + +

3 Tamra varna + + + + + -

4 Rookshata - + + + + +

5 Parusha - + - - - -

6 Daha - + + + + -

7 Kandu - + + + + -

8 Romadwamsi - + + + + -

9 Ghanam - + + + + -

10 Bahalam - + - - - -

(C.S - Charaka Samhita, S.S - Susrutha Samhita,A.H - Ashtanga Hridaya B.P - Bhava Prakasha, M.N - Madhava Nidana, H.S - Harita Samhita)

Classification of Switra

Vitiligo is an organ specific autoimmune disease of the skin characterised by

the development of well-circumscribed white macules associated with local

melanocyte loss37.

Most of the Acharyas in Ayurveda mentioned the Switra varieties as three

only. All the authors of Brihatrayee and Laghutrayee mentioned three types of Switra.

But according to Kasyapa it is of five types. Bhoja described two types, doshaja and

vranaja. In Harita Samhita it is mentioned as two types sadhya and asadhya.

52

Samhita

Classification by Charaka is based on the colour that in turn is depending on

the Dhatugata - Dosha38. Charaka opines that daruna, Aruna and Switra are the

synonyms of Switra and also are three types it self, tridiscordance in origin.

When Dosha dislodged in Rakta

Rakta varna Daaruna

When Dosha dislodged in Rakta Mamsa

Tamra varna Aruna

When Dosha dislodged in Rakta Medas

Sweta Switra

Vagbhata classified the Switra with direct relation of Doshas with

Dhatu39. Susruta40 followed the classification of Charaka with Tridosha

predominance.

Bhoja41 describes as Dohsaja and vranaja groups of classification, in which

Doshaja has been further classified into Atmaja - vitiation of the Vatadi Dosha as a

result of the indulgences of the person himself and paraja - by the contact with others

in whom the entity already exists. Varanaja refers to the discoloration that is

introduced in to the normal skin as a result of a scar tissue due to the healing of a

wound or as a result of burns - cicatrix.

Switra bhedas - various Acharyas

S.no Text Verities Names 1 Charaka Samhita 3 Daruna Aruna Switra 2 Susruta Samhita 3 Vataja Pittaja Kaphaja 3 Astanga Hridaya 3 Vataja Pittaja Kaphaja 4 Harita Samhita 2 Sadhya Asadya 5 Kashyapa Samhita 5 6 Madhava Nidana 2 Doshaja Vranaja 7 Bhava Prakasha 3 Vataja Pittaja Kaphaja 8 Sarngadhara

Samhita 3 Vataja Pittaja Kaphaja

53

Since long time researching several medicinal plants and their active

principles I picked-up those that could help in the toxins elimination, but also those

that could achieve balance in the function of organs that are responsible for

metabolization and excretion of these toxins.

Switra

Doshaja Vranaja

Paraja Atmaja

VYAVACHEDAKA NIDANA

Though the Nidana are same for the disease Switra and Kusta (M.N 49-37),

the lakshanas differ, and hence they are given in a tabular form.

Switra Kushta

1 Usually one dosha predominates All the three doshas are involved

2 Only three dhatus(rakta,mamsa,and

medo)are affected

All the dhatus may affected

3 Confines to the skin only (tamra-4th layer) Confines to the fifth layer of the

skin(vedhini)

4 It is of krimirahita Krimisahitam (may be)

5 It is non-infectious and non-contagious It is contagious on prolong contact

6 No destruction of dhatus occurs Destruction of dhatus may occurs

7 No loss of sensation in the lesion There may be loss of sensation in

8 No secretion occurs Often secretion is present

9 It is non-hereditary Found occasionally hereditary

54

SADYASADYATA

The disease Switra is told as krichrasadhya roga in most of the texts and as

asadhya in only the text "Kashyapa Samhita". The krichratva becomes more and

more in raktagata, Mamsagata and medogata respectively42.

In early stages, where the hairs of the patches are not turned into white

colour, which are not extensive. Not compound and not caused by burns are told as

'sadhya'. Patches opposite to these conditions and which are appeared in genital

area, palms, soles and lips, even if they are not short duration or of long duration are

mentioned as "asadhya".

VITILIGO - MODERN ASPECT

It is an idiopathic, acquired, localized or disseminated depigmentation of the

skin. Vitiligo, which though world wide in distribution, is most common in India, Egypt

and other tropical countries. Incidence of this disease is about 1-2% of the world

population.

It is a source of great social embarrassment and serious cosmetic problem to

dark skinned people. Even though it is not contiguous, common people

misunderstand that fact, which arouse mental problems. Victims especially females

feels social degradation. It is effects all age groups with no predilection to either see.

Many cases start at the ages of five to fifteen and at menopause.

ETIOLOGY

It is accepted that Vitiligo is a multi factorial melody. The various operative

factors in the genesis of Vitiligo are as below -

55

These various factors are enumerated and discussed in order of their sequence

in the pathogenesis.

1) Nutritional deficiency

a) Theoretically a diet poor in proteins particularly tyrosine can contribute to

the causation of Vitiligo.

b) Deficiency of B complex factors particularly thiamin, Riboflavin,

Pyrodoxine, Pantothenic acid and Folic acid is supposed to be casually

related to Vitiligo.

2) Amoebiasis - intestinal parasites: These are said to be responsible for Vitiligo by

interfering with the absorption of nutrients and by producing toxins.

3) Liver functions deficiency: By impairing detoxification of toxins is supposed to be

responsible for Vitiligo.

4) Achlorhydria: there are stray reports indicating achlorhydria to be a cause of

Vitiligo.

a. Deficiency of MSH

b. Other hormonal factors

c. Vitamin C d. Heredity e. Copper deficiencya. Nutritional deficiency

b. B – Complex deficiency c. Amoebiasis d. Liver function deficiency e. Achlorhydria

Tyrosinase Tyrosine DOPA

melanin

Neural concept melatonin

Exhaustion of melanocytes

Autoimmune mechanism

♦ Rubber friction ♦ Chemicals

56

5) Endocrinological factors :

Amongst endocrinological factors anterior pituitary is possibly the most important.

Intermediate lobe of pituitary secrets "melanocyte stimulating hormone"(MSH).

This MSH stimulates melanin formation and dispersal. Except MSH other

hormonal factors have a much less significance in the causation of Vitiligo.

Association between hyper thyroidism and Vitiligo is noticed many times.

ACTH and MSH have some structural similarity and slight functional overlapping.

Anterior Pituitary

Pancreas Thyroid MSH Adrenal Gonads Para Cortex Thyroids

Malanocytes

Oestrogen increases melanin synthesis and quantity of free melanin.

Progresterone is supposed to potentiate pigmentory action of oestrogen.

Androgens do not have any significant action on pigmentation.

6) Vitamin - C :

a) It increases tyrosine decomposition capacity of liver

b) It increases level of sulphydryl compounds in the tissues.

c) As a bio catalyst, by its reducing action it inhibits melanogenesis

d) Vitamin - C has a direct fading action on the formed melanin as a result of

these modes of action vitamin C appreciably depresses synthesis.

57

7) Copper deficiency: serum copper studies in Vitiligo by different workers show

conflict results. Thus copper deficiency may cause the Vitiligo.

8) Heredity: By definition only Vitiligo is an acquired disorder. A distance clear-cut

inheritance is normally never seen in Vitiligo. However, in many cases Vitiligo of

family history of the disorder is appreciably noticeable. No specific gene for

Vitiligo has been located. The disorder might be due an inform error of

metabolism.

There is no proof of its being hereditary

Nearly 40% of cases give a positive family history

Inheritance is probably determined by an autosomal gene of variable penetrence

9) Auto -immune mechanism: Antibodies against melanin have been isolated, from

the serum of Vitiligo patients. On this background Vitiligo has been claimed to be

an autoimmune disorder.

10) Neural concept: According to this theory in Vitiligo peripheral nerve endings

secrete cytotoxic substances. (Ex; melatonin). These cytotoxic substances have

a damaging or destroying action on melanocytes. This neural concept is

particularly useful in explaining segmental and unilateral occurrence of Vitiligo.

11) Melanocyte exhaustion theory: According to some workers graying of the hair and

Vitiligo are similar processes. Due to the continuous strai of producing melanin,

the melanocytes get tired and exhausted. Exhausted melanocytes fail to produce

the required quantity of melanin and Vitiligo results.

12) Drugs - chemicals: Like quinones, guanofuracin, amylphenol, chlorthiazide,

broad-spectrum antibiotics, and chloroquin may initiate Vitiligo.

58

13) Miscellaneous factors: Constant rubber friction, pressure, and trauma light

wearing of sarees and dhotis can precipitate the Vitiligo lesions.

Causes of localized hypopigmentation

Disorders Distinguishing features Vitiligo Destruction of melanocytes, common, acquired, multiple sharply

defined non-pigmented patches anywhere. Pityrias isverscicolor Superficial fungus infection leading to disturbance in pigment

production, common, multiple pale scaling patches on trunk. Pityriasisalba Mild patchy eczema of the face in children causing a disturbance in

pigment reductions. Leprosy One or several paler macules on trunk or limbs that are

hypoaesthetic. Albinism Congenital stationary disorder, distribution may complete or partial.

Hairs and eyes may be affected. White macules of tuberous sclerosis

Uncommon development of anomaly affecting CNS connective tissue and skin, several maple leaf shaped hypo pigmented macules.

Post inflammatory After inflammatory skin disease (often eczema) or trauma to the skin, irregular in shape and in depth of pallor.

Naevus anaemicus Rare developmental solitary white patch usually on trunk thought to have a vascular basis.

Chemical toxicity May took very like Vitiligo, seen in workers in the rubber industry exposed to paratertiary benzyltoluene.

CLINICAL FEATURES: APPEARANCE

Completely depigmented macules and patches of varying sizes and shapes

characterize it. Besides loss of colours, there is no other structural change. The

depigmented areas are paling white or slightly pink and ill defined at the start of the

disorder. In doubtful cases, the pigmentation can be made to appear more distinct by

pressing the patch with a glass side. This pressure momentarily obliterates the blood

supply and hence the depigmentation stands out more prominently. In early doubtful

cases examination under "woods lamp" is also helpful.

Often the depigmented patches are symmetrical, especially when the disorder

is distributed over the peripheral parts of the limbs and the face.

59

The border: A rim of hyper pigmentation generally lines the border of the

depigmented patch. It looks as the pigment is removed from the patch and is thrown

at the periphery.

Hair on the patch: Hair may or may not become depigmented in vitilliginous areas.

Presence of depigmented hairs (leucotrichia) or a patch is a strong point in favour of

the diagnosis of Vitiligo.

Distribution - lesions: Distribution of the lesions is determined by the supply and

demand behaviors of the pigment commodity. Whenever there is scarcity of any

commodity two diagonally opposite areas suffer most thus;

1) Peripherally situated, badly supplies areas, which are even normal at a critical

level of supply with little or no stored material, suffer commonly. Hence

mucocutaneous junctions. Finger tips, palms, soles and toe lips are commonly

involved in any extensive Vitiligo.

2) Areas where the consumption rate is normally very high suffer most in any

scarcity or pigment commodity. Pigmented like nipples, scrotal skin, scalp

(because of hair) and moles are also commonly involved in any extensive Vitiligo.

Clinical forms

a) focal

b) segmental

c) acrofacial - lip-tip

d) generalized

60

Common lesions:

a) scalp

b) retro-auricular folds

c) upper eye lids

d) lips

e) finger tips, palms

f) nipple

g) waist

h) scrotum, glands

i) legs

j) Toe tips and soles.

Often the depigmented patches are symmetrical, especially when the disorder

is distributed over the peripheral parts of the limbs and the face.

Zosteriform Vitiligo - lesions develop along the distribution of a peripheral nerve.

Halo neavus (sutton's nevus) - a related disorder in which the depigmentation begins

around one or a few compound naevi.

Occupational Vitiligo (Oliver): it is seen on the dorsum of the hands of tannery

workers caused by the use of rubber gloves containing agerite alba. Monobenzyl

ether of hydroquinone (MBEH), The chemical gets dissolved by sweat and acts on

the melanocytes in such away as to interfere with the formation of malanin. In early

cases, depigmentation may disappear spontaneously.

The onset of this disorder is slow and the course insidious but enigmatic. It

may continue to increase slowly or come to a halt and then increase again. There

may be spontaneous recovery in very small percentage of cases. This malady starts

and much more noticeable in the summer.

61

Classification: Vitiligo has been divided into three stages

a) active progressive stage

b) quiescent stage

c) repigmenting stage

Clinical criteria for classification of Vitiligo

Stages of Vitiligo Clinical feature Active stage 1 New lesions developing 2 Lesions increasing in size 3 Border ill - defined Quiscent stage 1 No new lesions developing 2 Lesion stationary in size 3 Border hyperpigmented and well defined Improving stage 1 Lesions decreasing in size. 2 No new lesions developing 3 Border defined and signs of repigmentation

(follicular and peripheral) Zosteriform Vitiligo 1 Unilateral distribution of lesions, preferably

along the course of nerves. Clinical associations - Vitiligo:

1. Cutaneous

a) premature graying of hair

b) halo naevi

c) alopecia areata

2. Systemic

a) thyroid disorders

b) Diabetes mellitus.

c) Addisons disease

d) Pernicious anemia

e) Multi endocrinopathy syndrome

f) Oculo and auditory abnormalities

62

PATHOLOGY

a) A defect in enzyme tyrosinase is held responsible for Vitiligo. According to some,

"melatonin" a substance secreted at nerve endings inhibits tyrosinase, thus

interfering in pigment formation.

b) The Vitiligo appears to be due to an immunological attack on the melanocytes.

This would suggest that Vitiligo is an autoimmune disorder.

Histopathology

The essential feature is absence of melanin pigment. There are no other

histological changes. The area surrounding the white patches shows increased

pigmentation and the blood vessels hair follicles and glands are surrounded by

pigment cells.

The skin on the whole looks normal, melanocytes are not much reduced in

number with normal shape (appearance). But when the skin is incubated with DOPA

reagent, the melanocytes take smooth homogenic colouration, which indicates that

there are inactive melanocytes. Activity of melanocytes is indicated by their granular

appearance. Vitiligo is a functional and not a structural anomaly

Diagnosis:

1) History

2) Clinical features

Wood's lamp - are of great help in diagnosis of Vitiligo.

63

DIAGNOSTIC CRITERIA43

1. Medical history: Evaluation and diagnosis of Vitiligo require obtaining the

following information:

1. The age of onset of the white spots; Vitiligo rarely begins before the age

of 6 months.

2. Family history of Vitiligo and early graying of the hair (i.e., significant loss

of hair colour before the age of 30 years)

3. Inflammation, irritation, or rash preceding the white sports.

4. Potential precipitating events including emotional stress, physical illness,

sunburn, or other forms of cutaneous forms occurring within 2 to 3 months

prior to the onset of de pigmentation.

5. Personal stress to the patient resulting from the disease

6. Ocular or auditory dysfunction.

7. Previous forms of therapy, either systemic or topical, how the therapy was

prescribed, and the effects or toxicity of the treatment.

8. Stability or progression of the disease.

9. Allergies and personal family history of atopy.

10. Occupational hazards and hobbies to define chemical exposures that

might be responsible for chemically induced Vitiligo.

11. Personal or family history of associated diseases including thyroid

disorders, premature graying, alopecia areata, diabetes mellitus, collagen

vascular diseases, permicious anemia, and addision’s disease; personal

history of other disorders aggravated by photoexposure or of

photosensitivity.

64

2. Physical examination

The diagnosis of Vitiligo is based exclusively o the clinical examination of the

patient. The physical examination includes the following findings; the presence of

acquired asymptomatic depigmented macules or patches, usually without clinical

signs of inflammation. Hypopigmented lesions may coexist with depigmented lesions.

Such trichrome lesions are often observed in individuals with darker skin. Trichrome

Vitiligo is characterized by depigmented, hypopigmented, and normally pigmented

skin. About 2% to 5% of patients may exhibit one or more depigmented lesions with

dermatitic /inflamed borders.

Vitiligo lesions may be found in any area of the body. The initial lesions are

frequently found on the hands, forearms feet, face and lips. The borders of the

lesions are usually discrete and well defined.

The distribution of skin lesions, the number, and the approximate surface area of

the integument involved by de pigmentation should be determined in order to

establish the baseline extent of the disease. Some investigators classify Vitiligo into

two groups —generalized and segmental. Others subclass generalized Vitiligo into

three subcategories;

1. Generalized – symmetric marcules or patches occurring in a random

distribution over much of the body; acral/acrofacial—depigmented

macules or patches confined to the extremities and /or face;

focal/localized—isolated macules or patches on one or two sites of the

body.

65

2. Segmental---Vitiligo restricted to one portion of the body such as one leg,

one portion of the trunk, or the face. The lesions are rarely if ever

distributed in a dermatomal pattern.

Other important physical findings include acquired depigmented hairs within a

vitiliginous region and poliosis of scalp hair, eyelashes, eyebrows, and/or beard hair.

Agreas of hypopigmentation and hyperpigmentation of the choroid and retinal

pigment epithelium may be evident by ophthalmologic examination. The presence or

absence of uveitis also should be determined. This examination is best done by an

ophthalmologist. Referral to an ophthalmologist is of particular importance if the

patient has complaints of photophobia, decreasing visual acuity, or poor night vision.

For patients with fair skin, such as those with skin types I and II, detection of

depigmented or hypopigmented patches of Vitiligo may require the use of a wood’s

lamp to delineate the areas of involvement. In-patients with darker skin, a wood’s

lamp examination also can be helpful to assess the degree of hypopigmentation or

depigmentation in individual lesions.

Diagnostic tests

In most instances the diagnosis of Vitiligo is based on the history and physical

examination. However, I some instances additional diagnostic tests may be indicated

to differentiate Vitiligo from conditions that may mimic it clinically. These conditions

include piebaldism, nevus depigmentosus, nevus anemicus, postinflammatory

depigmentation hypopigmentation, pityriasis alba, tinea versicolor, discoid lupus

erythematosus, and scleroderma. In addition, certain tests are sometimes helpful to

detect the presence of associated systemic disorders such as thyroid disease,

66

pernicious anemia, diabetes, or Addison’s disease. Some useful tests include the

following.

1. Biopsy from the border stained with fontana Masson technique to

differentiate Vitiligo from some of the aforementioned conditions.

Melanocytes are decreased in the early stages of Vitiligo. As the disease

progresses, they are completely absent. Other changes include basilar

vacuolopathy, exocytosis of lymphocytes,spongiosis, and

lymphohistiocytic infiltrates, especially in inflammatory Vitiligo. For most

patients a biopsy is not necessary

2. Baseline blood chemistry may include a complete blood count, a

differential with erythrocyte sedimentation rate, and thyroid function

studies including thyroid stimulating hormone. In addition, tests for

antiparietal cell, antithyroid (thyroglobulin and microsomal), and

antinuclear antibodies are frequently indicated. These tests are more

important if signs or symptoms of endocrine disease or collagen vascular

disease are present. Abnormal test values should be followed clinically or

by laboratory examination as indicated.

3. If patients are to undergo photo chemotherapy, a baseline ophthalmologic

examination and antinuclear antibody determination are advisable. Some

physicians recommend a repeat of these tests at 6- month intervals. Other

at 12 month intervals while on PUVA therapy.

Inappropriate diagnostic tests include serum alpha-MAS levels, serum ACTH

levels, hair analyses, and trace metal analyses.

67

Differential diagnosis of Vitiligo

Causes for localized de pigmentation of skin: In many countries the fear of

leprosy makes differential diagnosis of a "white patch" an urgent and vitally important

issue.

Examination of the skin in long wave UVR helps distinguish whether these is

total de pigmentation (as in Vitiligo) or not. It may also detect areas of

depigmentation not easily seen in ordinary daylight as well as detecting a lemon-

yellow fluorescence seen in some cases of pityriasis versicolor.

68

CHIKITSA - KARMA

The description and various treatments for Switra mentioned in almost all the

Ayurvedic texts along with kushtas. Same general principles of treatment for Kusta

and Switra are similar. But the number of special preparations only for Switra is

available in many texts.

Which means, Switra is more complicated disorder than all types of kushtas,

which becomes incurable within small period of duration. The Chikitsa is advised as

soon as possible in this disorder, which is compared with a - "Burning building" which

needs a fast management.

Switra is a dosha-karmaja vyadhi. With this fact the treatment methods for

switra can be adopted under three headings - Daivavyapasraya, Yuktivyapasraya,

and Satvavajaya chikitsas.

Daivavyapashraya Chikitsa

The generally mentioned diavavyapasraya chikitsas for Kusta and Switra -

practice of vrata-dana-yama, tyagasheelata, friendship and mercy to all kinds of

beings, worship of brahmins-devas-guru, shiva and bhaskara aradhana etc, which

cure the effect of papakarmas44.

In Charaka Chikitsa 7th chapter mentioned as the shodhanadi other Chikitsa

karmas and above mentioned daivavyapasraya karmas (which relieves the effect of

papakarmas) together will give good prognosis.

Satwavajaya Chikitsa:

Controlling of the manas from ahita indriyarthas i.e., from causative aharas

and viharas for Switra. It is also named as Nidana parivarjana, which also plays a key

role in Chikitsa.

69

Yuktivyapasraya Chikitsa45

The person is made to undergo all types of shodhanas. Then once again is

made to drink malapurasa with guda to his capacity, which is preceded by oleation

and then made to expose to sunrays (suryapada santapam) as long as he can. This

drink will have a purging action. The procedure is repeated for three consecutive

days.

On doing so there may be formation of blisters on the regions of Switra. The

blisters so formed should be punctured with badara kantaka and the fluid allowed

oozing out completely. When undergoing this line of treatment he must be given to

drink the decoction prepared out of bark of malapu, asana, priyangu and satapushpa

taken in equal quantities, or palasa kshara along with phanita taken according to his

capacity.

Whatever else non-curative of Kusta in general is beneficial if taken with

khadirodaka. Internal usage of only khadirodaka is like wise beneficial46. The patient

should expose to sunrays and when blisters forms he advised to take food with takra

(nirlavana). Vagbhata also tells internal administration of gomutrarista47.

Bahiparimarjanam:

There are so many topical lepas prescribed in various texts. Some of them are as

below -

1. manahsiladilepa - manahsila, vidanga, kasisa, rochana, kanakapushpi and

saindavam.

2. Kadalikshara+burnt bone of donkey in cows blood.

3. Nilotpala, Kusta and saindavam in elephant urine.

4. Mulaka beeja and bakuchi-paste.

70

5. Kakodumbara, bakuchi seeds and chitraka in cows urine.

6. Manahsila in peacock bile.

7. Udayadityarasa.

8. Putikaranjadilepa.

9. Bakuchi with one fourth of talaka in cows urine.

10. Bringaraja, haridra, doorva, ajaji, vidanga, tila, chitraka, harichandana in cows

urine.

11. Bakuchi, karanja, jyothishmati taila in equal quantities.

12. Bakuchi seeds, laksha, cow-bile, anjanadwaya, long piper and kalaloharajah.

Shastrapranidhanam

In Charaka Samhita Chikitsa 7th chapter the raktamokshana is mentioned as

a part in treatment of Switra. The above mentioned shonitamokshana supports the

Switra as raktadushtiyanaya roga48.

Even though vamanarechanadi shodhanas, shonitamokshana, virukshana

and intake of saktu are done carefully, swithra can become sadhya only to those

persons whose effect of papakarmas are cured completely with vrata, dana,

dharmadi karmas.

PATHYAPATHYA

As the Nidana factors mentioned it for both the Kusta and Switra in almost all

Ayurvedic texts. Hence the pathya apathyas for both disorders may appear similar

(almost) with each other49.

71

a) Ahara : Atilavana - atiamla padartha sevana, dadhi, ksheera, guda,

anupamamasa, tila, masha, vasa, kulutha, nishpava, lkshu, pistavikara, virudha -

adhayasana, ajeerna, vidaha - abisyandahara etc.,

b) Vihara : Diwaswapna and vyavayam

Above mentioned dravyas and causative factors mentioned for swithra are said to be

apathyas in kishta as well as in swithra.

Pathyas in Kusta: the following are indicated as usual ahara, achara - vibhaga for

are who suffers from Kusta.

♦ Ahara: Shashtika shali, koradushaka, uddalak, mudga, adaki,

peya, tiktasaka, jangala mamasa, saktu sevana, pachagavya

sataa sevana.

♦ Ausadha: Avalguja, nimba, arushkara, aragwada, chakramarda,

palasakshara, atarusha, mandukaparni and khadira - their various

preparations.

♦ Vihara: Vrata, dwija-sura-gurupuja, bhaskararadhana,

ravivaravrata, dana dharma, tyagasheelata, goseva and

satyadharmata etc.

Modern view of treatment

As a border organ, the skin is crucial for the body's homeostasis, to which it

contributes through a number of particles specialized in receiving stimuli and

forwarding them to the central organs of the nervous system. Along with these, there

is a special family of receptors, the melanocytes, whose task is to react to the light

stimulus by synthesizing a special protein, melanin, constituting the most important

skin-protection factor.

72

Local treatment:

For understanding the role of local treatment, it is necessary to realize that -

1. Systemic treatment is like "feeding a horse with nutrients and attending to its"

general well being while

2. Local treatment is merely like "mild irritation and stimulating the horse with a

whip" irritation through the local therapy should be started at the lowest intensity

and should be gradually increased to reach the optimum level.

Topical preparation

Bauchi oils

Bauchi preperations

Ludermol oint/oil

Manaderm oint

Psoralen oint/lotion

Ammi majus preparation

Meladinine or melanocyl oint/lotion

Synthetic preparations

Neopsoralen lotion (TMP)

Macsoralen lotion (8 MOP)

If excessive irritation after local applications poses a problem, the duration of

the exposure is reduced. Alternatively in similar situations, diluting can also reduce

the strength of the topical preparations. For eyelids, lips and genitalia topical

preparations are normally required to be sufficient diluted.

Local applications should not be carried right up to the outermost border of a

patch. Should always be kept uncovered by local applications. If this precaution is not

followed, the normally hyper pigmented living border of a patch becomes still more

73

hyper pigmented and the colour contrast between the Vitiligo patch and the normal

skin becomes unnecessarily more obvious.

If any time, extreme erythema and visculations appear as an untoward

reaction of a topical preparation, the application should be suspended for some

weeks. Soothing creasm, para-amino benzoic acid creams or topical corticosteroid

preparations should be applied on the inflamed areas.

Tanning, specific effect of U.V light

The increased melanin pigmentation of human skin following exposure to

sunlight or to U.V light from various sources is known as tanning. Two separate

reactions are recognised immediate pigment darkening (PD) and delayed tanning

reaction. IPD is induced by both long wave (320-380mm) and also by visible light.

This reaction is instandeous and then reaches a maximum about 1-2 hours following

irradiation. It then slowly decreases, between 3-24 hrs. Ultra structural studies have

shown that in this reaction there are alterations in the distribution of pre-existing

melanosomes with in the keratinocyte and melanocytes.

Delayed tanning involves the formation of new melanosomes and is a gradual

process, which occurs 48-72 hrs, following irradiation of skin. In the delayed reaction

the DOPA is markedly increased, and the melanocytes are often increased in

number and have well-developed dendrites.

Intralesional infiltration

Bakuchi oil preparations (ludermol injections etc) are available for

intralesional injections. Intralesional infiltration should be undertaken only after

getting convinced that the patient is tolerating topical psoralen well. One drop per

74

swuare cm of the patch is the normal dose. Since the lesion is in the epidermis the

infiltration should be as superficial as possible.

The time interval between two infiltrations on a patch should not, normally be

less than two weeks.

Chemical tattooing

With flesh-coloured dyes (Conway) is not effective at all. To conceal the

disfigurement temporarily, the use of a 'cover mark', walnut juice, silver nitrate or

potassium permanganate is recommended.

Surgery

In controlled cases defying different measures recommending surgical

measures are beneficial i.e., melanocyte grafting with thin thiersch's autolougous

grafts under local or general anaesthesia. This technique has been used with

success (Behla)

Role of sun light in the management of Vitiligo

In Ayurveda the importance of sun light in the management of Switra is

described very clearly. Charaka, in the treatment of Switra after the internal

administration of malayurasa with guda the sunlight exposure is advised. The same

procedure has to continue for 3 days. The duration of exposure is mentioned as

"yadabala suryapadasantapam". Blistering in the lesions may follow this exposure.

It is an astonishing fact that, at the period of samhitas out Acharyas had good

awareness about the pigmentory action of sunlight. The bhaskararadhana,

suryanamaskara, ravi vara vrata etc. daiva vyapashraya chikitsas, which are directly

75

related to exposure to sunlight also mentioned by some Acharyas in the

management of Switra.

The same sunlight exposure in the management of Vitiligo has been followed

by western system in the topic of tanning. The western medical science advises the

exposure to sunlight to the Vitiligo lesions after 2 hours of psoralen tablets (trioxalen

etc) internal administration and after topical application.

The essential oil bakuchi seeds and the sunlight these both are having the

melanocyte stimulating action. Being radiant energy the sunlight may potentate the

permeability action of the bakuchi's essential oil. By the psoralen preparations

internal administration the psoralens get concentrates in cytoplasm of the

melanocytes, which is connected with the production of pigment melanin. Psoralens

themselves cannot initiate melanin formation, they requires radiant energy by

exposure to sunlight or ultra violet light to activate enzyme tyrosinase responsible for

the melanin formation.

Drugs affecting skin pigmentation

Drugs can be used either as skin-bleaching agents to treat localised hyper

pigmentation such as freckles and post inflammatory pigmentation, or to increase

pigmentation in acquired localised, skin disorders of hypo pigmentation such as

Vitiligo.

Hydroquinone and monobenzone are used as skin bleaching agents whereas

the psoralen compounds (trioxsalen and methoxsalen) are used concurrently with

exposure to U.V light for stimulating melanin synthesis and re-pigmentation.

76

Trioxsalen

This compound is available as 5mg tablets. Given orally. It is effective in the

treatment of vitiligo. By increasing the skin pigmentation, it increases the tolerance of

the skin to U.V light. For large lesions of Vitiligo, It is given in the dose of

0.6mg/kg/day 2-3 times a week 2 hours before exposure to 15-20 minutes of direct,

mid-day sunlight. Exposure is increased by 10-20 minutes per day until erythema

sets in. if the desired effect is not obtained after 90 minutes of exposure, the dose of

the drug is increased gradually up to a maximum of 80 mg daily.

Re-pigmentation is usually evident after 3-4 months of treatment. Blue-gray,

plastic sunglasses, opaque to U.V rays, and a light screening lipstick should be used

during exposure in order to protect the eyes and help and the lips. The drug

sometimes causes cutanious reaction. It is contraindicated in-patients with diseases

associated with photo sensitive such as porphyria and systemic lupus erythematosus

and should not be given concurrently with other photo sensitising drugs.

Methoxsalen

This drug is used topically and orally to treat small vitiligenous lesions.

Topical application of a 0.1 to 1-% lotion is followed by exposure to sunlight or a U.V

lamp. Topical use can cause acute, vesicular cutaneous photosensitivity reaction.

The drug can also be given orally in the dose of 20mg per day (single dose), 2-4

hours before exposure to U.V light. It can cause gastric discomfort. Precautions

similar to those while using trioxsalen should be taken during the use of this drug.

The risk of severe sunburn is considerable with this drug.

77

DHATRYADI YOGA

Materials required

Bakuchi 4 Kg

Khadira bark (decoction reduced to quarter) Q.S.

Amalaki

Gomootra Q.S. for purification

Method of preparation of Amalaki decoction

• 2 Kg Amalaki is taken and physically purified for unwanted materials and mixed

with 8 litres of water and exposed to constant regularised heat till it reduces to

one fourth of the taken quantity i.e. 2 litres.

• 2 Kg Khadira bark is collected and physically purified for unwanted materials and

mixed with 32 litres of water and exposed to constant regularised heat till it

reduces to one sixteenth of the taken quantity i.e. 2 litres.

Method of preparation of Dhatryadi yoga

Prescribed quantities of Bakuchi were taken and soak in to Gomootra for

purification for 3days. Then it was dried under shade. Afterwards Bakuchi was

soaked in Khadira and Amalaki decoction. Once again it was dried after soaking in to

the prescribed decoctions and finally made as fine powder and filled in to 500mg

capsules.

Dose –2 Capsule thrice daily with water.

AWALGUJADI LEPA

Materials required

Bakuchi 4 Kg

Gomootra Q.S. for purification

78

Prescribed quantities of Bakuchi were taken and soak in to Gomootra for

purification for 3days. Then it was dried under shade. 1 Kg Haritala made in to small

pieces is boiled in 8-litre limes water up to 3 hours in Dola yantra. After wards it was

washed and thoroughly mixed with purified Bakuchi and grind with cow urine till it

becomes as fine paste. That paste was made as varti of 5 gms each and dried under

sunshade. Finally packed in tight polythene packs and offered for trial patients Q.S.

Analytical findings of Dhatryadi yoga and Avalgujadi lepa

Name of the sample: Dhtrayadi Yoga (sample 1)

The main ingredients of this compound formulation are –

1) Bakuchi : Psoralia cordifolia (seeds)50

It contains two important active coumarine compounds viz. Psoralen and Iso-

psoralen. These compounds stimulate melenoblast (pigment forming cells). This

in turn reddens the white patches of leucoderma. At the later stage, these

patches turn in to normal skin colour.

Bakuchi also has other important organic compounds like,

a) Bakuchinol (Monoterpenoid phenol) C18 H24 O - 0.7%, BP 145-147º C

b) Psoralidin MP 315º C

c) Iso-Psoralidin C17 H14 O4 MP 283 - 284º C

79

d) Coryliflolin C17 H18 O3 MP 183º C

The important minerals present in it are -

Calcium 1.9%

Phosphorus 0.2%

Stigmatsterol - traces and

hydroxy flavone - which imparts pigments.

2. Amalaki - Emblica officinalis (Fruits)51 The decoction of Amalaki contains the compounds, which have the

dyeing action. The tannins containing gallic acid and ellagic acid.

Garlic Acid Ellagic Acid C14 H6 O8 3. Khadira – Acacia catechu (Hard wood)52

The decoction of khadira has the important ingredients like:

Catecnin (faavanoid) 4 – 7 %

Catechutannic acid and tannins (C27H24O8) 57%

From the above information it can be inferred that, the Bakuchi, stimulates the

pigment formation cells, Amalaki imparts the dye and Khadira helps for better

absorption.

Sample – 2 (External Use)

An important ingredient Harital (orpiment) As2 S3 is used as a pigment.

80

Analytical Findings of Dhatrayadi Yoga and Avalgujadi Lepa Type of Analysis Sample 1 Sample 2

Organoleptic study Colour Dark brown Mud colour with

yellow specks Smell Cow's urine Cow's urine Touch Hard Hard

1

Taste Slightly Bitter Acrid Quantitative estimation % of loss on drying 8.13 7.8 % of Ash 7.58 8.10 % of Acid insoluble Ash 1.54 1.82 % of solubility - water 12.8 11.2 % of solubility - Alcohol 10.64 9.62 % of extractive principles Petroleum ether 7.04 6.42 Benzene 2.32 1.77 Chloroform 1.88 2.3

2

Ethanol 8.72 8.4 3 Inorganic constituents Ca, Fe, Na, K, Cu

(trace), Co, SO4, Chloride & phosphate (trace)

Ca, Fe, Na, K, Arsenic, CO3,SO4, & Chloride

Organic constituents Steroid ++ ++ Triterpenoid - - Flavanoid ++ ++ Phenol ++ ++ Tannins ++ ++ Saponins + - Sugars ++ + Alkaloids ++ ++

4

Glycosides + +

Visible rays UV Rays 254 µ UV Rays 365 µ 5 Fluorescence Analysis Sample 1 Sample 2 Sample 1 Sample 2 Sample 1 Sample 2

As such DG DG DG NF NF NF With methanol Black Black NF NF NF NF With Methanolic

NaOH Black Black DG DG NF NF

Hydrochloric acid (diluted)

DG Black DG DG NF NF

NF = No Fluorescence, DG = Dark Grey

81

BAKUCHI

Botanical name psoralia corylifolia

Family legu-papilionaceae

Sanskrit charaka - avalguja

Nigantu

bakuchi, somaraji, somavalli, suvalli, avalguja, krisnaphala, putiphala,

chandralekha, indulekha, sesilekha, putikarni, kalamesi, durgandha,

kushtanasini, wakuchi, somavalika, suvalika, sita, sitavari, candri, suprabha,

kushtahantri, kamboji, pratigandha, valuja, vara, amrutha, malayu, induraji,

chandrabhida, raji, aindavi, kishtadoshapaha, kantida, prabhayukta etc.

Vernacular and other languages

Hindi Babchi, babachi, bavanchi, bavanchiyan, bavaj, bukchi

Telugu Karubogi, bogivithulu, bavanchalu, kalaginja

Urdu Babechi

Tamil Karpokarishi, karpuvanshi

Punjabi Babchi

Marathi Babachi, bakchi, bavachya

Malaya Knoochee, kutzu

Gujarathi Babichi, bavacha, bawchi

Chinese Kutzu, puki chih

Assam Phaco

Bengal Bavachi, hakuch, latakasturi

Ceylon Ravoti

Bombay Bawachi etc.

82

Meanings of few terms of bakuchi Somaraji that which gives good complexion like soma

Avalguja which takes its origin from a foul smelling seed

Suvalli which has a beautiful and tender stem

Krisnaphala plant which has black fruits or seeds

Putiphala that gives bad smelling fruits.

Habitat and distribution A herbaceous weed distributed all over India.

Common in dehradun, bengal, bombay, carnatic etc.

Morphology Whole plant

An erect annual about 0.6-1.2 m high, Stem and branches strated vertically

with a few spread out white hairs. Leaves simple, about 3.8-7.5 cm, by 2.5-5cm,

broadly ellipticle, incisodenate, rounded and mucronate at the apex. Stipules

lanceolate, persistent, flowers close, in dense axillary solitary 10-30 flowered

racemes, pedicles short, calyx 3 to 4 mm long hairy outside, corolla bluish purple

nearly twice as long as the calyx. Pods 5mm long, avoid ablong, somewhat

compressed closely pitted, mucronate, black glabrous, one seeded, smooth adhering

to the pericarp.

Parts used seeds - characters

Macroscopic

The fruits are dark brown to blakish in colour and oily or greasy to touch. They

are ablong, avoid ablong or reniform in shape somewhat flattened and closely pitted

and slightly rough. They are 3 to 5 mm long and about 1.5 3 mm wide. The hilum is

situated at the lower end of the concave margin. The entire fruit in most cases is

found enclosed within peristant clayx which is adherent to fruit. The seed which is

easily separated from the fruit is somewhat ovate and of a dark brown colour. It has

83

rather horny borwnich testa and an embryo with dry yellowish cotyledons. The fruit

have an aromatic odour with pungent or bitter taste.

Microscopic –

Pericarp consist of small thin walled parenchymetous cells in early stage. At

maturity the pericarp gets reduced and the parenchymatous cells composing it

collapse a good dead. The testa of the seed is represented by 4-5 layers of cells - a

layer of prismatic cells into outermost side. A layer or two of parcenchymnatous cells

on the inner side. The seed is attached with the pericarp by a small fan shaped

funicle.

Chemical composition –

The seeds of psoralea coryfolia contains essential oil (in pericarp to the extent

of about 0.05 - 0.12%), a fixed oil, a resin, a volatile terpenoid oil and two crystelline

principles psoralen (c11 H6 o3)m.p 162 c. Iso - psoralen m.p 112c. A crystelline

substance called psorolidin (c16 H14 o4)m.p 315c has been isolated from the

pericarp. Psoralin and Iso-psoralen are oil soluble furocoumrins.

Pharmacological action of essential oil: -

The oil has an irritant and specific effect on the skin and mucous membrane.

Its action on the undifferentiated protoplasm such as paramoecium is quite marked. It

has a powerful effect against the skin streptococci. On voluntary muscle, the

essential oil in high dilutions (1 in 50,000 to 100,000) has a distinct stimulat action.

Sturated solutions of the oil injected intravenously have no effect on the blood

pressure. The essential oil, however, varies enormously in its effects on different

persons. With the majority (95%) it causes only redness of the leucodermal patches,

84

but in a small number (5%) there is extreme sensitiveness to the oil, so much so that

blistering may be produced.

The strength of the oil should, therefore, be varied in such a way as not allow

its action to go beyond the state of redness of the leucodermic patches. The oil being

an essential oil is able to permeate through the epidermis to the prickle cells of the

lymphatics and so it finds its way to the subcapillary area and stimulated the cells

situated there. The advantage of this oil over the skin irritants, is that it does not

produce desquamation or any change of keratolytic nature resulting in loss of

pigment of the epidermis.

So far as is know P.corylifolia is the only drug that has a dual action i.e.

Action on both rouget's cells and the melanoblastic cells of the skin. In leucoderma

the malanoblastic cells are not functioning properly and their stimulation by the oil

leads them to form and exude pigment which gradually diffuses into the decolorised

area.(chopra) Cally active

Therapeutic uses of seeds: -

Seeds are useful in bilious affections and are also used to make a perfumed

oil, and its powder is specially recommended by vaidyas in leprosy and Leucoderma

internally, and are also applied in the form of paste or ointment externally. The drug

has been considered to be so efficacious in skin disorders that it was given the name

"kushtanshini".

" Sen, Chatterjee and Datta found the unsaponified oil to be

pharmacologically active and they used it with success in cases of Leucoderma and

psoriasis". The oleo resinous extract of the seeds given to non-syphilitic Leucoderma

patients has been found beneficial by action. In syphilitic cases it had no effect.

85

" The effect of the essential oil is purely local. If affections of the

gastrointestinal tract such as E. histolytica infections etc, are present, these should

be treated at the same time" (chopra). Seeds are given inscorpion-sting, snake-bite

leucoderma and other skin diseases.

Dr. N.C. Basu says that "the bowchi oil changes white skin, gray hair., rough,

scaly, discoloured skin, nails, hair etc to normal colour within 3 months, and that it is

well tried and prescribed by eminent doctors".

Oleo-resinous extract of the seeds (containing most of the essential oil

present in the seeds) diluted with chaulmugra oil, both internally and as a simple

ointment externally, is recommended as an application, gently rubbing once or twice

daily, in leucoderma, white leprosy, psoriasis and other inflammatory skin diseases

and febrile conditions. (K.L.Dey). ointment may be prepared by combining one part of

an alcoholic extract of the seeds with two parts of chaulmugra oil and two parts of

lanoline. The proportion of the active ingredients may be increased if the action is

delayed.

Ayurvedic consideration: -

Under the general classification of dravyas "somaraji" is classified in the

"audbhida" group, meaning vegetable kingdom. It is supposed to function as Kapha

Pitta hara. It is included in the sakavarga of Charaka Samhita as a drug in

haritakyadivarga. The leaves of the plant were used for preparing a cooked

vegetable.

Charaka mentions the Rasa of saka as madhura and Susruta and Vagbhata

do not appear to mention about the rasa etc. The rasa-virya-vipaka of the seeds

seems to be omitted by these authors. It is strange that Charaka mentions the Rasa

86

both as tikta and madhura in the same chapter. Nighantus mention the rasa as tikta

and tikta-katu. It is also surprising to note that the nighantus. Mention virya of the

seed both as sita and ushna. Although charaka mentions virya as sita, there appears

to be unanimity in vipaka. Which is mentioned as katu. Amongst the other properties

described to the somaraji appear the terms - rasayana, kushtaghna, twagdosahara,

krimihara, kanduprasamana etc.

Kalpas :- Various types of preparations (kalpas) are used such as lepa, gutika,

kasaya, taila, churna etc. the following table gives approximately the number of

preparations given by different authors, containing bakuchi.

Number of preparations of bakuchi in different texts

A few preparations containing bakuchi, mentioned by sarangadhara are in use, as

• Brihanmanjistadi kashaya

• Laghumanjistadi kashaya

• Kaishora guggulu

• Mahatiktaka gritha

• Khadirarishta

• Kasisadigritha

Mathra (dose): - The exact dose of the seeds does not appear to be mentioned in

the ancient Ayurvedic texts. The latest texts mentioned the dosage of bakuchi seeds

as 1-3 grams.

Shodana (purification): - The shodana for somaraji seeds appears in the text

"Dravyaguna vignana" by acharya P.V. Sarma. Which is described as - keeping the

seeds in Gomutra or ardraka swarasa for 7 days, with changing the everyday

dravadravya.

87

KHADIRA

Botanical name Acacia catechu

Family legu-mimosoideae

Sanskrit: khadir, raktasara, dantad awana, kantaki, yagniya, balapatra. Tiktasara,

susaradruma. Yupadruma, bahusalya, yajaka, kushtasudana, gayathri, kshatikshama

geeta, kushtagne, salyaka, gourata, kandara, syama etc.

Vernacular and other languages:

Hindi khair

Telugu chandra,

Marathi kahir

Kannada kaggali

Malayala khadiram

English cutchtree

Khadirasara: -

Hindi - khairsar, katha,

Marathi - kotah,

Gujarati-katha,

Malayala- kathu,

Telugu-kachu,

English-catechu

Meanings for few terms of khadira :-

Khadira - which destroys the diseases and which restores the

sareera sthirata

Raktasara - which is having a raktavarna sarabhoga

88

Dantadwana - useful in cleaning the teeth

Kantaki - the tree with prickles

Balapatra - tree with small leaves

Yagniy - which is used in yagna

Kushtagna - which cures the kushtas

Habitat and distribution: -

This is a common tree in most parts of India and Burma, ascending to 3000

feet in the Himalayan valleys, generally growing gregariously. It is also found in

Ceylon. But is probably not known out of Asia.

Parts used –

Extract, bark, woods, flowering tops and gum.

Constituents –

catechu- tannic acid 35%, catechuic acid or catechin; catechu red tannin,

gum, quercetin and ash. Catechutannic acid loccurs as dark reddish brown powder

which oxidises in the air. "dye extracted from the inner wood is a brittle compact

substance of choclatre colour containg much tannin and acid called catechuic acid it

has a astringent taste but no smell and is soluble in water." "dye occurs in dark

brown masses with a very astringent taste"

Action.-

Powerful astringent.

Preparations.-

Gum catechu, powder, tincture and decoration. Catechu is a resinious extract

prepared from the wood by boiling it in water and inspissating the decoration.

89

Morphology: -

A moderate sized tree, not reaching more than 30-40 feet high and often

smaller, with a short, somewhat crooked trunk, and numerous irregular straggling

branches, bark brown or dark gray, rough, red and fibrous within, young branches

smooth or pubescent, with a pair of sharp. Hooked, brown prickles, just below the

position of the stipules of each leaf, and leaves numerous. Alternate stalked petiole

with a prominent gland on the upper surface about the middle. And often armed with

a few prickles, bipinnate, 5-8 inches long, pinnae in 10-20 pairs, 1-2 inches long,

blunt, 1/8-1/4inch long, glabrous or pubescent, entire. Flowers in -mat-oct, pale

yellow in long spikes, calyx villous, petals villous pods thin brown, shining, and

dehiscent.

Chemical composition: -

The cutch essentially composed of "catechin" or catechuic acid (upto30%)

and catechu-tannic cid or mimotannic acid (about 50%). The pale-coloured cutch is

also, almost entirely composed of the former.

90

Amalaki

Emblica officinalis (N.O.Euphobiaceae)

Sanskrit

Dhatriphala

Amraphalam

Amalakam

Sriphalam

Amalaki

Vayastha

English Emblica Myrobalan (Indian gooseberry)

Hindi Amala, Aoula, Aura and Anuvurah

Habitat: The deccan, the sea coast districts and kashmir.

Parts used. Dried fuit, the nut or seed, leavesroot, bark and flowers. Ripe fruits used

generally fresh dry also used.

Action- fresh fruit is refrigent diuteric and laxative. Green fruit is exceding acid. Fruit

is also carminative and stomachic. Dried fruit is sour and astringent. Flowers are

colling and apreient. Bark is astringent. Rasa all except lavana, kashyam dominates,

setha veeryam, mathura viprakam, tridosha, haram, rasayanam, increases sukram.

Indications: - Raktapittam, prameham, vata-raktam, giddiness, and vertigo. Extrnal

use: in method disorders as a paste and tailum to head. 'Tara-dravam'.

Preparations: - Decoction and infusion of leaves and seeds; a liquor, a fixed and an

essential oil; confection; powder; paste and pickles. An astringent extract equal to

catechu is prepared from the root by decoration and evaporation.

Dose: - 1/2 to 2 tolas vehicle being goat’s milk. This is a nutritive tonic, useful in

phthisis and improves all conditions of deblity. The drug is also used in scopion

string.

91

Arsenic trisulphidum (As2 S3)

Sanskrit Harital

English orpiment; yellows sulphuret of arsenic,

yellow arsenic trisulphade or Trisulphuret of Arsenic

Hindi Hartala.

Action: Haritala is purified for internal administration by being successively boiled in

kanjika the juice of the fruit of benincasa cerifera sesame oil and a decoration of the

three myrobalans for three hours in each fluid together to save time as done by some

physicians. The dose of the purified orpiment if 2 to 4 grains. It is generally known as

harital bhasma.

As an antiperiodic and alternative tonic it is given to cure fevers and skin

diseases. It is to increase strength and beauty and to prolong life also in incipient

phthisis and asthma, paraplegia, hemiplegia, monoplegia and facial paralysis, in

cough, chronic fever, gonorrhoea, epilepsy, dropsy etc. it is generally used in

combination with other ingredients. Pills known as Ramban Rasa composed of

orpiment, sulphur and asafoetida are recommended in asthma and chronic skin

diseases as eczema, psoriasis etc. in doses of 1 to 4 pills of one grain each with

ghee three times a day after meals. "this preparation was administered to cases of

asthma and rheumatism and was fairly beneficial in giving relief to the patient in

those diseases" (Ind. Drugs Rept., Madras). A preparation called mahalakshmibilas

composed of mercury and sulphur, arsenic, iron, mica, tin, copper, aconite, camphor,

nutmeg, mace, and seed of gmelina asiatica is recommended in vayu and kapha

(asthma). It is given rubbed with betel leaf juice.

92

Switra is an achromatic macular disorder, where the depigmented patch al over

the skin spread irregularly, causes cosmetic problem initially and there after results into

various complications pertaining to skin53. The incident of this disorder varies from 3-4 %

in India54, draw the attention of researcher to said problem. Meanwhile is the great

protector of the skin against the actinic rays of the sun55. Vitiligo is due to patchy loss of

melanin that develops after birth and it is progressive in nature56. ACTH has also had an

effect on melanocytes similar to that produced by Melanocyte stimulating Harmone

(MSH). MSH release inhibiting Harmone (MRIH), which have been extracted from the

hypothalamic area. Transported to the pars intermedia through the nervous pathway

rather than through portal vessels57. Not only the cosmetic but also psychological

intervention of the Switra has to be studied at backdrop contemporary medical faculty’s

failure in such aspect and also to provide a reasonable remedy for the Switra.

Review of literature:

Ayurveda has elaborately explained the evaluation of the skin and in further

divided into seven layers58. The Switra appears in fourth layer of the skin, which is

93

known as tamra, where the involvement of rare metals such as copper, zinc etc. has

been established Switra as a condition of disease described since the ages of Rigveda

(6000 year B.C.)59. Vitiligo is due to autoimmune distortion of melanocytes over

circumscribed area of the skin60. Ayurveda Acharyas has classified it as one of the

Kusta61. Many of the scholars62 of the Ayurveda have suggested medicaments63 or the

Switra64. Chakrapani Dutta’s Chakradatta is a one of such valuable text offers the

treatment of Switra, internally and externally65. Switra Kusta like other Kusta indicated

with muhurmuhur sodhana. As Switra Kusta is Kapha predominant, it is indicated with

Vamana as one of the best eliminative therapy66. The present study includes Dhatrayadi

yoga67 and Avalgujadi Lepa68 as a treatment of internal and external respectively.

Objectives of the study

1. To evaluate the efficacy of the Dhatrayadi Yoga (internal) and Avalgujadi

Lepa (external) over the achromic maculae of the Switra

2. To evaluate the effect of the Dhatrayadi Yoga (internal) and Avalgujadi

Lepa (external) in Switra over melinocytogenesis

Materials and Methods

Source of the data

(a) Literary: Literary aspect of the study is collected from classical Ayurvedic

and modern texts and is updated through journals along with search.

(b) Drug: the drug part is discussed here under:

Ingredients

1) Dhatryadi Yoga (internal)

a) Avalguja (Psoralia cordifolia)

b) Amalaki (Emblica officinale)

c) Khadira (Acasia catechu)

94

2) Avalgujadi Lepa (External)

(a) Avalguja (Psoralia cordifolia)

(b) Haritala (Arpiment)

The herbal and mineral origins are well identified and purified (if subjected) before to

the preparation of medicine.

(c) Patient: - patients with switra are selected after screening with inclusive and

exclusive criteria from OPD/IPD of post Graduation and Research Center of

DGM Ayurvedic Medical College, Gadag.

Method of collection of data

(A) Study design:

The study is a prospective clinical trial. Study will be done in two groups :-

a. Trail over Sodhita Rogi

b. Trial over Asodhita Rogi

(B) Sample size :

Minimum 30 patients divided in two groups

(C) Exclusive criteria :

(1) Lepromatus and pityriasis alba patches are excluded from the study.

(2) Patients below the age of 15 and above the age of 55 are excluded as

disease starts at generally in early adolescence69.

(3) The patients those who are prone to risk, such as Diabetes Mellitus and

psychotics are excluded.

(D) Duration of trial

♦ Sodhana: vamana is done at the interval of 21 days

♦ Shamana drug: 70 days (inclusive the days of sodhana; for the second

group continously)

95

(E) Posology

Vamana

According to prescribed directions of texts.

Dhatrayadi yoga

2gms TDS or 100mg/kg body weight.

Avaigujadi lepa

External application Q.S

(F) Assessment of result :-

Results will be assessed on the basis of subjective and objective

parameters to the baseline

Investigation (Objective parameters)

♦ Hemoglobin %

♦ Random blood sugar

♦ Serum copper

Ethical clearance

Ethical clearance has been obtained from the principal of the college as

chairman of the ethical clearance committee.

The detailed case sheet for the Switra is as follows.

102

1A - Demography Sodhana therapy

Sex Religion Economical status occupation Diet Result S.No OPD

No Age

M F H Mu C O E1 E2 E3 E4 O1 O2 O3 V Mix Best Responded

Responded

Not Responded

1 408 19 - + + - - - - + - - - + - + - + 2 413 26 + - + - - - - + - - - - + + - + 3 418 30 - + - + - - - - + - + - - - + + 4 428 42 - + + - - - + - - - + - - + - + 5 429 50 - + - + - - - + - - + - - - + + 6 572 15 + - + - - - - - + - - + - + - + 7 577 27 + - + - - - - + - - - - + - + + 8 584 15 - + + - - - - - + - - + - + - + 9 851 18 + - + - - - - + - - - + - - + +

10 866 18 + - + - - - - + - - - + - + - + 11 870 17 - + + - - - - + - - - + - + - + 12 914 18 + - - + - - + - - - - - + - + + 13 984 20 + - + - - - - + - - - + - - + + 14 985 33 + - + - - - - - + - + - - - + + 15 1140 16 + - + - - - - - + - - + - + - +

Total 364 09 06 12 03 00 00 02 08 05 00 04 08 03 08 07 9 6 0

M = Male, F = Female, H = Hindu, Mu = Muslim, C = Christian, O = Others, E1 = Poor, E2 = Middle Class, E3 = Higher middle class, E4 = Higher Class, O1= Sedentary, O2= Active, O3= Labor, V = Vegetarian, Mx = Mixed diet

103

1B - Demography Shamana therapy

Sex Religion

Economical status Occupation Diet result S.No OPD No

Age

M F H M C Ot E1 E2 E3 E4 O1 O2 O3 V Mix Best Responded

Responded

Not Responded

1 170 17 - + + - - - - + - - - + - - + + 2 171 15 - + + - - - - + - - - + - - + + 3 395 21 - + + - - - - + - - - + - + - + 4 404 50 + - + - - - - + - - + - - + - + 5 406 60 + - + - - - + - - + - - + - + 6 414 45 + - + - - - - + - - + - - + - + 7 420 20 + - + - - - - + - - - + - + - + 8 422 44 + - + - - - - + - - - - + + - + 9 426 45 + - + - - - - + - - - - + + - +

10 432 29 + - + - - - - + - - - - + - + + 11 878 50 - + - + - - + - - - - - + - + + 12 1159 15 - + + - - - - - - + - + - - + + 13 1160 15 - + + - - - - + - - - + - - + + 14 1190 34 - + + - - - - - + - + - - + - + 15 1383 18 + - + - - - - + - - - + - + - +

Total 478 08 07 14 01 00 00 02 11 01 01 04 07 04 09 06 9 6 0

M = Male, F = Female, H = Hindu, Mu = Muslim, C = Christian, O = Others, E1 = Poor, E2 = Middle Class, E3 = Higher middle class, E4 = Higher Class, O1= Sedentary, O2= Active, O3= Labor, V = Vegetarian, Mx = Mixed diet

104

2A -complaints (Sodhana Group)

SN Hands Forearm Palm Thigh Leg Foot Abd Back Face Chin Checks Lips genitals R L R L R L R L R L R L R L R L R L R L

1 - - - - - - - - + + - - - - - - - - - - - - - 2 + + - - + + - - + + - - + - - - - - - - + + - 3 + + + + + + + + + + + + - - - - - - - - - - - 4 + + + + + + + + + + + + + + + + - - + + + + - 5 - - - - - - - - + - + - - - - - - - - - - - - 6 - - - - - - - - - - - - - - - - - - - + - + - 7 + + + + + + + + + + + + + - + - - - + + + + - 8 - - - - - - + + + + + + - + - - - - - - - - - 9 + + - - - - - - - - + + - - + + - - + + + + - 10 - + - - + + - - - - + + - - - - - - + + + + - 11 + + - - + + + + + + - - - + - - - - + + + + - 12 - - - - - - - - - - - - - - - - - - - - - - - 13 - - - - + + - - - - + + + + + + - - - - - - - 14 + + - - - - - - + + - - - - - - - - - - - - - 15 + + - - - - - - - - + + - - + + - - - - - - - Total

8 9 3 3 7 7 5 5 9 8 9 8 4 4 5 4 0 0 5 6 5 7 0

Abd = Abdomen

105

Table 2A1 - complaints (Sodhana Group)

Vata Pitta Kapha S.No Rooksha

twa Gati

kshaya Roma

vidwahi Daha Vrana Srava Toda Sweda Spota Kleda Gurutwa kandu

1 - - + - - - - - - - - - 2 + - - + - - + - - - - - 3 - - - - - - - - - + + - 4 - - + - - - - - - - - - 5 - - - - - - - - - - - - 6 + - - - - - - - - + - - 7 - - - - - - - - - + - - 8 + - - - - - - - - + - - 9 - - - + - - - - - - - - 10 + - - - - - - - - - - + 11 + - - - - - - - - - - - 12 + - - - - - - - - - - - 13 + - - - - - - - - - - - 14 + - - - - - - - - - - - 15 + - - - - - - - - - - -

Total 09 00 02 02 00 00 01 00 00 04 01 01

106

2B -complaints (Shamana Group)

SN hands Forearm Palm Thigh Leg Foot Abd Back Face Chin Checks Lips Genitals R L R L R L R L R L R L R L R L R L R L

1 + + + + + + 2 + + + + + + + 3 + + 4 + 5 + + 6 + 7 + + + + 8 + + 9 + + + + + 10 + + + + + + + + + + + + + + + + + + + + + + 11 + + + + + + + + + + + + + + + + + + + + + + + 12 + + + + + 13 + + + + 14 + + 15 + + + + Total

5 4 4 2 4 4 2 3 9 10 5 5 3 6 3 3 2 2 2 2 4 4 2

Abd = Abdomen

107

Table 2B2 - complaints (Shamana Group)

Vata Pitta Kapha S.No Rooksha

twa Gati

kshaya Roma

vidwahi Daha Vrana Srava Toda Sweda Spota Kleda Gurutwa kandu

1 + - - - - - - - + - - - 2 + - - - - - - - - - - - 3 + - + - - - - - - - - - 4 + - - - - - - - - - - - 5 + - - - - - - + - - - - 6 + - - - - - - - - - - - 7 + - - - - - - - - - - + 8 + - - - - - - - - - - + 9 - - - - - - - - - - - - 10 + - - - - - - - - - - - 11 + - - + - - - - - - - - 12 + - - - - - - - - - + + 13 + - - - - - - - - - - - 14 - - - - - - - - - - + - 15 - - - - - - - - - - - -

Total 12 00 01 01 00 00 00 01 01 00 02 03

108

Chart number 3A – Hetu (Sodhana Group)

Physical Hereditary Burns trauma P

Psychological

Systemic

F M Br Si

B

1 2 3 4 5 a b c d e A B X Y Z

L G H I J

1 + 2 3 + + + 4 + + 5 6 + 7 8 9

10 11 + 12 13 + + 14 + + + + 15 + T 02 01 00 03 0 0 0 0 0 0 0 0 0 0 0 00 4 5 00 00 00 00 00 00 00 00

F= Father, M = Mother, Br = Brother, Si = Sister, B = Contagious, 1 = Thermal, 2 = Direct Heat, 3 = Electric 4 = Sun, 5 = Chemical, a = Accident, b = Abrasion, c = Scratch of itch, d = post surgery, e = Post inflammatory, P = Pregnancy, A = Psychological trauma,

B = Emotional Upset, X = skin problem. Y = GIT problems, Z = Malnutrition, L = Leprosy, G = Protozoa, H = Endocrinal, I = Idiopathic, J = Iatrogenic

109

Chart number 3B – Hetu (Shamana Group)

Physical Hereditary

Burns trauma P Psychological

Systemic

F M Br Si

B

1 2 3 4 5 a b c d e A B X Y Z

L G H I J

1 + 2 + + 3 + + + 4 + 5 + 6 7 8 9 +

10 + + + + + 11 12 + + + 13 14 + 15 Total

03 01 00 02 0 0 0 0 0 0 0 3 0 0 1 00 3 4 00 01 00 00 00 00 00 00

F= Father, M = Mother, Br = Brother, Si = Sister, B = Contagious, 1 = Thermal, 2 = Direct Heat, 3 = Electric 4 = Sun, 5 = Chemical, a = Accident, b = Abrasion, c = Scratch of itch, d = post surgery, e = Post inflammatory, P = Pregnancy, A = Psychological trauma,

B = Emotional Upset, X = skin problem. Y = GIT problems, Z = Malnutrition, L = Leprosy, G = Protozoa, H = Endocrinal, I = Idiopathic, J = Iatrogenic

110

CHART 4A - Ahara & Vihara (Sodhana Group)

Ahara Vihara S.No A1 A2 A3 A4 A5 A6 A7 A8 A9 A10 A11 A12 A13 A14 A15 V1 V2 V3 V4 V5 V6 V7

1 + + + + + + + + + 2 + + + + + + + + + + 3 + + + + + + + + + 4 + + + + + + + + 5 + + + + + + + + + + 6 + + + + + + 7 + + + + + + + + 8 + + + + + 9 + + + + + + + 10 + + + + + + + 11 + + + + + 12 + + + + + + + + 13 + + + + + + 14 + + + + + + + + 15 + + + + + + + + + + + Total

07 15 04 04 00 02 15 00 15 00 06 06 01 00 15 04 09 00 02 00 09 03

A1 = Adhyasana, A2 = Navanna, A3 = Dadhimatsya, A4 = Lavana, A5 = Masha, A6 = Moolaka, A7 = Pistapadartha, A8 = Tailam,

A9 = Viruddha Annapana, A10 = Drava., A11 = Snigdha, A12 = Guru, A13 = Chirajeernam, A14 = Ajeerna Ahara, A15 = Ksheera Guda vikriti, V1 = Excess work after food, V2 = Drinking cold water after food, V3 = Vegarodha,

V4 = Bath with cold water, V5 = Diwaswapna, V6 = Papakarma, V7 = Tight cloth

111

CHART 4B- Ahara & Vihara (Shamana Group)

Ahara Vihara s.No A1 A2 A3 A4 A5 A6 A7 A8 A9 A10 A11 A12 A13 A14 A15 V1 V2 V3 V4 V5 V6 V7

1 + + + + + + + 2 + + + + + + 3 + + + + + 4 + + + + + + 5 + + + + + + + + 6 + + + + + + 7 + + + + + 8 + + + + + 9 + + + + + + 10 + + + + + + + 11 + + + + + + + 12 + + + + + 13 + + + + + 14 + + + + 15 + + + + Total

10 07 05 07 00 00 15 01 15 01 00 01 00 01 00 00 10 00 00 03 10 00

A1 = Adhyasana, A2 = Navanna, A3 = Dadhimatsya, A4 = Lavana, A5 = Masha, A6 = Moolaka, A7 = Pistapadartha, A8 = Tailam,

A9 = Viruddha Annapana, A10 = Drava., A11 = Snigdha, A12 = Guru, A13 = Chirajeernam, A14 = Ajeerna Ahara, A15 = Ksheera Guda vikriti, V1 = Excess work after food, V2 = Drinking cold water after food, V3 = Vegarodha,

V4 = Bath with cold water, V5 = Diwaswapna, V6 = Papakarma, V7 = Tight cloth

112

Chart no 5A – Poorvaroopa (Sodhana Group)

Sparsha Sweda Loma Varna Twak Vrana General 1 2 3 4 5 6 7 8 9 1

0 11

12

13

14

15

16

17

18

19

20

21

22

23

24

25

26

27

28

29

30

31

32

33

1 + + + + + 2 + + + 3 + + + 4 + + + 5 + + + + + 6 + + 7 + + 8 + 9 + +

10 + 11 + + + 12 + 13 + + + 14 + 15 + + +

T 0 4 7 3 2 0 3 0 0 8 0 0 1 0 0 3 0 0 0 0 0 0 0 0 0 0 0 0 7 0 0 0 0

113

Chart no 5B- Poorvaroopa (Shamana Group)

Sparsha Sweda Loma Varna Twak Vrana General 1 2 3 4 5 6 7 8 9 1

0 11

12

13

14

15

16

17

18

19

20

21

22

23

24

25

26

27

28

29

30

31

32

33

1 + + + + + 2 + + + + 3 + + + 4 + + 5 + + 6 + + + 7 + + + 8 + + 9 + + + +

10 + + + + 11 + + + 12 + + + + 13 + + + 14 + + 15 + + + +

T 0 7 8 2 3 0 3 1 0 0 2 0 4 0 0 3 0 0 0 0 0 0 0 0 0 0 0 0 15

0 0 0 0

114

6A sadhya-asadhyata of Sodhana Group

Sadhya Asadhya Asukla Aloma Bahula Asamslis

ta Nava Anagnid

agdha Gyhyaga

ta Ostagata Padatala

gata Hastatala

gata Chiram kilasam

Result

1 + + Responded 2 + + + + + + + Responded 3 + + + Best Responded 4 + + + + + + Responded 5 + + Responded 6 + + + + + + + Best Responded 7 + + + + + + + Best Responded 8 + + + + Best Responded 9 + + + + + Best Responded

10 + + + + + Best Responded 11 + + + Responded 12 + + + + + Best Responded 13 + + + + + + + Best Responded 14 + + + + + Best Responded 15 + + + + + + + + Responded T 10 7 7 2 5 15 0 8 6 8 8 0

115

6B sadhya-asadhyata Shamana group

Sadhya Asadhya Asukla Aloma Bahula Asamslis

ta Nava Anagnid

agdha Gyhyaga

ta Ostagata Padatala

gata Hastatala

gata Chiram kilasam

Result

1 + + + + + + Responded 2 + + + + + Responded 3 + + + Best Responded 4 + + Responded 5 + + + Best Responded 6 + + Best Responded 7 + + + Best Responded 8 + + Responded 9 + + + + + + Responded

10 + + + + + Responded 11 + + + + + Best Responded 12 + + + + + + Best Responded 13 + + + + + Best Responded 14 + + + + + Best Responded 15 + + + + + + Best Responded T 13 6 6 1 5 15 1 3 5 4 5 0

116

7 A - Sodhana therapy Assessment

Serum copper

Patch area

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

S.No

B A B A %R B A B A B A B A B A B A B A B A B A B A B A B A B A B A

1 147 295 4 1 75 - - 2 0 10.3 1.1 2 0 2 0 2 0 - - - - + + - - - - - - - - - - 2 106 158 12 4 75 - - 3 1 10.4 2.1 2 1 2 1 2 1 - - - - - - - - - - - - - - - - 3 400 198 14 1 93 - - 2 0 6.6 0 3 1 3 1 1 0 - - - - - - - - - - - - - - - - 4 310 210 20 4 80 - - 2 1 10.3 2.6 3 1 3 1 1 0 - - - - + + - - - - - - - - - - 5 150 175 2 2 0 - - 3 2 20.4 12.7 3 2 3 1 1 0 - - - - + + - - - - - - - - - - 6 175 160 2 0 100 - - 1 0 2.4 0 1 0 2 0 2 1 - - - - - - - - - - - - - - - - 7 75 160 22 5 77 - - 3 1 1.1 0 3 2 3 1 1 0 - - - - - - - - - - - - - - - - 8 74.9 168 10 2 80 * - 1 0 6.1 0 3 1 2 0 2 0 - - - - + + - - - - - - - - - - 9 356 200 10 0 100 - - 2 0 1.5 0 2 0 1 0 3 1 - - - - - - - - - - - - - - - -

10 100 172 10 0 100 - - 3 0 4.5 0 2 0 2 0 2 0 - - - - - - - - - - - - - - - - 11 190 138 15 3 80 - - 3 1 20.3 8.7 3 1 3 1 1 0 - - - - + + - - - - - - - - - - 12 130 140 1 0 100 - - 1 0 2.1 0 1 0 1 0 3 1 - - - - - - - - - - - - - - - - 13 160 158 12 4 66 - - 3 1 3.4 0 3 1 2 1 2 0 - - - - - - - - - - - - - - - - 14 148 156 8 0 100 - - 2 0 4.3 0 2 0 2 1 2 0 - - - - - - - - - - - - - - - - 15 172 156 6 2 66 - - 2 1 6.6 2.1 2 1 2 1 2 1 - - - - - - - - - - - - - - - -

Total 2693.9 2644 148 28 1 0 33

8

110.3 29.3 35

11

33

9 27

5 0 0 0 0 5 5 0 0 0 0 0 0 0 0 0 0

1) Number, %R = % of Recovered 2) Position: * = spreading, - = Not spreading 3) Extent 4) size in Sq. Cms 5) surface

6) Margin; 3= thin, 2 = medium, 1 = thick, 0 = Normal 7) colour;0 = Normal 1 = deep,2 = Medium, 3 =less, 8) Inflammations 9) Bleeding 10) hair discoloration 11) Oedema 12) Ulceration 13) Local temperature 14) pain 15) Skin texture, (B= Before, A = After, + = Present)

117

7 B -Shamana therapy Assessment

Serum copper

Patch area

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

S.No

B A B A %R B A B A B A B A B A B A B A B A B A B A B A B A B A B A

1 68 102 9 3 66 - - 1 0 4.6 1.3 2 1 2 1 2 1 - - - - - - - - - - - - - - - - 2 102 140 7 1 85.7 - - 1 0 3.3 1.2 1 0 2 1 2 1 - - - - - - - - - - - - - - - - 3 80 160 4 0 100 - - 1 0 4.2 0 2 0 2 1 2 0 - - - - - - - - - - - - - - - - 4 136 120 14 5 64.3 * - 2 1 14.1 2.2 2 1 2 1 1 0 - - - - - - - - - - - - - - - - 5 120 150 4 0 100 - - 1 0 4.3 0 1 0 2 0 2 0 - - - - - - - - - - - - - - - - 6 270 175 2 0 100 - - 1 0 3.4 0 1 0 1 0 1 0 - - - - - - - - - - - - - - - - 7 80 125 6 1 83.3 - - 1 0 4.8 0 2 0 1 0 1 0 - - - - - - - - - - - - - - - - 8 204 180 6 1 83.3 - - 2 0 4.6 0.1 2 0 1 0 1 0 - - - - - - - - - - - - - - - - 9 254 195 5 1 80 - - 3 1 10.9 2.8 3 1 3 2 2 1 - - - - - - - - - - - - - - - -

10 92 91.7 21 5 76.2 - - 3 1 12.8 2.2 3 1 3 2 2 1 - - - - - - - - - - - - - - - - 11 190 160 10 2 80 - - 3 1 12.1 0 3 1 3 2 3 0 - - - - - - - - - - - - - - - - 12 70 110 8 1 87.5 - - 1 0 2.1 0 1 0 1 0 1 0 - - - - - - - - - - - - - - - - 13 100 145 4 0 100 - - 1 0 4.3 0 1 0 1 0 1 0 - - - - - - - - - - - - - - - - 14 158 140 2 0 100 - - 1 0 2.1 0 1 0 1 0 1 0 - - - - - - - - - - - - - - - - 15 140 130 4 0 100 - - 1 0 4.2 0 1 0 1 0 1 0 - - - - - - - - - - - - - - - -

Total 2064 2123.7

106 20

1 0 23

4 91.8 9.8 26

5 26

10

23

4 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

137.6

2) Number, %R = % of Recovered 2) Position: * = spreading, - = Not spreading 3) Extent 4) size in Sq. Cms 5) surface 6) Margin; 3= thin, 2 = medium, 1 = thick, 0 = Normal 7) colour;0 = Normal 1 = deep,2 = Medium, 3 =less, 8) Inflammations 9) Bleeding 10) hair discoloration 11) Oedema 12) Ulceration 13) Local temperature 14) pain 15) Skin texture, (B= Before, A = After, + = Present)

118

Chart 8A - Statistical Assessment before treatment

Criteria Group Mean SD SE PSE "t" Value P value Remarks A 179.59 98.68 25.48 Serum

Copper B 137.6 65.34 16.87 30.56 1.37 < 0.25 Significant

A 9.87 6.31 1.63 Number of patches B 7.07 5.0 1.29

2.08 1.35 < 0.25 Significant

A 2.2 0.77 0.19 Extent B 1.53 0.83 0.21

0.28 2.39 < 0.25 Highly Significant

A 7.35 6.12 1.58 Size B 6.12 4.09 1.06

1.9 0.65 > 0.25 Not Significant

A 2.33 0.72 0.18 Surface B 1.73 0.79 0.2

0.27 2.22 < 0.25 Highly Significant

A 2.2 0.68 0.18 Margin B 1.73 0.79 0.2

0.27 1.74 < 0.25 Significant

A 1.8 0.68 0.17 Colour B 1.53 0.64 0.16

0.23 1.17 > 0.25 Not Significant

As the Vitiligo is a psychosomatic disorder which can not be treated with in a limited period, we wish to prove this remedy is effective even with in 60 days of trail period. A 75% of accuracy is assumed at the present study with P value as 0.25. The

non-significant criteria can be comprehended as statistically highly significant.

119

Chart 8B - Statistical Assessment after treatment

Criteria Group Mean SD SE PSE "t" Value P value Remarks A 176.26 38.87 10.04 Serum

Copper B 141.58 29.45 7.6 12.59 2.75 < 0.25 Highly

Significant

A 1.87 1.77 0.46 Number of patches B 1.33 1.72 0.44

0.64 0.84 > 0.25 Not Significant

A 0.53 0.64 0.16 Extent B 0.27 0.46 0.12

0.2 1.3 > 0.25 Not Significant

A 1.95 3.75 0.97 Size B 0.65 1.0 0.26

1.0 1.3 > 0.25 Not Significant

A 0.73 0.7 0.18 Surface B 0.33 0.49 0.13

0.22 1.81 < 0.25 Highly Significant

A 0.6 0.51 0.13 Margin B 0.67 0.82 0.2

0.25 0.28 > 0.25 Not Significant

A 0.33 0.49 0.13 Colour B 0.27 0.46 0.12

0.18 0.33 > 0.25 Not Significant

As the Vitiligo is a psychosomatic disorder which can not be treated with in a limited period, we wish to prove this remedy is effective even with in 60 days of trail period. A 75% of accuracy is assumed at the present study with P value as 0.25. The

non-significant criteria can be comprehended as statistically highly significant.

120

Chart 8C - Statistical Assessment Individual study of group "A"

Criteria Mean SD SE "t" Value P value Remarks Serum Copper

69.07 61.66 15.92 4.34 < 0.001 Highly significant

Number of patches

8.0 5.23 1.35 5.93 < 0.001 Highly Significant

Extent 1.67 0.62 0.16 10.44 < 0.001 Highly Significant

Size 5.47 3.47 0.89 6.14 < 0.001 Highly Significant

Surface 1.4 0.51 0.13 10.76 < 0.001 Highly Significant

Margin 1.07 0.26 0.067 15.94 < 0.001 Highly Significant

Colour 1.27 0.59 0.15 8.47 < 0.001 Highly significant

121

Chart 8D - Statistical Assessment Individual study of group "B"

Criteria Mean SD SE "t" Value P value Remarks Serum Copper

37.62 25.33 6.54 5.75 < 0.001 Highly significant

Number of patches

5.73 3.45 0.89 6.44 < 0.001 Highly Significant

Extent 1.27 0.46 0.19 6.68 < 0.001 Highly Significant

Size 5.47 3.47 0.89 6.15 < 0.001 Highly Significant

Surface 1.4 0.51 0.13 10.77 < 0.001 Highly Significant

Margin 1.07 0.26 0.067 15.97 < 0.001 Highly Significant

Colour 1.27 0.59 0.15 8.47 < 0.001 Highly significant

122

DISCUSSION AND CONCLUSION

The disease Switra and its description have been existing from the Veda

period and the detail about knowledge regarding this disease is advanced up to the

period of Samhita kala. As per Ayurveda this disease is of two types. One is causing

somatic signs symptoms like shoola etc. and second variety caused severe mental

agony and lesser somatic disturbance. Vitiligo first appeared due to somatic

disturbance, but due to improper knowledge about it in society whether effected

person’s engulfed in psychic stress. But in same problem is not in every where.

Whether the person has a proper knowledge about this disease are not worried

about this disease. For example among the pategar community of Gadag distracts,

have 10:1 Vitiligo. But they are completely happy, neither stress nor any thing else

about this disease. They came to us to take medicine by knowing that medicine

distribution is free. A survey conducted by Dr.G. D Mukherjee retired Assistant

Director, RRI Calcutta with a association of psychologist Dr. A. K. Sikdar shown that

most of the patient exhibited mental depression, anxiety neurosis, psychosis, leading

to dilution thought of suicide insomnia, inferiority complex etc. Switra according to

Ayurveda is an ashukari Vyadhi i.e., fast spreading, which needs immediate

treatment to stop further spreading and relieve the already progressed disease.

Keeping in view these present clinical studies has been undertaken.

123

The following are the vital points observed:

1) Even though many causative factors for Switra under aharaja

(virudhahara, mithyahara etc,) viharaj (suppression of vegas etc,)

viprakrista (puruvajanmakritha papa etc,) groups are described in

Ayurveda.

2) In this thesis it is described with complete references, that copper has a

important role about formation of marinocytes-melanin by tyrosinase in

presence of copper. Scientist has mentioned that lesser percentage of

serum copper is may cause Vitiligo. But in the locality of surrounding

Gadag distracts, out of ten one person has Vitiligo. Total out of 60 cases

(included and excluded) not a single cases has shown lesser percentage

of serum copper. Majority have a higher percentage of serum copper viz.

300 - 400 micro gram per dl. There by it had to be considered that serum

copper have a no any a specific role in formation of melinocyte which is

decreased in case of Vitiligo.

3) Vihara; Vihara have an important role in relation of this disease. Most of

patients and their family member’s nature are much crazy, unfaithful, liar,

non-sympathatic, and unkind heart except children of below eight years.

For example one person bring two patient’s for trial, one person’s age was

below eight years there by we refuse to give medicine, but we given

medicine to a person whose age was around fifteen years. The aged

person who brought the patient has not given medicine to a real patient

whose age was around fifteen years and he given medicine to his son

whose age was below eight years. His son was cured by the medicine but

124

by dishonestly he not given medicine to real patient. He also not recorded

actual residential address. This is the mentality of most of Vitiligo effected

family.

4) Dosha dushya sammuruchana is another interesting point for discussion.

As a result of indulgence and practice of the etiological factors the

tridoshas get vitiated and occupies the three dhatus namely rakta, mamsa

and medhas, as a result Switra occur. This sammuruchana is termed as

“thridhatudbhava samshrayam”. This thridhatudbhava samshrayam leads

to a bit of confusion for the lesson of Switra is manifesting in twak. The

explanation is that it is only the vitiated Doshas that are dislodged, which

in turn have got displaced in to the rakta, mamsa and medodhatu. In fact

the Dhatu are not yet vitiated at his juncture, which is early stage of the

manifestation. As such treatment at this stage is highly successful. The

same way observed in the present study were in two out of 30 cases were

below three months of duration and responded dramatically favorable.

5) On careful observation of history of patients it is observed that there are

two types of progression disease pattern- one is quick spreading, another

is very slow in spreading. This type of disease pattern may be due to

involvement of Doshas. For instance when Vata predominated in the

samprapthi naturally Switra spreads very rapidly, since vat is ashukari in

swabhava. On the same analogy, if Kapha dominates naturally disease

pathology develops very slowly, as Kapha is mandakari in swabhava. The

same pattern of disease progress in Vitiligo has also been described in

the western medical since under two categories sudden and delayed.

125

6) In this treatment of Switra, Charaka specifically mentioned the

atapasevana (exposure to sunlight) after the intake of internal medication.

And the same has been followed in western system of medicine in the

topic of tanning.

It is an astonishing fact that, at the period of Samihitas, our Acharyas had

good awareness about the pigmentary action of sunlight. The bhaskaradhana,

suryanamaskara, ravivara vrata etc. daiva vyapashraya Chikitsa which are

directly related to exposure to sunlight, also explained by some Acharyas in the

management of Switra.

In the present clinical study the external application is followed by exposure to

sunlight. The both sunlight and essential oil of Bakuchi are having the action of

the melanocyte stimulation. The sunlight being radiant energy it may potentate

the action of external application. Thus may results in perfect permeability of drug

through epidermis and which results in perfect stimulation of the melanocytes for

their normal function melanogenesis. By the internal medication (Dhatryadi Yoga)

the psoralens get concentrates in cytoplasam of the melanocytes, that is

connected with the production of pigment melanin. Psoralens them self cannot

initiate melanin formation they requires radiant energy by exposure to sunlight or

ultra –violet light to activate enzyme tyrosinase responsible for the melanin

formation.

7) The drug Bakuchi is drug of choice in Vitiligo and which has been

successfully using by various systems of medicines in various forms.

“So far as is known psoralia is the only drug that has a dual action i.e., action

on both Rouget cells and the melanoblastic cells of the skin. In Vitiligo the

126

melanoblastic cells are not functioning properly and their simulation, the oil leads

them to for and exudes pigment, which gradually diffuses in to the decolorized area”-

Chopra.

In the present study Bakuchi, which used in internal preparation was purified

in Gomutra for 7 days. Dr.P.V.Sharma takes this reference from the text Dravya guna

vignana. Ardraka swarasa is also advised for Bakuchi Sodhana. Being Kusta

Switrahara lekhanadi gunas Gomutra has been selected for Bakuchi beeja shodhana

in present clinical study.

In the western system of medicine the available drugs for Vitiligo, obtained

from Bakuchi are trioxalen and methoxalen. The internal administration of these

drugs may show the side effects such as gastric irritation, nausea, vomiting,

giddiness, rashes etc and according to some, repeated liver function tests were

advised during the course of prolong these drugs administration. And these

preparations are contradicted in-patients with diseases associated with

photosensitivity such as porphyry and systemic lupus erythematosus.

Whereas as in our present study the Gomutra shodita Bakuchi done bhavana in

khadiramalaki kashaya not shown any kind of adverse effects like gastric irritation etc

by its internal administration. It is accepted by western science that the impaired

detoxification function of live is supposed to be responsible for Vitiligo. In Ayurveda

the Gomutra has been successfully using in cirrhosis of liver, jaundice anemia,

ascities and other conditions by various Ayurvedic physicians. Being yakruttuejakadi

specific gunas it can be said that Gomutra may support the normal liver functions.

Cows urine has been used to mitigate the effect of poisonous drugs, organic

and inorganic in origin of Ayurvedic medicines. With 7days process of Gomutra

127

Sodhana, the Gomutra with its teekshana, ushna, laghvadi gunas it may mitigates

the adverse effect of Bakuchi seeds and may helps in quick assimilation of drug

Bakuchi. And this Gomutra with its Switra kushtaharadi gunas it may potentate the

action of Bakuchi in management of Switra.

8) The western system of medicine opines the Vitiligo as autoimmune

disorder. The internal proportion of the present study contains the drugs-

Amalaki, Khadira, Haritaki and Bakuchi. The drugs Amalaki, Khadira,

Haritaki were chemically rich in tannins. These tannins were described in

modern pharmacology as “tanins are non nitrogenous plant constitutes

characterized by their astringent action upon mucous membrane, they

precipitate proteins from the cell of mucous membrane and thus exert a

“protective action”.

In Ayurvedic literature the term Rasayana mostly correlates with the immune

system of the western science. Amalaki and Haritaki were explained as best

Rasayana and on the other hand the Bakuchi also told in some texts as Rasayana.

The drug Khadira is mentioned as utama kushtahara dravya and this property is

chiefly related to present study.

If the Vitiligo is accepted as auto immune disorder the drugs used in this present

study being rasayanadi specific gunas they may play an effective role in protecting or

correcting or toning of the immune system (vyadhi kshamatva shakti) of the body and

thus may result in curing the Vitiligo.

The chief internal preparation of present trial (Dhatryadi Yoga), Gomutra shodhita

Bakuchi powder done bhavana in khadiramlaka kashya and the effect of this

compound appropriated on Switra is explained as hantiswitram nasamshyam.

128

In this way the systematic correction with internal preparation and the local

stimulation by external application may appeared effective in this present trial.

9) The topical preparation used in the present trial consists of Bakuchi beeja,

harithala (patra) and gomutra. “The essential oil of Bakuchi is able to

permeate through the epidermis to the prickle dells of the lymphatics and so it

finds its way to the subcapillary area and does not produce desquamation of

any change of keratolytic nature resulting in loss of pigment of the epidermis.”

– Dr.K.M.Nadkarni.

The Harihala and Gomutra in this preparation with their ushna, teekshana,

lekhandi gunas they may potentiate the action of Bakuchi in he management of

Switra. And these may give support in permeating of drug through epidermis, thus

may result in perfect stimulation of the melanocytes for their normal melanogenisis.

Bakuchi, Harihala, Gomutra and sunlight, all these factors are having the role in

stimulating the melanocytes for melanogenisis. Thus the efficiency of this preparation

is mentioned in Ayurveda as savarnakaranam param Switra the best curative method

in Vitiligo.

10) Previous survey shows the prevalence of incidence of Vitiligo is more in

females and according to the present study also it is more in males. Youth

and adolescents are more susceptible to this disease. In sixties also it is

in remarkable percentage. In the present study the incidence of males is

57% and of females 43%. The tabular form of incidences and

demography charts follows in the sequential headings.

129

So.Male30%

So.Female20%

Sh.Male27%

Sh.Female23%

1. Sex incidence:

“Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa

(external) along with and without Sodhana (Vamana) in Switra (with special

reference to Vitiligo)” has the following data in sex incidence. From the available

data we can draw a conclusion, that the incidence of Vitiligo is more in males I.e.

57% (9 + 8 = 17 patients) including Sodhana and Shaman. Where as females are

of 43% (6+7=13 patients). The detailed data is as follows in tabular form.

S.No Sex and Group Number of patients included

Percentage Number of patients Best responded

Percentage

1 Sodhana Male 9 30 6 66.66 2 Sodhana Female 6 20 3 50 3 Shamana Male 8 27 4 50 4 Shamana Female 7 23 5 71.42 Total 30 100 18 -

Graph - 1 :- Showing the sex incidence

130

15 – 2554%

35 – 4513%

45 – 5513%

25 – 3520%

2. Age incidence

In the present study the age incidences are as follows. The study according to

inclusion and exclusion criteria includes between ages of 15 to 55. The study for the

convenience classified in to regular intervals of 10 units. The distribution of patients is

as follows.

S.No Interval Sodhana Group

% Shamana Group

% Total %

1 15 – 25 9 59 7 47 16 54 2 25 – 35 4 27 2 13 6 20 3 35 – 45 1 7 3 20 4 13 4 45 – 55 1 7 3 20 4 13 Total 15 100 15 100 30 100

Over all expression is found, as the age group below 25 years of age is more

then half of the study i.e.54%. The rest of the groups are 46%. Perhaps cosmetic

values commenced in the Vitiligo might be dragged more youth then that of aged

people. Disease long term association and incurability would have dissappointed the

elder groups not to attend the traatment schedules. The graphical representation is

as follows.

Graph – 2 :- Showing the Age incidence

131

Sh.Others0%

Sh.Hindu47%

So.Christian0%

So.Hindu40%

Sh.Christian0%

Sh.Muslim3%

So.Muslim10%

So.Others0%

3. Religion distribution: -

At the present study it is observed more Hindu patients (40 + 43 = 83%) are

reported. It doesn't mean that Hindu patients have more incidence of Vitiligo. In the

locality where study is done has more population of Hindus and especially Pategar

families are prone to get this disease in their families it is hereditary and the ratio is

1:10. This is only a segmental study of one area in Gadag. The reported cases are

grouped as under.

Group Number of

patients Before

Percentage Number of patients Best Recovered

Percentage

Sodhana Hindu 12 40 7 58.33 Sodhana Muslim 3 10 2 66.66 Sodhana Christian 0 0 0 0 Sodhana Other 0 0 0 0 Shamana Hindu 14 47 8 57.14 Shamana Muslim 1 3 1 100 Shamana Christian 0 0 0 0 Shamana Other 0 0 0 0 30 100 18 -

Graph – 3:- Showing the Religion distribution

132

Shamana higher

3%

Shamana Poor7%

Sodhna H.Middle

17%

Sodhna Poor7%Shamana

H.Middle3%

Shamana Middle36%

Sodhna Middle27%

Sodhna higher0%

4. Economical Status distribution

Present study is done under four categories of distribution. Much of the

patients fall under middle class, probably they undergo insecurity feeling or crave for

the higher status. For the above region they strain and stress them selves and get

captured in to the clutches of Vitiligo. The data and flow-chart as follows.

Group Number of patients

Percentage Number of patients Best Recovered

Percentage

Sodhana Poor 2 7 1 50 Sodhana Middle 8 27 4 50 Sodhana Higher Middle 5 17 4 80 Sodhana higher 0 0 0 0 Shamana Poor 2 7 2 100 Shamana Middle 11 36 5 45.45 Shamana Higher Middle 1 3 1 100 Shamana higher 1 3 1 100 30 100 18 -

Graph – 4:- showing the Economical Status distribution

133

Shamana Active23%

Sodhana Labor10%

Sodhana Sedentary

13%

Shamana Labor13%

Sodhana Active28%

Shamana Sedentary

13%

5. Occupation distribution: -

This is done under three categories. It seems that sedentary and active group

patients have high incidence of Vitiligo and the labor group has very less. It may be

because of sedentary lifestyle in which Kapha is predominant or obstruction to the

srotases is seen. Out of present study it is being observed that the people who are

more dynamic and active are prone to get this condition as they are over exerted and

exited. The psychological intervention can not be ruled out, as it is a psychosomatic

disorder. The distribution and diagram as follows.

Group Number of patients

Percentage Number of patients Best Recovered

Percentage

Sodhana Sedentary 4 13 2 50 Sodhana Active 8 28 5 62.5 Sodhana Labor 3 10 2 66.66 Shamana Sedentary 4 13 3 75 Shamana Active 7 23 5 71.42 Shamana Labor 4 13 1 25 30 100 18 -

Graph – 5:- Showing the Occupation distribution

134

Shamana50%

Shamana Vegetarian

30%

Sodhna Vegetarian

27%

Sodhna Mixed diet23%

Shamana Mixed diet

20%

6. Diet distribution:

Food plays an important role in disease development. As such salt, wheat

floor, curd and milk mixed with food which more practiced in this area are the

common causative factors of this disease to develop. Thus it is necessary to

emphasize diet regulations in the research study. Present study has the distribution

of food regulations 17:13 to that of vegetarian and mixed diet. The data as follows.

Group Number of

patients Percentage Number of

patients Best Recovered

Percentage

Sodhana Vegetarian 8 27 6 75 Sodhana Mixed diet 7 23 3 42.85 Shamana Vegetarian 9 30 6 66.66 Shamana Mixed diet 6 20 3 50 Total 30 100 18 -

Graph – 6:- Showing the Diet distribution

135

Responded40%

Not Responded0%

Best Responded60%

Result in Group study: For the convenience and evaluation present study undertaken in two groups

"A" and "B". Group "A" was defined as Sodhana therapy followed by Shamana

therapy and group "B" Shamana therapy, following the treatment for same length of

period. Equal number of distribution is taken in both groups, each group consists of

15 patients. Present study under taken 30 patients in two groups.

The result was studied under the symptomatic and Patch area readings along

with serum copper studies. Over all result is emphasized as explained earlier. Out of

30 patients all satisfied with the treatment schedule and expressed normalcy both

symptomatic and on patch colour index. The P value also shows high significance as

P<0.001. The result is as follows. 60% of patients got cured and 40% have

remarkable relief. Thus the present study combination under the title Evaluation of

the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with

and without sodhana (Vamana) in Switra (with special reference to Vitiligo) is said to

have efficacy in relation to regulate Switra i.e. Vitiligo.

Graph – 7: - showing the result of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana)

in Switra (with special reference to Vitiligo)

136

Result of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external) along with and without sodhana (Vamana)

in Switra (with special reference to Vitiligo) in tabular form

S.No Category Number of patents Percentage 1 Best responded 18 60 2 Responded 12 40 3 Not responded 00 00 Total 30 100

CONCLUSION:

So it can be concluded that the preparations-

1) Avalgujadi lepa – (bakuchi beeja – 1part, Haritala – ¼ part, bhavana in

Gomutra = vatikas).

2) Dhatryadi Yoga- (Gomutra shodhitha Bakuchi beeja churna, bhavana

in Khadiramalaki kashaya).

Of present clinical study were best choice of compound preparations in the

management of Switra, with out showing any kind of adverse effects.

♦ A separate study with external application group and internal medication

group is required to assess the effect of the individual preparations. Since

the present study highlights the combined action of he both external and

internal preparations vis a vis to sodhana and sodhana shamana groups.

♦ Finally it can be very safely concluded that the above mentioned drug

combinations has a positive role in the management of the disease Switra.

The premising results observed in the present study calls for further

enlarged clinical study at different centers.

i

Summary

Of Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and

Avalgujadi lepa (external) along with and without sodhana (Vamana) in

Switra (with special reference to Vitiligo)

Vitiligo is a common chronic and progressive skin disease characterized by

the lack of melanin pigments producing skin patches with sharp and often hyper

pigmented edges. This disease affects approximately 1% of the worldwide

population. White patches of skin usually on exposed areas of the body- can occur

symmetrically. Emotional stress may the onset of Vitiligo. Out of which kandas 1,5,6

and 19 mention the terms under this study. The other terms used in the place of

swetha Kusta, Kilasa and Palita are synonymous. The term hence was used for a

person who shows white patches on the body.

The remedy gives for sweta Kusta in Atharvanaveda chiefly consist of four

plants. Which go under the terms 'Rama, Krishna, Asikni and Rajani. According to

some authors these four terms are synonymous.

The knowledge regarding Kusta appears very ubiquitously in these centuries

and Charaka treats the clinical conditions of Kusta in all its aspects. The term 'Kilasa'

appears in Chikitsa chapter, along with Kusta. Chikitsa Sthana of Charaka devotes

7th chapter entirely to the treatment of Kusta and allied conditions. The mention of

'Somaraji' as a remedy for Kusta appears in the Charaka Chikitsa Sthana although

the drug appears to be mentioned in sutra Sthana for other uses.

Vagbhata mentions all the important terms - Kusta, Switra and Kilasa, but he

mentions Krimi with Kusta and Switra in one and the same chapter. All authorities of

Ayurveda accept the limitation of Switra up to the skin. According to Ayurveda,

ii

vitiation of Bhrajaka Pitta brings changes in the normal colour of the skin, in vitiligo,

which is something like defective melanin formation.

This is an unappealing yet harmless skin disorder characterised by white

patches of skin that have seemingly lost their ability to produce the normal colour of

the skin. The description of Switra is available since vedic literature only. The terms

used in the place of Switra in vedic literature are sweta Kusta, Kilasa and palita. The

term's palita and sweta Kusta are also supports the changing of the normal colour of

skin into white. The term Switra is firstly appears in Ayurvedic classes only. The term

Switra derives from the root - "swita varne swita" - that means which gives white

colour. So Switra can be defined as the disease which turns the normal colour of the

skin to white.

In Amarakosha gurubala prabhodhini the term Switra is defined as "swetate

twaganena Switram" - means by which the colour of skin - turns into white. The

cardinal symptom of the Vitiligo is localised de pigmented patches. The all above-

mentioned definition gives support to Vitiligo and its cardinal symptom perfectly.

In further how skin cells interact with one another via cell to cell signalling and

attachment, how the skin protects itself from the external environment has to be

studied in detail.

Many other skin diseases are inflammatory without being autoimmune.

Studying the skin as an active immune organ, with a focus on immunocompetent

cells that are both resident within skin and trafficking through skin. Skin stem cells

include that necessary for the continued repopulation of the skin itself as well as

those related to skin appendages, hair, nails, and eccrine and apocrine glands.

iii

Is VITILIGO a melanin malfunction or a skin disease?

Abnormally functioning nerve cells may make toxic substances that injure

melanocytes. The body’s immune system may destroy melanocytes. Pigment-

producing cells may self-destruct. While pigment is forming, toxic by products could

be produced and destroy melanocytes.

The layers of Twak forms in the stages of grabhavastha, as layer of scum

formation on boiling milk. According to "Susruta" Twak is composed of seven layers

and six layers by "Charaka". The specific "Bhrajaka Pitta" is located in Twak.

Bhrajaka Pitta is stated to be located in the skin and to impart to this structure

its characteristic colour and luster. Bhrajaka is located in the skin. The production of

normal and abnormal colour of the skin, as whole, and parts and structures of the

body viz. hands, feet, sides, back etc., (Bhela). The central cells of the solid down

growth undergo alteration to form the hair, while the peripheral cells are retained to

form the living cells of the hair follicle. Microscopic anatomy of the skin:

Structurally the skin consists of two principal parts. The epidermis is

cemented to the inner, thicker, connective tissue part called the dermis. Beneath the

dermis is a subcutaneous layer. Fibers from the dermis extend down into the

superficial fascia and anchor the skin to the subcutaneous layer. The epidermis

consists of 5 layers, which are

♦ Stratum corneum

♦ Stratum lucidum

♦ Stratum granulosum

♦ Stratum spinosum (prickle cell layer)

♦ Stratum germinatinum

iv

The vellous hair covers all thin skin, so that the vellous is the body hair of all

the infants and children. Terminal hairs from the scalp hairs body hairs, axillary hairs

and genital hairs of the adult and are coarse and pigmented.

Eccrine glands are the common sweat glands, occurring all over the body, but

their population is most dense over the thick skin. Sebaceous glands

Sebaceous glands develop from the hair follicles and therefore, they are not found

over the thick skin.

In the skin and hair it is probable that melanin serves a protective action

against the harmful effects of sunlight. The colour of skin is due to melanin, a

pigment in the epidermis, carotene, a pigment in the dermis, and blood in the

capillaries in the demis. The amount of melanin varies the skin colour from pale

yellow to black. Melanin is synthesized in cells called melanocytes. The number of

melanocytes is about it in allreces, difference in skin colour is due to the amount of

pigment the melanocytes produce and disperse.

Melanocytes are situated In between the keratinocytes of the based layer of

the epidermis. Epidermal melanocytes reside in the epidermal basal layer and

synthesize melanin within specialized organelles called melanosomes. melanoblast -

precursor to melanocytes and melanophores

♦ melanocyte - a cell that synthesizes melanosomes

♦ secretory melanocytes - distribute their melanosomes into neighboring cells

♦ continent melanocytes - retain their melanosomes within themselves, not

secretory

♦ nevocellular melanocyte (nevus cell) - a subtype of epidermal melanocytes that

are continent with their melanosomes

v

Melanocytes:

Melanin pigmentation in the skin in man is a dual process which involve not

duly the production of melanosomes within the melanocyte, termed melanogenesis,

but also the distribution and transfer of these pigment granules to surrounding

epidermal keratinocytes.

Melanoblast migration seems to depend on the c-kit proto-oncogene, which

is, expressed on melanocytes, mast cells, germ cells, enteric ganglion pacemaker

cells of the intestine, and bone marrow stem cells.

In the basal layer of the human epidermis there are about two billion

melanocytes. A reduction in the number of melanocytes occurs in the skin with

advancing age. Total adult epidermal melanocyte population is about 2(109) cells with

a volume of 1-1.5 cm3. The mean density is about 1500 melanocytes / mm2. In

adults, sun exposed skin (especially the head and forearms) have approximately

twice the melanocyte density as sun protected skin (except the genitalia). There is an

age-related decrease in melanocyte density of 6- 8%/decade in both sun exposed

skin (especially the head and forearms) and sun protected skin (except the genitalia).

The position and distribution of melanocytes is influenced by keratinocytes

since melanocytes are clustered, both basally and suprabasally, when cultured in

fetal skin equivalents, Whereas in neonatal skin equivalents they are singly

distributed along the basal layer only.

Melanocytes undergo mitosis infrequently in unstimulated skin (thymidine

index 0.7% of melanocytes are labelled) relative to keratinocytes (thymidine index

15% of KCs), but are activated to divide in UV-stimulated skin (thymidine index 2.1%

of density in sun-exposed skin over sun-protected skin.

vi

Melanocyte has comparatively large nucleus and Melanin granules also take

enzymatic activity. Appear as clear cells resting on the basement membrane in the

basal layer. The Vertical sections have a melanocyte: basal keratinocyte ratio 1:10.

Epidermal melanocytes are dendritic cells whose dendrites interdigitate among

neighboring keratinocytes within the malpighian (cell cycling) layer. Each melanocyte

provides melanin for keratinocytes within its "epidermal melanin unit". a. Melanin is

argyrophylic. Silver stains, e.g. Fontana-Masson stain melanin.

The melanosome-containing dendrite ends are pinched off and endocytosed

by neighboring keratinocytes within the epidermal melanin unit.

Melanocytes on exposed surfaces are more responsive to UV-induced

pigmentation. Skin color on most skin surfaces is due to the sum of constitutive and

facultative melanization. Best-seen in dark skinned people, Does not involve new

melanin sythesis or melanosome transfer and can be seen in UV-exposed cadaver

skin. There are more than 80 genetic loci that determine skin, eye, and fur colour.

Melanin, whenever it is found, is formed in the local cells by the enzyme -

tyrosinase of melanase. Staring product of melanogenesis is tyrosine by the action of

the enzyme tyrosinase, tyrosine is converted to DOPA and then DOPA is converted

to melanin as follows.

Melanin formation in both human and amphibian skin is augmented by the

hormone known as intermedin or melanocyte stimulating hormone (MSH) secreted

by the pars intermedias of the pituitary gland. These are branched tubular structures

arising from the melanocytes. It is held that melanocytes, keratinocytes should be

viewed together as an integrated epidermal melanin unit.

vii

From the melanosomes are formed the melanosomes and these

melanosomes are having tyrosinase activity. From melanosomes melanin granules

are formed. Melanin granules are amorphous and take enzymatic activity. Melanin

granules enter dendrites, travel through these tubules and enter keratinocytes of the

basal cell layer. In the keratinocytes of the basal cell, melanin granules either remain

as a supranuclear cap is distributed diffusely.

The visual colour of the skin is caused by this arrangement of the melanin granules

within the keratinocytes. While in Negro skin, they are distributed diffusely. From the

keratinocytes of the basal cell layer, melanin gets carried to the stratum corneum, by

the progressive differentiation of keratinocytes, through various layers.

The essential factors for Samprapthi are Nidana, Dosha and Dushya strength

of relation between these factors decides severity of the disease. "Agni" and

"Srothas" are the secondary factors in the production of the disease (samprapthi),

with the association of the above mentioned essential factors. The secondary factor

is Agni and between Dosha and Dhatu it is Srothas.

There are different opinions of Brihatrayee in the layer of skin, in which the

Switra manifests. Susruta described seven layers of skin, while Charaka six only.

More over the diseases that are occurring in the first three layers of skin described by

Susruta occurs in the third layer of Charaka. For the definite factor 'aparisravi' signs

of Switra exists no longer. According to ' Hareetha Samhita', Pitta is the main Dosha

in Switra, which vitiates Rakta and causes Switra Kusta with the help of motive force

Vata.

Oestrogen increases melanin synthesis and quantity of free melanin. Copper

deficiency: serum copper studies in Vitiligo by different workers show conflict results.

viii

Thus copper deficiency may cause the Vitiligo. Zosteriform Vitiligo is said as lesions

developed along the distribution of a peripheral nerve and Vitiligo is a functional and

not a structural anomaly.

A defect in enzyme tyrosinase is held responsible for Vitiligo. The area

surrounding the white patches shows increased pigmentation and the blood vessels

hair follicles and glands are surrounded by pigment cells.

Personal or family history of associated diseases including thyroid disorders,

premature graying, alopecia areata, diabetes mellitus, collagen vascular diseases,

permicious anemia, and addision’s disease; personal history of other disorders

aggravated by photoexposure or of photosensitivity.

The description and various treatments for Switra mentioned in almost all the

Ayurvedic texts along with kushtas. Same general principles of treatment for Kusta

and Switra are similar. Switra is a dosha-karmaja vyadhi.

In Charaka Samhita Chikitsa 7th chapter the raktamokshana is mentioned as

a part in treatment of Switra. The above mentioned shonitamokshana supports the

Switra as raktadushtiyanaya roga.

If excessive irritation after local applications poses a problem, the duration of

the exposure is reduced. For eyelids, lips and genitalia topical preparations are

normally required to be sufficient diluted.

The increased melanin pigmentation of human skin following exposure to

sunlight or to U.V light from various sources is known as tanning. Two separate

reactions are recognised immediate pigment darkening (PD) and delayed tanning

reaction.

ix

Charaka, in the treatment of Switra after the internal administration of

malayurasa with guda the sunlight exposure is advised. The duration of exposure is

mentioned as "yadabala suryapadasantapam". Blistering in the lesions may follow

this exposure. The bhaskararadhana, suryanamaskara, ravi vara vrata etc. daiva

vyapashraya chikitsas, which are directly related to exposure to sunlight also

mentioned by some Acharyas in the management of Switra.

The western medical science advises the exposure to sunlight to the Vitiligo

lesions after 2 hours of psoralen tablets (trioxalen etc) internal administration and

after topical application. The essential oil bakuchi seeds and the sunlight these both

are having the melanocyte stimulating action. Psoralens themselves cannot initiate

melanin formation, they requires radiant energy by exposure to sunlight or ultra violet

light to activate enzyme tyrosinase responsible for the melanin formation.

Drugs can be used either as skin-bleaching agents to treat localised hyper

pigmentation such as freckles and post inflammatory pigmentation, or to increase

pigmentation in acquired localised, skin disorders of hypo pigmentation such as

Vitiligo. At the present study the following herbs are included in the study.

1. Bakuchi

2. Khadira

3. Amalaki and

4. Haritala

Two yogas as internal and external medicine with the names -

♦ Dhatryadi Yoga (internal)

♦ Avalgujadi Lepa (External) -

are distributed to the patients who included in the study.

x

Patients with Switra are selected after screening with inclusive and exclusive

criteria from OPD/IPD of post Graduation and Research Center of DGM

Ayurvedic Medical College, Gadag.

As per Ayurveda this disease is of two types. For example among the pategar

community of Gadag distracts, have 10:1 Vitiligo. Keeping in view these present

clinical studies has been undertaken.

Even though many causative factors for Switra under aharaja (virudhahara,

mithyahara etc,) viharaj (suppression of vegas etc,) viprakrista

(puruvajanmakritha papa etc,) groups are described in Ayurveda.

Scientist has mentioned that lesser percentage of serum copper is may cause

Vitiligo.

Vihara have an important role in relation of this disease. In the present clinical

study the external application is followed by exposure to sunlight. The both

sunlight and essential oil of Bakuchi are having the action of the melanocyte

stimulation. The drug Bakuchi is drug of choice in Vitiligo and which has been

successfully using by various systems of medicines in various forms.

In the present study Bakuchi, which used in internal preparation was purified in

Gomutra for 7 days. Ardraka swarasa is also advised for Bakuchi Sodhana.

Being Kusta Switrahara lekhanadi gunas Gomutra has been selected for Bakuchi

beeja shodhana in present clinical study.

In the western system of medicine the available drugs for Vitiligo, obtained from

Bakuchi are trioxalen and methoxalen.

xi

Whereas as in our present study the Gomutra shodita Bakuchi done bhavana in

khadiramalaki kashaya not shown any kind of adverse effects like gastric irritation

etc by its internal administration. The western system of medicine opines the

Vitiligo as autoimmune disorder. The internal proportion of the present study

contains the drugs- Amalaki, Khadira, Haritaki and Bakuchi.

The drug Khadira is mentioned as utama kushtahara dravya and this property is

chiefly related to present study.

The topical preparation used in the present trial consists of Bakuchi beeja,

harithala (patra) and gomutra.

The Harihala and Gomutra in this preparation with their ushna, teekshana,

lekhandi gunas they may potentiate the action of Bakuchi in he management of

Switra. In the present study the incidence of males is 57% and of females 43%.

“Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa

(external) along with and without Sodhana (Vamana) in Switra (with special

reference to Vitiligo)” has the following data in sex incidence. Where as females

are of 43% (6+7=13 patients).

At the present study it is observed more Hindu patients (40 + 43 = 83%) are

reported. It doesn't mean that Hindu patients have more incidence of Vitiligo in

the present study.

It seems that sedentary and active group patients have high incidence of Vitiligo

and the labor group has very less.

Food plays an important role in disease development.

xii

Result in-group study

For the convenience and evaluation present study undertaken in two groups

"A" and "B". Equal number of distribution is taken in both groups, each group

consists of 15 patients. Present study under taken 30 patients in two groups. The

result was studied under the symptomatic and Patch area readings along with serum

copper studies. 60% of patients got cured and 40% have remarkable relief.

CONCLUSION:

So it can be concluded that the preparations-

1) Avalgujadi lepa – (bakuchi beeja – 1part, Haithala – ¼ part, bhavana

in Gomutra = vatikas).

2) Dhatryadi Yoga- (Gomutra shodhitha Bakuchi beeja churna, bhavana

in Khadiramalaki kashaya).

Of present clinical study were best choice of compound preparations in the

management of Switra, with out showing any kind of adverse effects.

♦ A separate study with external application group and internal medication

group is required to assess the effect of the individual preparations. Since

the present study highlights the combined action of he both external and

internal preparations vis a vis to sodhana and sodhana shamana groups.

♦ Finally it can be very safely concluded that the above mentioned drug

combinations has a positive role in the management of the disease Switra.

The premising results observed in the present study calls for further

enlarged clinical study at different centers.

Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external)

along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Dr. Satish Kumar Tiwari

References 1 Charaka Samhita 7th Chapter 2 Susruta Samhita Shareera 4/4 3 Astanga Hridaya Shareera 1/59 4 Ibid 12/14 5 Susruta Samhita 6 Astanga Hridaya Sutra 12/14 7 Charaka Indriya 1/7 8 Charaka Sutra 17/16 9 Ibid 17/15 10 Ibid 17/3 11 Ibid 12/11 12 Susruta Samhita Sutra 21/10 13 Astanga Hridaya Sutra 12/14 14 Gary Quinby, MD PhD and Christine Lin, MD 15 Kunisada et al, 1998 Development 125(15):2915-23 16 Grichnik et al 1998, JID 111:233-8 17 Rosdahl et al, 1983, JID 81:278-81 18 Haake et al, 1991, JID 96:71-7 19 Iyenger, 1994 Experientia 50(7):669-72 20 Gilchrest et al, JID May 2000 21 Can et al, 1998 JID 111:485 22 Schauer et al 1994 J Clin Invest 93:2258-62 23 Chakraborty et al 1999 JID 112:853-60 24 Madhava Nidana 49/37 25 Charaka Samhita Chikitsa 7/177 26 Susruta Samhita Nidana 5/2 27 Harita Samhita 2-1 & 3-38-1 to 3 28 Astanga Sangraha Sutra 22/89 29 Astanga Hridaya Nidana 14/2 30 Madhava Nidana 49/37 31 Charaka samhita Shareera 7/4

Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external)

along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Dr. Satish Kumar Tiwari

32 Susruta Samhita Shareera 4/ 33 Charaka Samhita Chikitsa 7/174 34 Astanga Hridaya Nidana 14/37 35 Madhava Nidana 49/37

Astanga Sangraha Nidana 14/39 36 Charaka Samhita Chikitsa 7/173 37 Mosher D.B.; Dermatology in General medicine, 3rd edition, Newyork, 1987, pp810-821 38 Charaka Samhita Chikitsa 7/173 39 Astanga Hridaya Nidana 14/74 40 Susruta Samhita Nidana 5/5 41 Madhava Nidana 49/37 Madhukosha 42 Charaka Samhita Chikitsa 7/174 43 Dermatologic Clinics, Vol 11 – Number1- January 1993 44 Astanga Hridaya Chikitsa 20/1 45 Ibid 20/2 46 Charaka Samhita Chikitsa 7/166 47 Astanga Hridaya Chikitsa 20/76 48 Charaka Samhita Chikitsa 7/172 49 Susruta Samhita Chikitsa 9/ 50 Wealth of India published and information SSIR – N.D 1982 pp. 296-97 51 Pharmacopoeia of India manager publication N.D. 1966 pp. 821-881 52 Fluorescence of powdered Vegetable Drugs (1949) Amer. Pharm assoc, 38. Pp. 324-25 53 API Textbook of medicine P-1208, Edited by G.S.Sainani,

Published -Typo Graphics Mumbai 1999 54 I.A.D.V.l. Textbook & Atlas of Dermatology, p-518, Edited R.G. Valla,

Published by Bhalani, 1994 55 Boyd’s Textbook of pathology pp-1991, published by lea & Febiger, London, 1990 56 API Text book of medicine p-196, Edited by G.S. Sainani,

Published by -Typo Graphics Mumbai 1999 57 Samson’s Wright’s Applied Physiology, p-525 & 534, Oxford University press, 1993

Evaluation of the efficacy of Dhatrayadi Yoga (Internal) and Avalgujadi lepa (external)

along with and without sodhana (Vamana) in Switra (with special reference to Vitiligo)

Dr. Satish Kumar Tiwari

58 Susruta Samhita, Shareera 4/4, p-28, Edited by Ambikadutta Shastri,

Published by Choukamba Sanskrit series office Varanasi, 1972 59 I.A.D.V.l. Textbook & Atlas of Dermatology, p-518, Edited R.G. Valla,

Published by Bhalani, 1994 60 API Textbook of medicine P-197, Edited by G.S.Sainani,

Published by -Typo Graphics Mumbai 1999 61 Madhava Nidana 49/37-39, p-288, Edited by vaidys vachaspati,

Published by Choukamba Orientalia, Varanasi, 1986 62 Charaka Samhita, Chikitsa, 7/161-179, p-224

Published by Choukamba Sanskrit sansthan, Varanasi, 1997 63 Bhavaprakash Madhyakhands, 54/45-48,pp-532-533, edited by Brahmasankar Mishra,

Published by Choukamba Sanskrit sansthan, varanasi, 1988 64 Susruta Samhita Nidana 5/17, pp286-287 Edited by Jadavji Trikamjee Acharya,

Published by Choukamba Orientalia,Varanasi, 1980 65 Chakraduta of Chakrapani 50/70-71, p-399 Edited by P.V. Sharma,

Published by Choukamba Sanskrit sansthan, Varanasi, 1998 66 Chakrapani on Charaka Chikitsa 7/167, p-224, Edited by Ganga Sahaya Pandey,

Published by Choukamba Sanskrit sansthan, Varanasi, 1997 67 Chakradutta of Chakrapani 50/70-71, p-399, Edited by P.V.Sharma,

Published by Choukamba Sanskrit sansthan, varanasi, 1998 68 Bhaisajya Ratnawali, 54/47 & 54, pp-621-622, Edited by Atridev Gupta,

Published by Choukamba Sanskrit sansthan, Varanasi, 1998 69 I.A.D.V.l. Text book & Atlas of Dermatology, p-519, Edited R.G. Valla,

Published by Bhalani, 1994

Bibliography

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Published by Association of Physicians of India, Bombay.

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By Harisastry paradakar Vaidya1939

Published by Nirnaya sagar press Bombay.

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By Prof K.R.Srikantha Murthy.

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1959 Published by Chowkhamba publication, Varnasi.

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Vol II, 16th edition,

• Clinical Surgery

By S.Das, 3rd edition, 1992

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by Vaidya Satyanaryana Shastri.

Published by Chowkhamba Vidya Bhavan. Varanasi.

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By Vaidya Satyanaryana Shastri.

Published by Chowkhamba Vidya Bhavan. Varanasi.

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Published at Great Britain, Oxford University Press.

Bibliography

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By John Maclod

1992, Published by Pitman press, Great Britain.

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Baidyanath Publications, Calcutta.

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By Douglas M. Anderson. 24th edition 1989

Published by Oxford & IBH publishing Co. Pvt. Ltd. Bombay.

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By Prof Dr. V.V.S.Sastri. 1999

Published by Publication Division,

PGARC, DGM Ayurvedic Medical College, Gadag

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• Gray’s Anatomy

by Henry Gray, 1973 Published by Longman group Ltd.

• Human Physiology By Dr C.C.Chatterjee, 11th edition 1992

Published by Medical Allide Agency. Calcutta.

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2nd edition 1982Published by Popular Prakashan Bombay

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by Kirtikar & Basu, Vol 1 - 3 2nd edition 1975

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By C. Dwarkanath,

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by Vridha Jeevaka,

1953 Published by Chowkhamba Vidya Bhavan. Varanasi

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By Acharya Sri Narindranath shastri.

1st edition 1989Published by Motilal Banarasidas, Varnasi.

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• Principles of Internal Medicine

By T.R. Harrison and Co. 1962

• Rajanighantu By Pandit Narahari.

2nd edition 1998Published by Krishnadas Academy, Varansai.

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By Dr. M.S.Baghel. 1st edition 1997

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By Kaviraja Ambikadutta shastri.

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By Kaviraja Ambikadutta shastri.

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By M. Ramasundar Rao, 2nd edition 1994

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by william Boyd. 1974

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By Swami Sada shiva Tirtha.

1st edition 1998 Published by Indian books centre, Delhi.

96

SPECIAL CASE SHEET FOR “SWITRA”(VITILIGO) POST GRADUATE AND RESEARCH CENTER, (KAYACHIKITSA)

SHRI. D.G.M.AYURVEDIC MEDICAL COLLEGE. GADAG. Guide : Dr.Ch.Ranga Rao Dr Satish. Kumar.Tiwari . M.D. (Ay) M.D.Scholar Co-guide : Dr. Sivarama Prasad Kethamakka. M.A.(Astro),M.D.(Ay) 1. Name of the Patient Sl.No. 2. Father’s/Husband’s Name OPD No 3. Age - Years IPD No 4. Sex - M F Bed No 5. Rel igion Hindu Musl im Christ ian Other Date of Schedule ini t iat ion Date of Schedule completion 6. Occupation - Sedentary Active Labour

7. Economical status Poor Middle class Higher middle class Higher class 8. Diet - Veg Mixed 9. Address Pin 10. Selection Included Excluded A Shodhita

B Ashodhita 11. Result Cured Pal l iat ive Responded Not responded Discontinued

CONSENT I am ful ly educated with the disease treatment and I got sat isf ied, whole heartedly, I accept for medicinal tr ial over me.

Patients Signature

97

Grand Father

1. Complaints with Durat ion :-

a) White patches over - Durat ion Part Right Left Before 21 days 42 days After

Hands Forearm Palm Thigh Leg Foot Abdomen Back Face Chin Chicks Lips Genitals

b. Sl Lakshana Present Absent + ++ +++

1. Rookshatwam (V) 2. Gati kshayam (V) 3. Roma vidwahi (P) 4. Daha (P) 5. Vrana (P) 6. Sravam (P) 7. Toda (P) 8. Sweda (P)

9. Spota ( i ) Pani (P) ( i i )Pada

10. Kleda in sandhi i . Twacha (K) i i . Astisandhi

11. Gurutwa in body (K) 12. Kandu (K)

2. Vital data.

Pulse BP Temp Resp Wt Height

3. Hetu A. Is i t Hereditary ? Yes / No

I f so, who have i t ?

Brother Sister

Father

Grand Father

Grand Mother Grand Mother

Mother

98

B. Do you feel i t is contagious? Yes / No. I f so from whom ?

C. Physical

i . Burns Yes / No What Sort of ?

Thermal Direct heat Electr ic Sun Chemical i i . Trauma Yes / No What Sort of ?

Accident Abrasion Scratch of I tch Post Surgery Post Inf lamatory

i i i . Natural Pregnancy

D. Psychological :-

a. Psychological trauma Yes / No What Sort of ? b. Emotional upset Yes / No What Sort of ?

E. Systemic :-

i . Any skin problems reported ? Yes / No I f so explain : i i . Any GIT Problems ? Yes / No I f so explain : i i i . Is there any Malnutri t ion ? Yes / No

F. Bacterial : - Leprosy Yes / No G. Protozoal :- Dermal Leishmaniasis Yes / No H. Endocrinal :- Hypopigmentat ion Yes / No Myxoedema Yes / No I . Idiopathic :- Not explainable Yes / No J. Iatrogenic :- Yes / No

99

K. Ahara :- Adhyasana Navanna Viruddh Annapana Dadhi matsya Drava Lavana Snigdha Masha Guru Moolaka Chirajeerna Ahara Pista padartha Ajeerna Ahara Ti lam Ksheera guda vikr i t i Drinking cold water after

- Sweating - Strain - Bhaya

Excess work after food Vyavaya at ajeerna or immediately after food.

L. Vihara Vamana nirodha Vata rodha Mootra rodha Pureesha rodha Bath with cold water – after - sweating

strain bhaya

Divaswapna Papakarma - Dharma Viruddha Sastra Viruddha Nyaya Viruddha Guru dooshena Tight cloths – Dothi / Sari / Jeans

4. Poorvaroopa Sl Poorvaroopa Sl Poorvaroopa 1 Asparsha (V) Ki lasa (K) Khara (V) 6 Kopana (P)

Sparsha

slakshna (K) Adhikyata (P) 2 At isweda (P) Pooyakam (R)

Sweda Asweda (R)

Vrana

Sambheda (Me) 3 Harsham (V) 7 Shoola (V) Aruna varna (V) Bhrama (V) Tamra varna (P) Daha (P) Aloma (P) Chirakari twam (K)

Loma

Sweta varna (K) Swapa avayava (R) 4 Rukshaaruna(V)(R) Toda (M) Tamra (P) (M) Switra bahulam (M)

Varna

Swetha (K) (Me) Vakra sodha (M) 5 Karkasham (M) Kanshuyam (Me) Spotest iratwam (M) Gati kshayam (Me) Kandu (R) Dalanam (Me)

Twak

Kodha (P)

General

v- Vataj, P-Pittaj , K-Kaphaj, R-Raktaj , M-Mamsaj, Me-Medaj.

100

5. Sadhyasadhyata

Sadhya Asadhya Asukle Guhyagata Aloma Ostagata Bahula Padatala gata Asamslistam Hastatalagata Nava Chiram Anagnidagdha ki lasem

6. Assessment Criteria a. Lab Investigat ion

Sl No Investigat ion Before After 1. RBC Total count 2. RBS 3. S. Cu

b. Patch Area

Sl No Patch area Before After 1. Number 2. Posit ion not/Spreading 3. Extent Deep / Superf ic ial

Size a. b. c.

4.

d. 5. Surface

Margin – Thick / Thin Coloured Deep / less

6.

Inf lamatory Yes/ No 7. Bleeding Yes / No 8. Hair discoloured / No 9. Oedema Yes/No 10. Ulcerat ions Yes/No 11. Local temperature r ise/No 12. Pain Present / Not 13. Skin texture changed / No

101

7. Vinischaya

8. Treatment schedule

Sodhita Asodhita

Poorvakarma :- Sadyasnehana : Salavana Panchatikta ghri ta Vamana :- Madana phala yoga (Madana phala + Yast imadhu) Quanti ty :-

Quanti ty of S.No Date Time Liquid given vomit No of Vegas Remark

1. 2. 3.

Yoga :- Internal :- Dhatrayadi yoga Anupana :- Sahapana :- External :- Avalgujadi lepa

S.No. Date Dose Adjustments Complaints Advises Remarks

Signature of Student Signature of Supervisor

Atmajam

Samsparsh

Vataja

Doshajam

Vranajam

Dagdha

Pit taja

Kaphaja

Sankara Parajam

Abhighata

“Evaluation of the efficacy of

Dhatrayadi Yoga (Internal) andAvalgujadi lepa (external)

along with and without sodhana(Vamana) in Switra

(with special reference to Vitiligo)”

ByBy

Guidance : Guidance : Dr. Ch. Dr. Ch. Ranga RaoRanga Rao

CoCo--Guidance :Guidance :Dr. K. SivaDr. K. Siva RamaRama PrasadPrasad

H i s t o r yH i s t o r y• Swetavarne twaganena switram -

• Amarakosha• "Celcus" of Rome first mentioned the term

Vitiligo • Latin word "vitilious" interprets with a 'calf'

comparing the whiteness of the skin of the calf to the human skin.

• Holy 'Qhuran' describes as 'bars' (6th century)• 'Unani' physicians suggested it can be

transmitted from parents to progeny.

Vitiligo looks withWhite patches of skin usually on exposed

areas of the body- can occur symmetrically.

Hair may go grey in patches.Switra - (Leucoderma - Vitiligo) is a

common chronic, progressive and an unappealing yet harmless skin disorder

characterised by the lack of melanin pigments producing skin patches with

sharp and often hyper pigmented edges.

ShareeraFunction of skinFunction of skin

• Temperature regulation• Colour and complexion through melanin• Protect the body from hazardous

elements• Sense perception• Water proof mechanism• Absorption of materials in Abhayanga etc.

Rachana of the skinAyurveda Contemporary

• Avabhasini Stratum corneum• Lohita Stratum lucidum• Sweta Stratum granulosum• Tamra Stratum spinosum• Vedhini Stratum germinatinum• Rohini Papillary superficial layer• Mamsadhara Deep reticular layer

Melanin FlowMelanin FlowRibosome of endoplasmicreticulum

Melanin granules

Keratinocytes of the basal cell layer

Supraneuclearcap diffuse

•Desquamation•Transfer to lymph nodes•G. I. tract and kidneys

Golgivesicle Premelanosome

MelanosomeMigration towards stratum corneum

Dendrites

Melanin FormationAnterior Pituitary

Malanocytes

Gonads

ThyroidMSH

Adrenal Cortex

Para ThyroidPancreas

Suntan in Melanin PigmentationUV Rays

Stimulus +

Pituitary

SKINSKIN

MSH

Adrenal

Inhibitory medullary hormones

Nidana• Mithyahara &

vihara• False behaviours• Blaspheme against

god and teacher• Adhyasana• Vyavaya (Sex)

immediately after food

• Suppression of natural urges

• Excessive intake of • Navanna• Dadhi• Matya• Moolaka• Pistanna• Amlarasa• Tila• Kshira• Guda etc.

Samprapti• Dosha - Vata, Pitta and Kapha• Dushya - Rakta, Mamsa and Meda

NidanaVata - Vyanavata Rakta

Impaired Twacha -Upadhatu

Pitta - BhrajakapittaKapha

Mamsa

Medas

Mamsa Agni

AmaDoshaja

ParajaVranajaAtmaja

LakshanaLakshana• Kaphaja• Swetavarna• Snigdha• Bahal• Kandu• Ghana • Guru

• Vataja• Mandala• Arunabha• Parusha• Paridhwanshi• Pittaja• Padmapatra varna• Daha• Tamravarna

Switra Lakshana from Various Samhita

Chiktsa Sutra

Materials required for

• DHATRYADI YOGA• Bakuchi 1 Part• Decoction of -• Khadira bark Q.S. • Amalaki Q.S. • Gomootra Q.S.

• for purification AMALAKI -

• AWALGUJADI LEPA• Bakuchi 4 Parts• Gomootra Q.S.

• for purification• Haritala 1 Part

BAKUCHI - Psoralia corylifoliaEmblica officinalis

KHADIRA - Acacia catechuHARITAL - (As2 S3)

Arsenic trisulphidum

Objectives of the study

• To evaluate the efficacy of the Dhatrayadi Yoga (internal) and Avalgujadi Lepa (external) over the achromic maculae of the Switra

• To evaluate the effect of the DhatrayadiYoga (internal) and Avalgujadi Lepa(external) in Switra over melinocytogenesis

Exclusive criteriaLepromatus and pityriasis alba patches

are excluded from the study.• Patients below the age of 15 and above

the age of 55 are excluded as disease starts at generally in early adolescence.

• The patients those who are prone to risk, such as Diabetes Mellitus and psychotics are excluded.

• Study design• Prospective clinical trial.

• over Sodhita Rogi and Asodhita Rogi• Sample size

• 30 patients divided in two groups• Duration of trial

• Sodhana: Vamana in 21 days interval• Shamana drug: 70 days (inclusive the

Sodhana days ; in 2nd group continuously)

• Posology • Vamana - As to prescribed directions of texts.

• Dhatrayadi yoga• 1gm TDS or 100mg/kg body weight.

• Avaigujadi lepa• External application Q.S

• Assessment of result :-• Results are assessed on the basis of subjective

and objective parameters to the baseline data• Investigation (Objective parameters)

♦ Haemoglobin %♦ Random blood sugar♦ Serum copper

Patient Showing Improvement in the studyAfter 20 daysBefore

Darkened edges

Patient Showing Improvement in the studyAfter 40 days

70% Melanocytesdeveloped

After 60 days

90% Melanocytes developed

6

6

00

9

9

0 2 4 6 8 10

Group ASodhita

Group BAsodhita

Best responded Responded Not responded

Not responded 0 0

Responded 6 6

Best responded 9 9

Group A Sodhita Group B Asodhita

RESULT GRAPH

Statistical Assessment Individual study of group "A"

Criteria Mean SD SE "t" Value P value RemarksSerum Copper 69.07 61.66 15.92 4.34 < 0.001 Highly

significantNumber of patches 8.0 5.23 1.35 5.93 < 0.001 Highly

SignificantExtent 1.67 0.62 0.16 10.44 < 0.001 Highly

SignificantSize 5.47 3.47 0.89 6.14 < 0.001 Highly

SignificantSurface 1.4 0.51 0.13 10.76 < 0.001 Highly

SignificantMargin 1.07 0.26 0.067 15.94 < 0.001 Highly

SignificantColour 1.27 0.59 0.15 8.47 < 0.001 Highly

significant

Statistical Assessment Individual study of group "B"

Criteria Mean SD SE "t" Value P value RemarksSerum Copper 37.62 25.33 6.54 5.75 < 0.001 Highly

significantNumber of patches 5.73 3.45 0.89 6.44 < 0.001 Highly

SignificantExtent 1.27 0.46 0.19 6.68 < 0.001 Highly

SignificantSize 5.47 3.47 0.89 6.15 < 0.001 Highly

SignificantSurface 1.4 0.51 0.13 10.77 < 0.001 Highly

SignificantMargin 1.07 0.26 0.067 15.97 < 0.001 Highly

SignificantColour 1.27 0.59 0.15 8.47 < 0.001 Highly

significant

Conclusion• Vitiligo is an autoimmune disorder.• lesser % of serum copper may cause Vitiligo. • In the present study the incidence of males is

57% and of females 43%.• In the study external application is followed by

exposure to sunlight.• The both sunlight and essential oil of Bakuchi

are having the action on the melanocytestimulation.

• Topical preparation in the trial consists ofBakuchi beeja, harithala (patra) and gomutra.

• The drug Bakuchi is drug of choice in Vitiligoand which has been successfully using by various systems of medicines in various forms.

• In the western system of medicine the available drugs for Vitiligo, obtained from Bakuchi are trioxalen and methoxalen.

• No adverse effects like gastric irritation etc by its internal administration.

• Present study undertaken in two groups "A" and "B”, each group consists of 15 patients. Studied 30 patients in 2 groups.

• Study highlights the combined action of the both external and internal preparations Vis a vis to sodhana and sodhana shamanagroups.

• It was the best choice of management to Switra, as all patients responded with out showing any kind of adverse effects.

• A separate study with external application group and internal

medication group is required to assess the effect of the individual preparations.• Finally it can be very safely concluded

that the above mentioned drug combinations has a positive role in the

management of the disease

Switra