type i leprosy reaction edit

TYPE I LEPROSY REACTION

KHUNADI HUBAYA

DERMATOVENEREOLOGY DEPARTMENT OF TUGUREJO GENERAL HOSPITAL, SEMARANG,

CENTRAL JAVA, INDONESIA

PRESENTED IN THE INDONESIAN DUTCH TROPICAL DERMATOLOGY MEETING, YOGYAKARTA, APRIL 7TH - 9TH ,2011

INTRODUCTION

Leprosy Reaction

State of symptoms and signs of acute inflammation in the lesions of leprosy

patients immunological disorder caused by hypersensitive reaction of M.leprae antigens.

Fifty percent (50%) of treated leprosy patients reactions

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Reaction occurs :◦ Leprosy occurs ◦ Occur due to of immunological

changes as a result of anti–leprosy treatment

◦ Occur spontaneously other infectious diseases, anemia, mental and physical stress, puberty, pregnancy, childbirth, surgery.

Anti-leprosy treatment most frequent trigger factors

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TYPE I LEPROSY REACTION T I LR = upgrading reaction, borderline reaction,

tuberculoid reaction, leprosy nonlepromatous reaction

Occurs in 30% of patients with borderline leprosy (BT, BB, BL)

Appears in: - First 6 months of treatment - Occur 2 years after the first treatment - Not received therapy

Jopling : delayed hypersensitivity reaction (type IV hypersensitivity reactions Coombs and Gell )

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Antigens from dead bacilli will react with T lymphocytes changes in celluler immune system.

Result : upgrading/reversal to tuberculoid form ( increase cellular immune system )

down grading to lepromatous form( decrease cellular immune system)

In fact, the type 1 reaction = reversal reaction most often encountered, down grading reaction is rarer

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CINICAL FEATURE

Prominent and shiny erythematous plaques, few days later, the color can change to purplish or brownish. The firm edge of the lesion, pressurized pain or feels hot when touched.

In severe reactions desquamation or ulceration due to necrosis.

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New lesions may show subclinical lesions

Neuritis of the nerves are located superficially.

Mild neuritis, painless enlarged nerves, anesthesia , paralysis.

In severe cases nerve enlargement, spontaneous or pressurized pain, anesthesia on the dermatomes.

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The biggest cause nerve function damage (30% patients) claw hand, drop foot, facial palsy with or without lagophtalmus , keratitis.

Mild systemic symptoms : facial and leg edema. Severe symptoms: malaise, fever, face hands and leg edema

Histopathological: epitheloidcell granuloma edema, dermal edema, plasma cells and granuloma fraction

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INFLUECE OF ANXIETY ON THE IMMUNE SYSTEM (WEBSTER, 1998)

Person experiences excessive anxiety symptoms CRH (Cortico Releasing Hormone) release catecholamin hormone more than the glucocorticoid.

Catecholamin hormone stimulate macrophages stimulate IL – 1O

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increasing the formation of T-helper cell (Th-2) more humoral immunity will be formed Manifestation type 2 leprosy reaction.

Minute glucocorticoid macrophage to slightly stimulate IL - 12 to secrete Th-1 cells the formed cellular immunity will be small Manifestation type 1 leprosy reaction

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MANAGEMENT

Rest or immobilizationElimination of triggering factorContinuing treatment of anti-leprosy drugsAnalgesic sedatives to cope with painProvision of anti reaction drugs

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Mild reaction ◦Nonmedicamentosa: rest, immobilization

◦Medicamentosa: paracetamol, mefenamic acid, aspirin, piroxicam, diclofenac sodium,cyclooxygenase 2 (COX 2)

Severe reaction◦Improvement of general condition by

improving fluid/electrolyte balance◦Must be given corticosteroid

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Provision of CorticosteroidPrednisone 40-60 mg/day single morning

dose, tapering slowly until a few months/years.

Corticosteroid > one month, required minimum dose and alternate-day treatment

Prednisone or prednisolone of 0.5 to 1.0 mg/BB kg/day single morning dose, tapering slowly and alternate-day treatment is more tolerated.

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Hospital for Tropical Diseases in London: prednisolone 30-40 mg tapering to zero over a period of 5-6 months.

Prednisolone 30 mg/day, slowly tapered to zero up to 20 weeks is better than 60 mg/day tapered up to 12 weeks.

Cyclosporin 5-10 mg/BB kg/day used if steroid fail,or as a steroid sparing agent.

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Reported that a case of borderline lepromatous leprosy with type 1 leprosy reaction treated with prednisolone 1 mg/BB kg/day for 4 weeks treatment condition did not improve and the skin lesions remained painful given topical therapy of 0.1% tacrolimus ointment twice daily healing of all skin lesions after 2 weeks and prednisolone dose become zero over a period of 12 weeks of treatment

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Tacrolimus: immunomodulatory and immuno suppressive agent

Surgery

During the treatment failure in the repair of some nerve function exploratory surgery to relieve mechanical compression

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Tugurejo General Hospital Semarang

Uses corticosteroid treatment : methylprednisolone dose = prednisone/prednisolone dependence and the side effect is smaller.

Astaxanthin 4 mg, twice a day orally, astaxanthin a strong antioxidant potential against strong free radicals and having anti-inflammatory effects by inhibiting cytokin and chemokin

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Zinc 200 mg a day stabilizing the cell membrane, machrophage and mast cells that play a role in the immune system.

Changes in zinc metabolism function of immune cells to become abnormal.

Zinc supplementation improve of zinc metabolism increasing immune response against M.Leprae.

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Tgl 9 Oktober 2009 hari pertama

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Tgl 15 Oktober 2009 (hari ke 6)

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Tgl 22 oktober 2009( hari ke 13)

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Tgl tgl 26 Oktober 2009 (hari ke17)

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Tgl 24 November 2009 (hari ke 45)

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“leprosy work is not merely medical relief; it is transforming frustration of life into joy of dedication, personal ambition into selfless service”Mahatma Gandhi

Sandra Dewi, Duta Lepra Indonesia

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PRESENTED IN THE INDONESIAN DUTCH TROPICAL DERMATOLOGY MEETING, YOGYAKARTA, APRIL 7TH - 9TH ,2011