hyper & hypo- pigmentation disorders
DESCRIPTION
hyper & hypo- pigmentation DISORDERS. Kenneth M. caranguian md. subtopics. Melasma Lentigo Freckles Juvenile lentigens Solar lentigens PIH. Nevus of ota Idiopatic gutate hypomelanosis pytiriasis alba vitiligo. MELASMA Acquired in genetically predisposed women. - PowerPoint PPT PresentationTRANSCRIPT
HYPER & HYPO- PIGMENTATION DISORDERS
KENNETH M. CARANGUIAN MD
SUBTOPICS
•Melasma • Lentigo • Freckles • Juvenile lentigens • Solar lentigens• PIH
•Nevus of ota • Idiopatic gutate
hypomelanosis• pytiriasis alba• vitiligo
MELASMA• Acquired in genetically predisposed women.• light-brown to gray-brown macules and
patches on sun-exposed areas.•Chloasma- synonymous term, aka “mask of
pregnancy”• 2nd or 3rd trimester, OCP or exogenous
estrogens• Fades slowly after pregnancy or
discontinuation of OCP
DISTRIBUTION:• sides of the face, forehead, upper lip, chin, malar
eminences and sides of the neck.PATHOPHYSIOLOGY:• Unknown or uncertain• Study - high expression of MSH in keratinocytes
that plays a key role in hyperpigmentation • Most common in women during reproductive
years, 90%• Family history of >30%
PHYSICAL FINDINGS:symmetric, intensity of pigmentation variescolor- uniform but may be blotchy,edges- irregular, well defined,(-) inflammation
DIFFERENTIAL DIAGNOSIS:1. Exogenous ochronosis• associated with bleaching agent hydroquinone. It is caused by
the deposition of polymerised homogentisic acid in the skin.2. PIH• dx is clinical• Skin that was previously inflamed due to dermatitis.• Hx: erythema, pruritus, and dermatitis 3. Phototoxic reaction• Dx is clinical• exposed to systemic or topical medicines or cosmetics, and
UV radiation.• Begins abruptly, in contrast to melasma, which develops
gradually.
TREATMENTNOTE:• The patient should not be promised great
therapeutic results.
1. Topical Bleaching AgentsA. HYDROQUINONE
• 2%- 5% cream or lotion b.i.d. for 2 months.• Compete with tyrosine oxidation by acting as an
alternate substrate for tyrosinase, the enzyme that converts tyrosine to melanin and selective damage to melanosomes and melanocytes
• m/c side effects: irritation and contact dermatitis - treated with topical steroids
• Common side effect among abusers is exogenous ochronosis- extended use of HQ
• Alternating HQ in 4-month cycles with other depigmenting agents can prevent or reduce side effects.
B.MONOBENZYL ETHER OF HYDROQUINONE (MBEH/Benoquin)
melanocidalSelectively taken up by melanocytes and
metabolized into free radicals that can destroy melanocytes permanently, leading to irreversible depigmentation
Reserved for generalized depigmentation with extensive vitiligo
Requires 9-12 months of continuous daily application to achieve complete depigmentation effect
C. KLIGMAN’S formula 5% HQ , 0.1% TRETINOIN, and 0.1% DEXAMETHASONE - in hydrophilic ointment
D. AZELAIC ACID• a naturally occurring dicarboxylic acid
derived from Pityrosporum ovale• 15- 20%• Applied BID x 3-12 months, well
tolerated• tx of acne- decreases comedo formation•Unlike HQ, it targets only hyperactive
melanocytes and thus will not lighten skin with normally functioning melanocytes
F. OTHER TREATMENTS – kojic acid glycolic acid (topical or peels 30-70%) Jessner's solution microdermabrasion•Alternative agents with potential therapeutic effects include aloesin (aloe vera), arbutin (bearberry fruits), licorice extract (Glabridin), soy, and vitamin C.
2. SUNSCREENS/ SUNBLOCKS• Because the ability of the sun to darken
lesions is much greater than HQ to bleach the pigment, strict avoidance of sunlight is imperative.
• Broad-spectrum with SPF 30 or > • Preferably containing, mexoryl,
avobenzone or physical blockers- titanium dioxide or zinc oxide that blocks both UVA and UVB
• IPL and Fractional CO2 laser may have additional benefits but results are variable
LENTIGO• Common, benign, circumscribed, 1-3 cm light yellow
or light brown macules from a localized proliferation of melanocytes due to acute or chronic sun exposure• Histologically - increased number of melanocytes in
the basal layer of the epidermis• affects 30 yrs old and above• May arise after sunburn or after PUVA overdosage• It is a localized hyperpigmentation in 3 patterns :
1. Freckles (Ephelides)2. Juvenile Lentigo3. Solar lentigo
1. FRECKLES HISTORY:• childhood, 5-7 yrs old• AD• M/c in redheads, blondes and fair skinned • Paradoxically, there are fewer melanocytes in a
freckle than in normal surrounding skin, but those that are present are large and able to form more melanin than usual
• Darkens during summertime and fade almost completely during winter
• Usually confined to face, arms, upper trunk
PHYSICAL FINDINGS:Appears as 1-2 cm, sharply defined, red or tan to light brown macules with uniform color
2. JUVENILE LENTIGENSHISTORY:• childhood• Lesions do not increase in number or size,
or darken in response to sunlight• characteristic feature of certain hereditary
conditions•May persist year round or may
spontaneously resolve
PHYSICAL FINDINGS:• appears as round to oval macules, 2 to 10 mm in diameter• Darker than freckles• Uniformly tan, or brown or black
3. SOLAR LENTIGENSHISTORY:
•Common in sun exposed skin• Increased in number and size in advancing
years• 75% of white people over 60 yrs have one or
more lesions• Aka- liver age spots •Usually in association with other changes
from sun damage, including wrinkling, dryness, and actinic keratoses
PHYSICAL FINDINGS:TEND TO BE LARGER (2- 20MM)OVAL TO GEOMETRIC MACULESUNIFORM IN COLOR, APPEAR AS FINE GRAINS, BLOTCHY, WITH BORDERS THAT ARE SHARPLY DEFINED
TREATMENT• Monitor existing lesions for interval change• Stable lesions do not require tx • HQ solutions, tretinoin, azelaic acid cream, glycolic
acid peels and creams are all valuable in reducing hyperpigmenation over weeks to months
POST INFAMMATORY HYPERPIGMENTATION (PIH)• Results from any skin injury• excessive irritation from cosmetic products
and procedures, pimples, scratching or any kind of trauma•Gradual darkening several weeks after the
original injury•More common in darker skin and sun exposed• Some are more prone to PIH than others• resolve after several months or years
NEVUS OF OTA• bluish gray spots (forehead, temples, upper cheeks,
around the eye, and eyebrow and nose, mucosa, conjunctivae, and tympanic membranes)• With shades of blue, black, purple or brown• More common in Asians in 1- 2 % of the population• can cause facial disfigurement - emotional and psychologic
distress• Females > males (4x)• Both dermal and epidermal components may co exist• Creams- ineffective• Can be effectively lightened with pigment lasers (ND-YAG,
Q switched) but multiple treatment sessions (about 7 to 10) are required
IDIOPATHIC GUTATE HYPOMELANOSISDESCRIPTION:• Common assymptomatic dermatosis of unknown etiology• Consists of white small macules in sun exposed upper and
lower extremitiesHISTORY:•middle aged and older people• 50- 70 % over the age of 50• F>M• Genetic predisposition • Although asymptomatic, it is cosmetically distressing• Lesions are stable in size but the number increases with
age
PHYSNICAL FINDINGS:
• Macules are white and hypopigmented, 2 to 5 mm, Borders regular and smooth to slight xerotic scaling
TREATMENT:
• Encourage sun protection with clothing• Sunscreens are less effective •Can be camouflaged with tinted make up• Self tanning creams that contains
dihydroacetone darkens the lesions, but the appearance is not pleasing• A light spray with liquid nitrogen may partially
fade the lesions although there is a potential to worsen the dyspigmentation•Reassurance is all that is required
PITYRIASIS ALBA• hypopigmented, slightly elevated, fine scaling patches
with indistinct borders typically on the lateral cheeks, lateral upper arms and thighs• young children, resolves in early adulthood• Asymptomatic• No history of prior rash, trauma or inflammation• Loss of pigment is often more noticeable and
distressing in darkly pigmented people
• Specific cause is unknown• Hypopigmentation due to both reduced activity of
melanocytes with fewer and smaller melanosomes• Often seen in children between the ages 3 and 16
years• males > females• Occurs more frequently in those of light skinned,
but is more apparent in those with darker complexion
• White macules are round to oval, varies in size, usually 2-4 cm in diameter• A fine surface scale often seen on close inspection• Lesions more common in lateral cheeks, lateral upper arms and thighs• Condition more obvious in summer and in darker skin types
DIFFERENTIAL DIAGNOSIS:• PIH history of another inflammatory skin disorder;• Atopic dermatitis, very itchy symmetrical plaques
that respond to topical steroids;• Psoriasis- symmetrical scaly plaques in typical sites
including scalp;• Pityriasis versicolor- affects upper trunk of
adolescents and adults and has positive microscopy;• Tinea corporis - has positive mycology• Nummular dermatitis - dry or crusted itchy round
patches;• Vitiligo - progressive macules with complete pigment
loss and no scale
TREATMENT:• Treatment is not necessary since it will resolve on
its own. • Reassurance- loss of pigment is not permanent
and fades with time• If the patches are red or itchy, mild topical steroid
can be applied. Sometimes these will help make the skin disorder disappear faster, but other times it may have absolutely no effect at all.
PROGNOSIS:• very good. • no scaring• However if forcefully remove with constant
washing with skin products it could remain longer than usual. But if the correct treatment is applied it can disappear more quickly
VITILIGOSex – equally affected but has a predominance to female- reflects
greater concern about cosmetic appearanceAge – begin at any age
50% (10-35y/o) old age – unusual
Incidence – common worldwideRace - all racesInheritance - >30%, family history, thyroid disease and DM
THREE SUBTYPES OF VITILIGO:• Localized or focal-• <20% body surface area• One or more macules in two single area. • limited to one or may only a few body areas.
• Generalized, aka vitiligo vulgaris; and universalis • -complete or near complete depigmentation.• most common pattern
• Segmental vitiligo- • much more common in children than adults • tends to spread rapidly within the segment of skin.
One or more macules in dermatomal or quasidermatomal pattern.• It corresponds to one or more dermatomes unilaterally
and may meet or slightly pass the midline.
•Common sites includes dorsal hands and fingers, face, body folds, axillae, genitalia•There is also predilection for orifices including eyes, nostrils, mouth, nipples, umbilicus, anus
PHYSICAL FINDINGS:• Consists of white depigmented 0.5 to 5 cm macules and
patches with well defined borders
DIFFERENTIAL DIAGNOSIS:1. Idiopathic guttate hypomelanosis• Small, circular macules, slowly
progressive accumulation of isolated lesions.
2. Pityriasis alba• Asymptomatic, ill-defined small patches
with fine scaling in children and adolescents
3. Discoid Lupus Erythematuses
4. Pityriasis versicolor• Polycyclic, well-demarcated, typical upper trunk
and shoulder distribution. 5. Seborrheic Dermatitis• Distribution pattern- (e.g., scalp, forehead,
eyebrow, nasolabial fold, periauricular, central chest, and back), greasy scales, dandruff.
TREATMENT:1.Psoralen plus ultraviolet A (PUVA) a combination treatment using Psoralen (P) and
exposing the skin to Ultraviolet A (UVA)= PUVAGeneral guide:
• if vitiliginous skin is <6 cm2 (the size of a quarter or half-dollar)- topical psoralens • large portion - systemic psoralens and
sunlight • extremely widespread (>50%),-
depigmentation with MBEH may be considered
• They radically increase the erythema response of skin to long-wave ultraviolet light (UVA) after either topical application or systemic administration.• 75% will have partial repigmentation
when treated twice a week for > 1 year.• Thus therapy be initiated gradually and
monitored carefully.
Successful therapy requires 9-18 months. 2. Narrowband UVB (NB-UVB)- also use as
monotherapy 3. Depigmenting the surrounding skin to blur
the margins or removing all remaining pigmentation in extensive cases may lead to cosmetic improvement.
Blurring of the margins may be attempted with HQ compounds.
4. Oil of Bergamot- contains psoralen as photosensitizer making skin sensitive to the tanning effect of sunlight
5. Broad spectrum sunscreens - at least spf 30
6. Concealing and Camouflaging agents 7. Topical immunomodulators- induce
repigmentation up to 90%. 0.1% tacrolimus ointment BIDx2
months, nearly as effective as superpotent topical corticosteroids and does not carry risk of adverse effects.
8. Surgical techniques- transplant of autologous melanocytes or cultured epidermal autografts to nonpigmenting areas
has promising effect with stable vitiligo that fails to respond to topical or phototherapies
The surgical technique include tissue and cellular grafting
Thank you!