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hyper & hypo- pigmentation DISORDERS

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.

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hyper & hypo- pigmentation DISORDERS

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  1. hyper & hypo- pigmentation DISORDERS Kenneth M. caranguian md

  2. subtopics • Melasma • Lentigo • Freckles • Juvenile lentigens • Solar lentigens • PIH • Nevus of ota • Idiopaticgutatehypomelanosis • pytiriasis alba • vitiligo

  3. 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

  4. 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%

  5. PHYSICAL FINDINGS:symmetric, intensity of pigmentation variescolor- uniform but may be blotchy,edges- irregular, well defined,(-) inflammation

  6. DIFFERENTIAL DIAGNOSIS: 1. Exogenous ochronosis • associated with bleaching agent hydroquinone. It is caused by the deposition of polymerisedhomogentisic 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.

  7. TREATMENT NOTE: • The patient should not be promised great therapeutic results.

  8. Topical Bleaching Agents A. 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

  9. m/c side effects: irritation and contact dermatitis - treated with topical steroids • Common side effect among abusers is exogenousochronosis- extended use of HQ • Alternating HQ in 4-month cycles with other depigmenting agents can prevent or reduce side effects.

  10. B.MONOBENZYL ETHER OF HYDROQUINONE (MBEH/Benoquin) melanocidal Selectively 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

  11. C. KLIGMAN’S formula 5% HQ , 0.1% TRETINOIN, and 0.1% DEXAMETHASONE - in hydrophilic ointment

  12. D. AZELAIC ACID • a naturally occurring dicarboxylic acid derived from Pityrosporumovale • 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

  13. 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.

  14. 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

  15. 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 Lentigo 3. Solar lentigo

  16. 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

  17. PHYSICAL FINDINGS: Appears as 1-2 cm, sharply defined, red or tan to light brown macules with uniform color

  18. 2. JUVENILE LENTIGENS HISTORY: • 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

  19. PHYSICAL FINDINGS: • appears as round to oval macules, 2 to 10 mm in diameter • Darker than freckles • Uniformly tan, or brown or black

  20. 3. SOLAR LENTIGENS HISTORY: • 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

  21. 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

  22. 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

  23. 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

  24. 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

  25. IDIOPATHIC GUTATE HYPOMELANOSIS DESCRIPTION: • Common assymptomaticdermatosis of unknown etiology • Consists of white small macules in sun exposed upper and lower extremities HISTORY: • 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

  26. PHYSNICAL FINDINGS: • Macules are white and hypopigmented, 2 to 5 mm, Borders regular and smooth to slight xerotic scaling

  27. 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

  28. 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

  29. 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

  30. 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

  31. DIFFERENTIAL DIAGNOSIS: • PIHhistory 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; • Pityriasisversicolor- affects upper trunk of adolescents and adults and has positive microscopy; • Tineacorporis - has positive mycology • Nummular dermatitis- dry or crusted itchy round patches; • Vitiligo - progressive macules with complete pigment loss and no scale

  32. 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.

  33. 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

  34. VITILIGO Sex – equally affected but has a predominance to female- reflects greater concern about cosmetic appearance Age – begin at any age 50% (10-35y/o) old age – unusual Incidence – common worldwide Race - all races Inheritance - >30%, family history, thyroid disease and DM

  35. 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

  36. 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.

  37. 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

  38. PHYSICAL FINDINGS: • Consists of white depigmented 0.5 to 5 cm macules and patches with well defined borders

  39. DIFFERENTIAL DIAGNOSIS: 1. Idiopathic guttatehypomelanosis • 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

  40. 4. Pityriasisversicolor • 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.

  41. TREATMENT: • Psoralen plus ultraviolet A (PUVA) a combination treatment using Psoralen (P) and exposing the skin to Ultraviolet A (UVA)= PUVA General guide: • if vitiliginous skin is <6 cm2 (the size of a quarter or half-dollar)- topical psoralens • large portion - systemic psoralensand sunlight • extremely widespread (>50%),-depigmentation with MBEH may be considered

  42. 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.

  43. Successful therapy requires 9-18 months. 2. Narrowband UVB (NB-UVB)- also use as monotherapy 3. Depigmentingthe 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

  44. 5. Broad spectrum sunscreens - at least spf30 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.

  45. 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

  46. Thank you!

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