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12. Vitiligo
Vitiligo is a common skin condition characterized by loss of pigment cells called melanocytes, resulting in chalky white patches on the skin. It affects around 0.5-2% of the population worldwide and has no known cause, though it may be related to an autoimmune response or genetic factors. The patches of depigmentation are well-defined, often appear on areas exposed to the sun like the face and hands, and may worsen with sun exposure. Treatment options include PUVA therapy which uses psoralen drugs and ultraviolet light to stimulate repigmentation, topical corticosteroids to reduce inflammation, and camouflage creams to hide patches.
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Introduction to Vitiligo presented by Dr. Bijay Kr. Yadav at Holly Vision Technical Campus.
Vitiligo is an idiopathic skin discoloration affecting 0.5-2% of the population, linked to melanocyte destruction and genetic factors.
Unknown exact cause of Vitiligo with familial ties; associated with autoimmune diseases; may be triggered by trauma or sunburn.
Sharply defined milky white macules often start in childhood; areas increase during summer due to sun exposure.
Classification includes Localized, Generalized, and specific types such as Segmental and Universal types of Vitiligo.
Vitiligo Vulgaris presents as a common, symmetrical pattern of depigmented skin.
Segmental Vitiligo occurs unilaterally, may start at an early age, often results in white patches on hair.
Universal Vitiligo denotes almost complete body depigmentation.
Acrofacial Vitiligo affects distal fingers and facial areas.
Mucosal Vitiligo primarily involves depigmentation of mucous membranes.
Management includes psoralens for repigmentation; use of sunlight at specific times is recommended.
PUVA therapy combines psoralens with UVA light; systemic or topical application recommended.
Psoralen treatments utilize ultraviolet light for therapy; includes PUVA method.
Cutaneous responses post-PUVA therapy include erythema and perifollicular pigmentation.
Options for management include topical corticosteroids, camouflage cosmetics, and skin grafting.
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12. Vitiligo
- 1. VITILIGO DR. BIJAY KR.YADAV Hollyvision technical campus Shankhamul, Kathmandu
- 2.
- 3. DEFINITION Vitiligo is acommon, acquired, idiopathic discoloration of the skin characterized by well circumscribed chalky white colored macules, which are flushed to skin surface in contrast to leukoderma where a cause of such change is known. There is destruction of Melanocytes in localized area of skin which is caused by immunological mechanism. Leukoderma is the term applied only to depigmented patches of known causes eg: following burns, chemicals, inflammatory disorder. Vitiligo - 0.5 to 2% of the population worldwide. both sexes and in all races Vitiligo has a genetic background; >30% of affected individuals have reported vitiligo in a parent, sibling or child
- 4. AETIOPATHOGENESIS Exact causeis unknown Involves focal area of melanocyte loss Positive family history of the disorder Associated with autoimmune disease such as DM, Thyroid disorder, Adrenal disorder & Pernicious anemia ( vit-B12 deficiency) Trauma & sunburn may precipitate the appearance of vitiligo.
- 5. CLINICAL FEATURES Sharplydefined areas of depigmentation appear. Increase in summer time, when the surrounding skin becomes slightly sun burn. Often start in childhood Macule of Vitiligo: Round, oval Milky white
- 6. CLASSIFICATION Localized Focal- One or more macules in 1 area. Segmental - One or more macules in a dermatomal pattern Mucosal - Mucus membrane alone Generalized Acrofacial - Distal extremities and face Vulgaris - Scattered macules Mixed - Acrofacial and vulgaris involvement, or segmental and acrofacial and/or vulgaris involvement Universal - Complete or nearly complete depigmentation
- 8. VITILIGO VULGARIS COMMONPATTERN symmetrical
- 9. SEGMENTAL VITILIGO Unilateralmacules in a dermatomal early age of onset patches of white hair, known poliosis
- 10. UNIVERSAL VITILIGO Appliesto cases where the entire body surface is depigmented
- 11. ACROFACIAL VITILIGO Typeaffecting the distal fingers and the facial orifices
- 12.
- 13. MANAGEMENT 1. Psoralens 0.6mh/kg is adequate to produce repigmentation, After oral administration maximum concentration of the photosensitizing drug in the blood is achieved after two hours. Maximum UVA radiation from sunlight is available between 9 to 11 A.M Thus to induce maximum photosensitization, it is advisable to take psoralen in the recommended dose after breakfast followed by exposure of the macule to sunlight at 11 A.M Initially exposed for 15 minutes Then exposure time is gradually increased to a maximum of 45 minutes
- 14. PUVA (PSORALEN +UVA) THERAPY Drug + light Systemic/ Topical Psoralen + UVA (320-400nm) UVA chamber, PUVASOL Photometer to measure output
- 15. PSORALEN PHOTOCHEMOTHERAPY (PSORGLEN &ULTRAVIOLET A THERAPY & PUVA THERAPY)
- 16. CUTANEOUS RESPONSE AFTERPUVA THERAPY Erythema Perifollicular pigmentation
- 17. 2. Topical corticosteroids: fluorinated steroid & clobetasol propionate 0.5% cream ( Beclovate) 3. (Cosmetics ) camouflage creams & covermask: It may be used to hide the patch if other modes of therapy have failed 4. Skingrafting : This is done if there is a patch on a exposed area & is cosmetically disfiguring.
Editor's Notes
- #7 Differ by anatomical location, and size of lesions Focal - a few isolated lesions Segmental – unilateral distribution Acrofacial – fingers and around mouth Universal – almost total depigmentation Generalized – most common, symmetrical distribution, form that will be discussed
- #9 Also termed vitiligo vulgaris, the most common pattern. Depigmented patches are widely and usually symmetrically distributed. Most commonly involving the face, upper chest, dorsal aspects of the hands, axillae, and groin Tendency for skin around orifices to be affected (eyes,nose, mouth, ears, nipples, umbilicus, penis, vulva, anus) Lesions also favor areas of trauma (elbows and
- #10 Segmental vitiligo (Fig. 72-2): or quasi-dermatomal distribution. This tends to have an and, unlike the other types, is not associated with thyroid disease or other autoimmune diseases. This type occurs more commonly in children. Alteration of neural peptides has been implicated in the pathogenesis of this type.
- #11 Universal vitiligo (Fig. 72-5): Depigmented macules and patches over most of the body, often associated with multiple endocrinopathy syndrome.
- #15 3.1.2 Psoralen plus UVA (PUVA) Psoralen photochemotherapy consists of the combined use of the photosensitizing chemical compound psoralen and UV radiation to induce a beneficial effect not produced by either alone. Absolute contraindications for PUVA therapy include skin type I, skin malignancies, pregnant or lactating women (for oral PUVA). Relative contraindications are patients younger than 12 years (for oral PUVA).[84,85]
- #16 Most effective treatment available in the United States. PUVA therapy is to repigment the white patches time-consuming, and care must be taken to avoid side effects Psoralen is a drug that contains chemicals that react with ultraviolet light to cause darkening of the skin. Psoralen is injected orally or is applied to the skin Then skin is carefully timed exposure to sunlight or to ultraviolet A (UVA) light that comes from a special lamp.