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VITILIGO
DR. BIJAY KR.YADAV
Holly vision technical campus
Shankhamul, Kathmandu
Vitiligo
DEFINITION
Vitiligo is a common, 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
AETIOPATHOGENESIS
 Exact cause is 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.
CLINICAL FEATURES
 Sharply defined 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
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
VITILIGO VULGARIS
 COMMON PATTERN
 symmetrical
SEGMENTAL VITILIGO
 Unilateral macules in a
dermatomal
 early age of onset
 patches of white hair, known
poliosis
UNIVERSAL VITILIGO
 Applies to cases where
the entire body surface is
depigmented
ACROFACIAL VITILIGO
 Type affecting the distal fingers and
the facial orifices
MUCOSAL VITILIGO
MANAGEMENT
1. Psoralens 0.6 mh/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
PUVA (PSORALEN + UVA) THERAPY
 Drug + light
 Systemic/ Topical
Psoralen + UVA (320-400nm)
UVA chamber, PUVASOL
Photometer to measure output
PSORALEN PHOTOCHEMOTHERAPY
(PSORGLEN & ULTRAVIOLET A THERAPY & PUVA
THERAPY)
CUTANEOUS RESPONSE AFTER PUVA THERAPY
 Erythema
 Perifollicular pigmentation
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.
12. Vitiligo

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12. Vitiligo

  • 1. VITILIGO DR. BIJAY KR.YADAV Holly vision technical campus Shankhamul, Kathmandu
  • 3. DEFINITION Vitiligo is a common, 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 cause is 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  Sharply defined 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
  • 7.
  • 8. VITILIGO VULGARIS  COMMON PATTERN  symmetrical
  • 9. SEGMENTAL VITILIGO  Unilateral macules in a dermatomal  early age of onset  patches of white hair, known poliosis
  • 10. UNIVERSAL VITILIGO  Applies to cases where the entire body surface is depigmented
  • 11. ACROFACIAL VITILIGO  Type affecting the distal fingers and the facial orifices
  • 13. MANAGEMENT 1. Psoralens 0.6 mh/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 AFTER PUVA 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

  1. 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
  2. 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
  3. 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.
  4. Universal vitiligo (Fig. 72-5): Depigmented macules and patches over most of the body, often associated with multiple endocrinopathy syndrome.
  5. 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]
  6. 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.