7. …VITILIGO…
• Vitiligo is an acquired , pigmentary
anomaly of the skin characterised by
depigmented white patches surrounded
by a normal or a hyperpigmented border
8. The Roman physician Celsus first
used the term vitiligo in the second
century AD.
It is interesting to note that the
Rigveda (6000 BC or earlier) named
leukoderma as kilas, meaning a
white spotted deer.
10. 2. AUTO-IMMUNE HYPOTHESIS
• Association with other autoimmune disorders-
alopecia areata and thyroid disorders
• Antibodies to melanocytes
• Lymphocytes in early lesions
19. Segmental vitiligo
• Occurs in children
• Not associated with autoimmune disorders
• Depigmentation- dermatomal/
quasidermatomal
• Stable course
• Leucotrichia
• Feathery margin
• Distant lesions- uncommon
• Poor response to treatment
20.
21. Generalised vitiligo
• Extensive lesions
Acrofacial
vitiligo
• Periorificially and
acral parts
• Resistant to
therapy due to
absence of hairs
Lip-tip vitiligo
• lips
• Tip of penis,vulva,
nipples
Vitiligo
universalis
• Widespread
• Multiple
endocrinopathies
25. Course
• Onset < 20 years
• Slowly progressive usually
• Segmental vitiligo – stable
• Spontaneous repigmentation- 10 –
20%
• Acrofacial vitiligo – resistant to
treatment
26. Absence of melanocyte and melanin in the
epidermis
e/m confirms the loss of melanocytes which
appears to be replaced by langerhans cells.
Increased cellularity of the dermis
27. Prognostic factors
• Long standing disease
• Leucotrichia
• Acro facial lesions
• Lesions on resistant
areas
Poor
prognosis
34. DIAGNOSIS
• Age of onset
• Depigmented macules with
scalloped borders
• Leucotrichia
• Koebner’s phenomenon
• Predeliction to sites of trauma
35.
36. vitiligo albinism
onset Later life At birth
course Depigmentation-
progress/regress
Freckling on
photoexposed parts
Eye involvement Not seen Always present
Response to
treatment
Partial/near complete
response
No response
Differential diagnosis
37.
38. Nevus
achromicus
Vitiligo
onset At birth Not present at
birth
Distribution Segmental/focal Segmental/focal/g
eneralised
Morphology Feathered
margins, uniform
pigment dilution
Scalloped
margins, islands
of pigmentation
Hair No leucotrichia leucotrichia
45. Physical modality
1.Photochemotherapy
Psoralens + UVA exposure – PUVA
• Mainstay of vitiligo therapy
• Psoralens – tricyclic furocoumarins
8- methoxypsoralen
topical/systemic
• UVA- in special chambers containing UVA
emitting tubes
PUVA sol – psoralen + sunlight
46.
47. REGIMEN
Topical therapy Alternate days Systemic therapy
Ointment/lotion psoralen (0.6mg/kg)
gradually increasing exposure
till mild erythema
sunlight PUVA – UVA lamps
Protect from sun for 8 hrs
(11:00 - 13:00)
Broad spectrum sunscreens- ZnO
48. RESPONSE TO PHOTOCHEMOTHERAPY
• Repigmentation- slow
• Begins in perifollicular area and periphery of
lesion
• Becomes confluent
• Most readily on face, neck and hairy regions
• Slow responders – acral and non hairy parts
49.
50. • Photo-toxicity
Excessive exposure to UVA / SUN
Topical psoralens
Treatment – withdrawal of psoralen
topical corticosteroids
severe – systemic steroids
• Nausea , vomiting, epigastric
discomfort, giddiness
51.
52. 2. Phototherapy – narrow band UVB (311nm)
• INDICATIONS – in extensive disease>10%
indicated in children and
pregnant women
in patients in whom psoralens C/I
• REGIMEN – Gradually increasing doses of
UVB, given from specialized chambers.
• Safe
53. Medical treatment
• Single lesions esp new
• adjuvantTopical
steroids
• Patient can’t be given
physical modalities
• Rapidly progressive vitiligo
with PUVA
• Vitiligo unresponsive to
psoralens
Systemic
steroids