VITILIGO

HYPOPIGMENTATION

MELANOPENI
C

HYPOPIGMEN
TATION
NONMELANOPENI
C

ANATOMICAL
DEFECTS OF
MELANOCYTE
S
FUNCTIONAL
DEFECTS OF
MELANOCYTE
S
ABNORMALITI
ES OF
VASCULATUR
E

MELANOPENIC HYPOPIGMENTATION
Anatomical
defect
Vitiligo
Piebaldism
Chemicalsrubber
Post
inflammatory

Functional
defect
Pityriasis
versicolor
Endocrine
disorders
albinism

VITILIGO
Vitiligo is an acquired , pigmentary
anomaly of the skin characterised by
depigmented white patches
surrounded by a normal or a
hyperpigmented border

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

ETIOPATHOGENESIS
1.GENETIC:
20 % PATIENTS- POSITIVE FAMILY HISTORY
POLYGENIC INHERITANCE- NALP gene , HLADR4,
CATALASE GENE, ..

2. AUTO-IMMUNE HYPOTHESIS
Association with other autoimmune disordersalopecia areata and thyroid disorders
Antibodies to melanocytes
Lymphocytes in early lesions

3. NEUROGENIC HYPOTHESIS
Segmental vitiligo
Nerve endings

toxin

destruction of melanocytes

Epidemiology
Incidence 1 % population
Race affects all races
No sex predisposition
Age peak -10-30 years

Clinical features
MORPHOLOGY

Depigmented macules- chalky/ milky white

Pigment loss- complete/ partial
Macules- scalloped outline
Geographical ptterns on fusion of adjacent lesions
Hairs in older lesion- leucotrichia

 Trichome vitiligo

LEUCOTRICHIA

SITES
Any part can be affected
Predilection to areas with
repeated friction and trauma
Dorsal aspect of hands and feets
, elbows , knees

PATTERNS
Vitiligo vulgaris
Segmental vitiligo
Generalised vitiligo

Vitiligo vulgaris
Commonest type
Second decade
Family history
Progression rapid/slow

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

Generalised vitiligo
Extensive lesions

Acrofacial
vitiligo

Lip-tip vitiligo

Periorificially and
acral parts
Resistant to
therapy due to
absence of hairs

lips
Tip of
penis,vulva,
nipples

Vitiligo
universalis
Widespread
Multiple
endocrinopathie
s

ACROFACIAL VITILIGO

ITILIGO

VITILIGO UNIVERSALIS

Course

Onset < 20 years

Slowly progressive usually
Segmental vitiligo stable
Spontaneous repigmentation- 10 20%
Acrofacial vitiligo resistant to treatment

HISTOLOGY

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

Prognostic factors

Long standing disease

Leucotrichia
Acro facial lesions
Lesions on resistant areas

Poor
prognosis

Associations
Endocrine disorders

Diabetes mellitus
Pernicious anemia
Addisons disease
Hypoparathyroidsm
Hypothyroidism
Hyperthyroidism

Cutaneous disorders
Alopecia areata

Halo nevus

Atopic dermatitis

Malignant melanoma

Morphea

DIAGNOSIS

Age of onset
Depigmented macules with scalloped borders
Leucotrichia
Koebners phenomenon
Predeliction to sites of trauma

Differential diagnosis
vitiligo

albinism

onset

Later life

At birth

course

Depigmentationprogress/regress

Freckling on
photoexposed parts

Eye involvement

Not seen

Always present

Response to
treatment

Partial/near complete
response

No response

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

Piebaldism

LEUCODERMA

All depigmented lesions

Idiopathic- vitiligo
Chemicals
Inflammatory skin diseases

TREATMENT
DEPENDS ON

Age of patient
Extent of disease
Pattern of disease
Cosmetic disability
Effect on quality of life

General measures
Physical modality
Medical treatment
Surgical treatment

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

REGIMEN
Topical therapy

Alternate days

Ointment/lotion

sunlight

Systemic therapy

psoralen (0.6mg/kg)

gradually increasing exposure

till mild erythema
PUVA UVA lamps
Protect from sun for 8 hrs

(11:00 - 13:00)
Broad spectrum sunscreens- ZnO

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

 Photo-toxicity
Excessive exposure to UVA / SUN
Topical psoralens
Treatment withdrawal of psoralen
topical corticosteroids
severe systemic steroids

Nausea , vomiting, epigastric discomfort,

giddiness

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

Medical treatment

Topical
steroid
s
Syste
mic
steroid

Single lesions esp new

adjuvant

Patient cant be given

physical modalities
Rapidly progressive vitiligo
with PUVA
Vitiligo unresponsive to
psoralens

ORAL MINI PULSE

ORAL
STEROIDSSINGLE DAY
OR ON 2
CONSECUTIV
E DAYS PER
WEEK

OTHERS
TACROLIMUS
,PIMECROLIMUS

FOR FACIAL LESION

CALCINEURIN INHIBITOR

LEVAMISOLE

IMMUNOMODULATER
WEEKLY/FORTNIGHTLY

MONOBENZYL
ETHER OF
HYDROQUINE

DEPIGMENTING AGENT

KHELLIN

PHOTOCHEMOTHERAPY

PLACENTAL
EXTRACT

SURGICAL TREATMENT
Indications- sites poorly responsive to
conventional therapy
Patient with stable disease

MELANOCYT
E TRANSFER

BLISTER
GRAFTING

PUNCH
GRAFTING

SPLIT
THICKNESS
SKIN
GRAFTING

Treatment guidelines
LOCALISED DISEASE
New lesions

Topical steroids

Old lesions

Topical PUVA/ PUVA sol

EXTENSIVE DISEASE
New lesions

Oral steroids + PUVA/PUVA sol NBUVB

Rapid increase

Oral steroids + PUVA/PUVA sol

/NBUVB

Old lesions

Oral PUVA/PUVA sol/NBUVB

Intolerence to PUVA/NBUVB

Oral steroids

GENERALISED LESIONS

Monobenzyl ether of hydroquinone