Vitiligo is a chronic disorder characterized by depigmented macules and patches due to the loss of melanocytes, with a prevalence of 0.5-2% and common onset before age 20. It has different classifications, primarily segmental and non-segmental, with various underlying etiological hypotheses including genetic and autoimmune factors. Treatment options include phototherapy, topical/systemic steroids, and surgical methods, though responses can vary significantly based on disease patterns and duration.

1. VITILIGO
REVATHY.M.P

2. INTRODUCTION
 DEFINITION: Vitiligo is an acquired chronic disorder of pigmentation
characterized by formation of :
Asymptomatic , depigmented/achromic macules and patches resulting from loss
of mature melanocytes .
 Recently our understanding of vitiligo has increased because of extensive
research in melanocyte biology and cellular immunity.

3. EPIDEMIOLOGY
 Incidence : Prevalence in general population : 0.5 – 2%
 Age : *Half of patients develop this disease before 20 years of age
*Peak incidence :10-30 years
*Congenital vitiligo has also been described
 Gender : Men and women are affected equally
 Sites : Face and acral areas are commonly involved initially

4. ETIOPATHOGENESIS
 Exact etiology not known.
 Different patterns of vitiligo have different pathogenesis.
 GENETIC:
*Genetic factors definitely important, 20% of patients have a positive family history.
*Inheritance may be polygenic.
 AUTOIMMUNE HYPOTHESIS : Evidences include-
*Frequent association with other autoimmune disorders like alopecia areata and thyroid disorders.
*Presence of antibodies to melanocytes.(Auto antibodies destroy melanocytes melanocyte
absent from the lesion)
*Presence of lymphocytes in early lesions.
 NEUROGENIC HYPOTHESIS:
*Segmental vitiligo is present along a dermatome in distribution of nerves , suggesting a neurogenic
origin.
*It has been hypothesized that a toxin , which destroys melanocytes , is released at the nerve endings.

5. CLASSIFICATION
 According to VGICC (Vitiligo global issues consensus conference),vitiligo is an umbrella
term ,including non segmental and mixed vitiligo
 1.SEGMENTAL VITILIGO
2.NON SEGMENTAL VITILIGO
3.UNCLASSIFIED/UNDETERMINED VITILIGO
4.RARE TYPES OF VITILIGO

6. 1.SEGMENTAL VITILIGO
 Onset : Occurs in children(early childhood)
 Course: Initially rapid(6-12 months), later stabilises
 Skin lesions:
• Unilateral
• Segmental
• Does not cross the midline
 Leucotrichia: On depigmented areas ,as well as away from vitiliginous areas . Seen early in the disease.
 Features:
• Margins are feathery.
• Not associated with an autoimmune disease.
• Depigmentation is dermatomal or quasi - dermatomal.
• Most frequently (50%) seen in distribution of trigeminal nerve(mandibular division).
• Distant lesions uncommon.
 Response to treatment:
• Less than satisfactory.
• Surgical intervention(Melanocyte transplanting , skin grafting)

7. 2.NON-SEGMENTAL VITILIGO
 Multiple small or large depigmented spots.
 Involves both sides of the body .
 Symmetrical distribution.
 Erythema in white skin after sun exposure.
 Mild hypopigmentation on the borders in dark skin on photo-exposed sites
• Acrofacial vitiligo :
*Vitiligo predominantly seen : Periorificially (around eyes and on lips on the face)
Acral parts –Periungual area ,palms and soles
*More resistant to therapy : As hair absent in the affected parts.

8. • Vitiligo vulgaris
*Commonest type.
*Occurs after second decade.
*May be slowly or rapidly progressive.
*Family history is frequently present.
• Vitiligo universalis:
*Widespread vitiligo(>80%-90%) with only few areas of normal pigmentation.
*Associated with multiple endocrinopathies.
• Lip-tip vitiligo:
*Involved areas : Lips , tip of penis , vulva and nipples
• Mucosal vitiligo
*Involves more than one site
• Generalized vitiligo

9. 3.UNDETERMINED/UNCLASSIFIED VITILIGO
 Focal vitiligo :
• Single , small , isolated, depigmented spot.
• Followed for at least 2 years.
• Not evolved to segmental or non- segmental disease.
4.RARE TYPES
 Vitiligo minor:
• Partly depigmented spots.
 Vitiligo punctate:
• Punctate 1-1.5mm spots.
 Follicular vitiligo:
• Involvement of follicular melanocytes in body and scalp.

10. CLINICAL FEATURES
MORPHOLOGY
 Depigmented macules : Chalky or milky white(melanocytes are absent).
 True Koebner’s phenomenon : New lesions appear at the site of trauma.
 Occasionally, three shades ( trichome) are seen in the same lesion - Depigmented center,
surrounded by a hypopigmented rim ,which in turn has normal pigmented skin around it.
 Macules : Have scalloped outline and form geographical patterns on fusion with neighbouring
lesions.
 Hairs : * May remain pigmented
*Older lesions ,hair lose their pigment : Leucotrichia

12. SITES
 Lesions occur in any part of the body
 Frequently affected sites : Areas subjected to repeated friction and trauma .
• Eg :The dorsal aspect of hands and feet ,elbows , and knees
 Figure

13. COURSE
 Onset usually before age of 20 years.
 Usually slow progressive.
 Sometimes, progress rapidly.
 Segmental vitiligo progress initially but stabilizes in about 6 months.
 Spontaneous repigmentation seen in 10-20% of patients ( especially in sun –
exposed parts).
 Acrofacial vitiligo is more resistant to treatment.

14. PROGNOSTIC FACTORS
 Following factors indicate poor response to treatment:
• Long- standing disease.
• Leucotrichia
• Acrofacial lesions
• Lesions on resistant areas :
Bony prominences , nonfleshy areas , nonhairy areas and mucosae and on ankles , wrist,
elbows, periungual areas , nipples and areolae, lips, and genitalia.

15. ASSOCIATIONS
 CUTANEOUS DISORDERS
• Alopecia areata
• Halo nevus
• Atopic dermatitis
• Malignant melanoma and morphea
 ENDOCRINE DISORDERS
• Diabetes mellitus
• Pernicious anaemia
• Addison’s disease
• Hypoparathyroidism
• Thyroid dysfunction
o Hypothyroidism
o Hyperthyroidism

16. DIAGNOSIS
 Age of onset ( Usually not present at birth)
 Wood’s lamp : Delineate actual extent ( especially fair skinned individuals and in
palms/soles)
 Dermatoscopy
• Diffuse white glow
• Reverse pigment network
• Sago grain
• Starbust depigmentation around parent patch
• Koebner’s phenomenon
*Also known as isomorphic phenomenon : New lesions of orginal disease develop at sites of
trauma.
 Depigmented macules( milky white) with scalloped borders
 Leurotrichia
 Predilection for sites of trauma

17. DIFFERENTIAL DIAGNOSIS
1.Albinism
2.Piebaldism
A: Depigmented macules with islands of normomelanotic macules within the area of
depigmentation in central area of trunk
B: Distribution of lesions. Central area of face and trunk and proximal parts of limbs with acral
sparing.

18. 3.Nevus achromicus
Feature Nevus achromicus Vitiligo
Onset Present at birth Not present at birth
Distribution Segmental/Focal Segmental/Focal/
Generalized
Morphology Feathered margins.
Uniform pigment dilution
Scalloped margins . Shows
islands of pigmentation
Hair No leucotrichia Leucotrichia

19. 4.Leucoderma
o Term includes all depigmented(white) lesions of skin including vitiligo
o Causes of leukoderma:
Idiopathic • Vitiligo
Chemicals • Hydroquinone(used in rubber
industry)
• Substituted phenols(used in
footwears)
• Adhesives(used in stick on
bindis)
Inflammatory skin diseases • Lupus vulgaris
• Discoid lupus erythematosus

20. TREATMENT
 Not satisfactory.
 Reasonable improvement expected in many patients.
 Depending factors :
• Age of patient
• Extent of disease
• Pattern of disease
• Cosmetic disability
• Effect on quality of life

21. I.GENERAL MEASURES
 Reassurance and psychological support to the patient and family.
 Explanation about prognosis

22. II. PHYSICAL MODALITIES OF TREATMENT
1.PHOTOCHEMOTHERAPY
 Photochemotherapy is use of psoralens in combination with UVA exposure (PUVA).
 It forms mainstay of therapy in vitiligo
 Psoralens:
• Naturally occurring tricyclic furocoumarins present in a large number of plants.
• Some are synthesized.
• The most frequently used psoralens is 8-methoxypsoralen (8-MOP).
• Depending on the extent of disease : either topical (for localized disease) or systemic (for extensive
disease) therapy is used.
 UVA:
• Is supplied by special chambers containing UVA emitting tubes.
• Sunlight is used , when therapy is called PUVA sol.

23. Regimen:
 Topical PUVA/PUVA sol:
• Psoralen application (on alternate days) followed by exposure to gradually increasing
doses (till mild erythema achieved) of sunlight or artificial source of UVA .
• Dose of UVA needed with topical therapy is less than that needed with systemic
therapy.
 Systemic PUVA/PUVA sol:
• 8-MOP, 0.6 mg/kg, orally on alternate days.
• Followed by exposure to gradually increasing doses (till mild erythema achieved) of
sunlight or to artificial source of UVA .
• Dose of UVA needed greater with systemic therapy.
 After exposure to UV rays, lesions are protected from the excessive exposure to sun by
using broad-spectrum sunscreens, e.g., zinc oxide and avoiding peak sunlight.

24. PSORALEN THERAPY : PRINCIPLES OF
TREATMENT

25. Response:
• Repigmentation is slow.
• It begins in perifollicular area and also periphery of lesions and gradually becomes
confluent
• Repigmentation occurs most readily on face, neck, and hairy regions .
• Acral and nonhairyparts are slow responders.
Side effects:
• Systemic psoralen therapy is generally well tolerated .
• Some patients complain of nausea, epigastric discomfort, and giddiness.
• Excessive exposure (to sun or to UVA) results in phototoxicity.
*Clinical manifestation: Painful erythema , edema , blistering.
*Its more frequent with topical psoralens .
*Treatment : Withdrawing psoralens and use topical corticosteroid therapy.
*Severe or widespread phototoxic reactions : Short course of systemic steroids

26. 2.PHOTOTHERAPY
Two forms of phototherapy have been used in vitiligo:
 Broadband UVB:
• Is no longer used.
 Narrow band UVB (311 nm):
Indications:
• In extensive disease (>10%).
• Especially : Children , pregnant women and in patients in whom psoralens are
contraindicated.
Regimen:
• In gradually increasing doses of UVB, given from specialized chambers.
Side effects:
• Generally safe.

27. III.MEDICAL TREATMENT
Steroids
 Topical steroids:
• Used for: Single lesions, (sometimes a few localized lesions) especially of recent origin.
• As adjuvant to other forms of therapy.
 Systemic steroids:
*Indications:
• Patient cannot be given phototherapy/photochemotherapy.
• In rapidly progressive vitiligo, along with PUVA/PUVA sol.
• In vitiligo, unresponsive to psoralens.
 Side effects to steroids limit their use.
 Recently devised weekly schedule (oral mini pulse) probably causes fewer side effects than
daily doses.
 OMP : Steroids given on a single day or on two consecutive days , every week.

28. Other therapies
 Many other drugs have been used, often empirically:
• Tacrolimus (calcineurin inhibitor)and pimecrolimus: For facial lesions where topical
steroids cause side effects and color match with photochemotherapy may not be
acceptable.
• Levamisole: As an immunomodulator, in weekly/fortnightly doses with variable results.
• Khellin: As part of photochemotherapy
• Placental extract
• Depigmenting agents
*Monobenzyl ether of hydroquinone.
*Used to depigment the few normally pigmented areas in patients with extensive
vitiligo.
*Depigmented skin of photo-exposed areas aggressively protected with sunscreens to
prevent spotty repigmentation.

29. IV.SURGICAL MEASURES
 Indications:
• At sites poorly responsive to conventional therapy (ankles and knuckles), in a
patient with stable disease (for at least 6 months).
 Techniques:
• Melanocyte transfer.
• Blister grafting.
• Punch grafting.
• Split thickness skin grafting

30. GUIDELINES FOR TREATMENT
 *PUVA/PUVA sol : Psoralens + UVA psoralens+ sunlight
 **NB-UVB: Narrow band UVB
LOCALIZED DISEASE
 New lesions
 Old lesions
 Topical steroids
 Topical PUVA */PUVA sol
EXTENSIVE DISEASE
 New lesions
 Rapid increase
 Old lesions
 Intolerance to PUVA/ NB-UVB
 Oral steroids +PUVA*/PUVA* sol or
NBUVB**
 Oral steroids + PUVA*/PUVA* sol/NB –
UVB**
 Oral PUVA*/PUVA*sol/NB-UVB**
 Oral steroids
GENERALIZED LESIONS Monobenzyl ether of hydroquinone

31. SUMMARY
 Etiology : Autoimmune etiology with familial predisposition
 Morphology: *Depigmented( milky white) macules with scalloped margins ,
leucotrichia in old lesions.
*Koebner’s phenomenon in active phase
 Site :Anywhere ,more on pressure points
 Patterns: Segmental vitiligo , nonsegmental vitiligo ( generalized , universal ,
acrofacial, and mucosal) , unclassified/undetermined(focal),rare types of vitiligo.
 Associations: Alopecia areata and thyroid disorders
 Treatment: * Localized lesions – Topical steroids(new lesions)
-Topical PUVA(old lesions)
*Extensive lesions-Systemic PUVA sometimes combined with oral steroids(if
rapidly progressing)

32. THANK YOU