Vitiligo is a skin condition characterized by loss of pigment cells called melanocytes, resulting in pale patches of skin. It affects 1% of the population and has no sex or racial predilection. The causes involve both genetic and autoimmune factors. Clinically, depigmented macules appear on the skin in various patterns including segmental, focal, acrofacial, and generalized forms. Diagnosis is made clinically and confirmed by skin biopsy. Treatment options include topical corticosteroids, phototherapy with narrowband UVB or PUVA, laser therapy, and surgical techniques like grafting.

1. VITILIGO
By
Mwachibua Sam
5th Year MBchB(MKU)

2. …Vitiligo…
• Vitiligo is an acquired, pigmentary anomaly of
the skin characterized by depigmented
patches surrounded by a normal or
hyperpigmented border.

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

4. ETIOPATHOGENESIS
1. GENETIC:
• 20% patients – positive family history
• POLYGENIC INHERITANCE – NALP gene,
HLADR4, CATALASE GENE

5. 2. AUTO – IMMUNE HYPOTHESIS
• Associated with other autoimmune disorders
eg alopecia areata and thyroid disorders.
• Antibodies to melanocytes
• Lymphocytes in early lesions

6. NEUROGENIC HYPOTHESIS
• Segmental vitiligo
• Nerve endings produce toxins which cause
destruction to melanocytes.

7. Clinical features
MORPHOLOGY
• Depigmented macules – chalky/ milky white.
• Pigment loss – complete / partial
• Geographical on fusion of the adjacent lesions
• Hairs – in older lesions - leucotrichia

8. PATTERNS
SEGMENTAL VITILIGO
• Manifest as one or more
macules that follow the
lines of
BLASCHKO/dermatomal
• It is unilateral and does
not cross the midline.
• Occurs most in children.
• Not associated with
autoimmune disorders.
• Feathery margin.
• Leucotrichia.

9. Non – segmental Vitiligo
• Includes all types of vitiligo
that cannot be classified as
segmental.
• Associated with markers of
autoimmune or inflammation
such as halo nevi and thyroid
antibodies.
• Non segmental vitiligo include:
• Focal- Xtd by one or more
macules in a limited area&do
not follow segmental
distribution.
• Generalize-Follows a non-
segmental distribution and is
more widespread than focal.

10. Subtypes of generalized vitiligo
1. Acrofacial vitiligo- Depigmentation occurs on
the distal fingers and periorificial area.
2. Vulgaris vitiligo- This is characterized by
scattered patches that are widely distributed.
3. Universal vitiligo- Complete or nearly
complete depigmentation of the body occurs.
Is associated with endocrinopathies.
4. Lip-tip vitiligo: Involves the lips ,Tip of penis,
Vulva, Nipple

11. Acrofacial vitiligo

12. Vulgaris vitiligo

13. Universal vitiligo

14. Lip-tip vitiligo

15. DIFFERATIALS OF VITILIGO and
DIFFERENTIATING SIGNS & S/O
1. Piebalism
• Present at birth,
nonprogressive, coalescing
depigmented patches,
usually near the midline on
the front, including a
forelock of white hair.

16. 2. Tuberous sclerosis
• Typical ash-leaf
hypopigmented
macules, seizures,
angiofibroma, and
mental retardation.
• Occurs predominately
on the thorax and legs.

17. 3. Lichen Sclerosus
• Women: typically
presents in females as
pruritic white plaques in
the genital area
associated with
epidermal atrophy and
scarring. Vulva
involvement may present
with dysuria and
dyspareunia.
• Men: Occurs almost
exclusively in those who
are uncircumsized.

18. 3. Nevus depigmentosus
• Congenital condition
usually noted at birth or
in early childhood.
• Hypopigmented solitary
patch with jugged
edges, typically on the
trunk. Usually remains
at the same site, but
may grown in
proportion to body
growth

19. 4. Pityriasis alba
• Asymptomatic ill-
defined small patches
with fine scaling
typically on the cheeks
of children and
adolescents, often with
with atopic dermatitis

20. 5. Pityriasis versicolor
• Polycyclic, well
dermarcated lesions
lesions with fine scaling,
on the upper trunk.

21. 6. Incontinentia pigmenti
• Distributed along
Blaschko lines, history
of vesicular eruption
perinatally, female
gender.

22. Diagnosis
• Skin biopsy
• ANA( Antinuclear Antibody). Helps to
determine if the patient has other
autoimmune disease.
• CBC with differential
• Thyroid functioning taste.

23. HISTOLOGY
• Absences of melanocytes 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.

24. TREATMENT
1. CHEMETHERAPY
• Topical corticosteroids: mometazone, hydrocortisone etc
• TCIs: tacrolimus ointment,Pimecrolimus cream
• Vitamin D analogues: Calcipotriol, Tacalcitol.
• Alpha-MSH analogues : Afamelanotide
2. PHOTOTHERAPY
• Narrow band ultraviolet UV-B.
• Photochemotherapy-Involves the use of psoralens combined with
UVA radiation.Psoralen is applied topically or taken orally followed
by exposure to artificial / natural UVA radiation.
3. LASER THERAPY
• laser produces monochromatic rays at 308 nm to treat limited,
stable patches of vitiligo.
4. SURGICAL
• Thin dermoepidermal grafting.
• Suction epidermal grafting.