Main for students or individuals in need to understand more about the disease

1. VITILIGO
By Reinfried Haule

2. Objectives
 Introduction
 Epidemiology
 Etiology
 Classification
 Pathophysiology
 Clinical presentation
 Diagnosis
 Differential diagnosis
 Treatment
 complications

3. Introduction
 To understand Vitiligo one must know about
the following terms;
 Melanocytes
These are one of the skin cells found at the bottom
layer (stratum basale) of the skin epidermis,
middle layer of the eye (uvea), inner ear and
vaginal epithelium which functions in the
production of Melanin.

4. Melanin
Is a dark pigment of the skin primarily
responsible for skin coloration. It also
acts in the protection of skin cells from
DNA(1)- (antagonist) which can lead to
skin cancer
 Vitiligo (simple definition)
corruption and murdering of melanocytes

5. VITILIGO

6. VITILIGO
Definition
Is a skin disease in which pigment cells of the
body (melanocytes) are destroyed in certain
areas of the body
• Its present by white skin patches (macules) in
any location of the body due to
depigmentation
• Vitiligo effects is also seen in hairs since they
also contain melanin

7. ALBINISM VITILIGO
Presents itself at birth Develops overtime or at anytime after birth
Genetic inheritance of faulty melanocytes
(melanocytes do not produce melanin)
melanocytes lose function, destroyed or
decreased
Covers whole skin including hairs. eyes and
skin
Covers only some points in the skin
Skin and eyes are directly affected due to
large coverage
only some white patches in skin than does
not affect the skin and eyes directly
Differences between Vitiligo and albinism

8. EPIDERMIOLOGY
 As long as every human being has got
skin, the it can affects all races though
its more noticeable to people with dark
skin.
 Estimated to affect 1% of the worlds
population
 May appear at any age but mostly
affects the age between 20 and 30
years

9. White patches of
Vitiligo
White patches of Vitiligo

10. ETIOLOGY
 The cause of Vitiligo is yet unknown
though some theories suggests the
defects in melanocytes functioning due
to auto immunity
 Its also possible due to history of family
members with Vitiligo

11. Classification of Vitiligo
Classification of Vitiligo
is based on its nature
of spread which
includes
I. Localized
(segmental)
II. Generalized (non
segmental)
III. universalis

12. I. Localized (segmental) Vitiligo
It’s a type that occurs at one or few areas of the skin its
divided in three types
Focal Vitiligo:
 Its Limited to one or few areas and there is no
progression. Its also not in a clear segmental distribution
Segmental Vitiligo:
 There is a unilateral and asymmetric in distribution of
patches. Thus only one side of the body is affected and
more common in children
Mucosal Vitiligo:
 Mucous membranes are affected including the
membranes of lips, mouth, lining of genitals (urethra and
vaginal) and the conjuctiva membranes of the eye

13. II. Generalized (non segmental)
Vitiligo
It’s the type of Vitiligo that occurs a large part of
the body. Its also contains three types
I. Vulgaris
 Involves the presence of scattered stains
extensively disseminated
II. Acrofacialis
 Contains patches that are localized on distal
extremities (hands and feet)
III. Mixed
 Coexistence of both Acrofacialis and Vulgaris

14. III. Universalis Vitiligo
 This is the uncommon and
the most severe non
segment Vitiligo whereas
the depigmented lesions
completely or almost
completely (≥ 80% of body
surface area) cover the skin.

16. PATHOGENESIS
 Vitiligo is a multifactorial polygenic disorder
with a complex pathogenesis. It is related to
both genetic and non genetic factors.
 Although several theories have been
proposed about the pathogenesis of vitiligo,
the precise cause remains unknown.
These theories includes;
 Autoimmune and cytotoxicity theory
 Intrinsic defect of melanocytes
 Neural hypothesis
 Oxidant –antioxidant mechanism

17. Autoimmune and cytotoxicity
theory
 Autoimmune theory proposes that there is
alteration in humoral and cellular immunity in
destruction of melanocytes. A theory gives
relevance to non segmental Vitiligo is more
frequently associated with autoimmune
conditions than in segmental
 It is due to circulating antibodies against
melanocytes proteins in patients with Vitiligo.
 Its destruction may also be mediated by
CD8+T cells (cellular immunity). Thus
activated CD8+T cells have been seen in
perilesional Vitiligo skin.

18. INTRINSIC DEFECT OF MELANOCYTES
 Melanocytes have an inherent abnormality
that impedes their growth and
differentiation in conditions that support
normal melanocytes
NEURAL HYPOTHESIS
 A neurochemical mediator destroys
melanocytes or inhibits melanin production.
OXIDANT-ANTIOXIDANT MECHANISM
 An intermediate or metabolic product of
melanin synthesis causes melanocyte
destruction

19. Clinical presentation
 There is no history of preceding
inflammation.
 Patients are very susceptible to sunburn.
 Lesions are often symmetrical and
frequently involve the face, hands and
genitalia.
 Trauma may induce new lesions.
 Spontaneous repigmentation can occur and
often starts around hair follicles, giving a
speckled appearance

20. Clinical presentation…………
 White patches of skin
 Whitening or graying of the hair on your
scalp,
 eyelashes, eyebrows or beard
(leukotichia – seen insegmental)
 Loss of color in the tissues that line the
inside of your mouth
 • Loss or change in color of the inner
layer

21. Investigations
 Proper history taking and physical
examinations lead to diagnosis of Vitiligo.
Examine and rule out other medical
problems such as dermatitis or psoriasis.
 Skin biopsy of the affected skin for cytology
 Wood lamp examination
 TSH levels [Thyroid disease].
 • CBC [Pernicious anemia].
 • Evaluation about Diabetes Mellitus.
 • Ophthalmological examination

22. Differential diagnosis
 Cutaneous melanoma
 Dermatologic manifestation of leprosy
 Idiopathic Guttate hypomelanosis
 Mycosis fungoides
 Pityriasis Alba
 Tinea versicolor
 Dermatologic aspects of Addison
Disease

23. Treatment
 There is no cure for vitiligo, but there are
number of treatments that can improve the
condition.
 Sun blocks should be used to prevent
burning. Potent topical steroids or
phototherapy help some individuals.
 Betamethasone valerate 0.1% 12 hourly for
2-4 months
 Finally, referral to a specialist camouflage
clinic is often the most helpful 'treatment'

24. Complications
 Social and psychological stress
 Sunburn and skin cancer
 Eye problems such as inflammation of
iris (iritis)
 Hearing loss.

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