Vitiligo presentation

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 Localized (segmental) Generalized (non segmental) 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.

15. 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

16. 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.

17. 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

18. 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

19. 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

20. 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

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

22. 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'

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

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