Vitiligo

Pathophysiology

Oxidative stress, specifically from hydrogen peroxide, in the setting of reduced cellular defence mechanism

Inherent functional defect of melanocytes

Reduction of melanocytes due to dysregulation of their survival and apoptosis

Toxicity from neuro chemical transmitters

Viruses eg: cytomegalovirus

Etoiology

Auto-immunity-Due to frequent associations with other auto immune diseases such as thyroiditis and type 1 diabetes, the presence of anti melanocyte antibodies and a response to immune suppressant therapy

Cytotoxicity- the possibility that metabolites formed during melanin synthesis may destroy melanocytes

Neural-chemical mediators released at nerve endings might destroy melanocytes or inhibit melanin production

Free radicals-excess free radicals might be toxic for melanocytes

Convergent- a combination of these theories.

Genetic- there appears to be several genes (such as NALPI) that cause an individual to be susceptible for developing vitiligo. what these genes control is yet to be determined

Triggering-it appears that some event must trigger the destruction of the pigment cells.There are many proposed triggers and they may not be the same for all vitiligo situations (such as sunburn, trauma, pregnancy etc)

Immune system can also be involved with the destruction of the pigment cells.That is why vitiligo is frequentely reffered to as an auto Immune disease.

Vitiligo is a condition in which the skin loses its pigment cells (melanocytes).this can result in discoloured patches in different areas of the body, including the skin, hair and mucous membranes. Patchy loss of skin colour, which usually first appears on the hands, face and areas areas around body openings and the genitals. Premature whitening or greying of the hair on your scalp, eyelashes, eyebrows or beard. Loss of colour in the tissues that line the inside of your mouth and nose (mucous membrane).

CLINICAL CRITERIA FOR CLASSIFICATION OF VITILIGO

In active stage v1 new lesions develops which are increasing in size but the border is ill defined.

Stable v2-no new lesions develop. Lesions are stationary in size border is hyperpigmented and well defined.

Improving v3-lesions starts to decrease in size, no new leisions developing. Border defined and signs of spontaneous repigmentation both (follicular and peripheral).

According to the area of spread:

Non segmental vitiligo(also known as bilateral vitiligo, vitiligo vulgaris,and generalized vitiligo)

This is the most common type of vitiligo and results in white patches appearing on both sides of the body. Colour loss comes in spurts over the course of one’s life, spreading and becoming more noticeable as time goes on.

Segmental vitiligo(also known as unilateral vitiligo)

The patches appears in one area of the body, such as one arm or one leg or along the course of nerves like that of herpes zoster(zosteri form is type)

ACCORDING TO THE PIGMENT LOSS

Localized-The vitiligo appears in just one or a couple of sports on the body.

Generalized-The patches of colour loss appear in many areas of the body.

Universal-This is a rare.Most of the original skin colour is gone.

Nutritional etiology

Defects in copper, protiens and vitamins in diet a scientists called Cunningham discovered

The skin of dark people contained more copper that that of white. Copper content was concentrated mainly in the epidermis, in vitro experiment demonstrated that the copper activated the oxidation of dopa by skin extracts containing dopa-oxidase. On the other hand addition of vitamin c neutralize the catalize effect of the copper.

Protien

Vitiligo is also considered as a genetically transmitted disorder. Studies have identified that NALPI, a protein coding gene that encodes a protein related to apoptosis, plays an important role in developing vitiligo.

Vit b12 and folic acid

Vit b12 inhibits the production of homocysteine, a homologue of amino acid cysteine. Homo cysteine down regulates the activity of tyrosinase, an enzyme responsible for melanin production as well as generates free radicals, leading to impaired melanin synthesis and destruction of melanocytes. In this whole process folic acid works in tandem with vit b12 as a methyl group donor.

Combination of vitb12, folic acid and sun exposure is a good strategy to regain the colour.

Supplementation of vit b12, folic acid and pantothenic acid removes white patches.

Vit A, C, E

These vitamins act as antioxidants and prevent epidermal oxidative stress, which is considered as a causative factor for premature destruction of melanocytes.

Vitamin d

Vitamin d increases the rate of melanogenesis by increasing the activity of tyrosinase. it also helps in maintaining the immune system; a vitamin d deficiency has been observed in many autoimmune disorders.

Beta carotene

Beta carotene is a precursor form of vitamin a with immense antioxidant activity. It plays a role in maintaining normal skin colour; moreover, skin deposition of dietary carotenoids provides photo protection for lightely pigmented skins. Vitamin A helps to normalize the appearance of pigmentation. It does so by normalising the activity of tyrosinase, an enzyme that plays a vital role in the production of melanin.