"Melanin"
is what gives our skin its natural colour. Thus whenever
Melanocyte ceases to function, the skin becomes white.
The Melanocyte Stimulating Hormone (MSH) is secreted
from the pituitary gland, which controls pigment cell
function. Vitiligo holds three prominent theories
- the auto immune, self-destruct and neural. Abnormal
nerve cells may injure pigment cells; the body might
be destroying its own tissue as an auto immune response
because it perceives the pigment cells to be foreign;
or the pigment cells may leave an auto toxic substance
that destroys the new pigment cells.
Heredity
plays a major role in the aetiology of cases of vitiligo.
Clinically, this disease may be associated with some
other ailments such as diabetes mellitus, thyroid
or endocrine disorders and anaemia.
Gastrointestinal
disorders too play a role. A past history of typhoid,
jaundice and amoebic dysentery has been quoted. Physical
and chemical agents are responsible for localised
lesions. Leucodermal patches may appear as a result
of an over indulgence with chemicals and physical
stimuli. I have found clinical cases of white skin
because of patients wearing rubber chappals, synthetic
innerwear and tight clothing. In cases of burns, hypopigmentation
occurs. The inflammatory process of psoriasis and
eczema can interfere with the melanin synthesis in
a few patients who report white discoloration of the
skin.
Prolonged medication is also found to produce pigmentary
disorders. Emotional and physical stress may precipitate
the ailment. In many cases we often have no clues
why one develops vitiligo.
Diagnosis of vitiligo does not need special investigation.
It is visible to the naked eye. Normally white patches
appear in two ways. In some cases the discoloration
may appear symmetrically on the lips, fingertips,
toes, around the eyes, the armpits, the areola of
the nipple and private parts. Progression is very
slow.
In the other type, the hypopigmentation starts asymmetrically
as a single or multiple lesion. The face, limbs, abdomen
and the back are affected. In some patients the depigmented
part remains the same size for years together. Sometimes
it spreads rapidly. Hypopigmentation starts as a small
brown spot and is trichromic. Fungal infections such
as Tinea alba, Tinea a versicolar and even leprosy
which look like vitiligo patches require differential
diagnosis.
There is no sensory and motor dysfunction. Whatever
the cause, the disease is never life threatening.
Normally sunlight promotes the pigmentation. Vitiligo
patients are unable to withstand sunlight as it could
produce blisters on over exposure.
Ascorbic acid tends to reduce melanin pigmentation.
Clinically, dietary regulations are necessary. Elimination
of lemon, pickles. Tamarind, Goose berry, Tomato,orange.
Latest clinical research shows that non-vegetarian
food has to be avoided too as it acts as a foreign
body to pigment cells. So no non vegetarians food,
even eggs.
In treatment, vitiligo patients move from one system
to another. Clinical studies have shown that homoeopathy
can cure this disease. Key of success lies in the
administration of minute doses to activate the immune
system to fight in natural way. The minute doses are
free from side effects and suitable for long time
medication..
We cannot treat vitiligo as a local malady as other
systems of medicines do. External applications with
creams and ointments, exposure to sunlight and ultraviolet
rays will not help restore normal body chemistry.
Pigmentation appears with external treatment, but
soon vanishes. These white patches are the local expression
of internal derangement.
The next point is the duration of treatment. Normally
the small patches respond very quickly rather than
the generalised spread. Dark complexioned patients
develop pigmentation very quickly. Even though the
length of the treatment depends individual, We have
seen pigmentation within four months in most cases
and in few cases one year or more.
