Toxic melanodermatitis is also known as melanodermatitis toxica Habermann-Hoffmann. Some patients develop asymptomatic, pin-point, hyperpigmented macular lesions which appear on any part of the body irrespective of whether the area is exposed to sunlight or not. Some lesions may remain discrete, but most of them coalesce with each other to form large irregular areas of hyperpigmentation.
On the forearms and legs the pigmentation commonly occurs around the hair follicles. New lesions keep on appearing for a few weeks or even a few months and then these lesions tend to disappear spontaneously over the next several months or may even take a few years.
The cause of this disease is not known. It seems to represent a post-inflammatory hyperpigmentation initiated by a substance which reaches the skin via blood. Till the exact aetiopathogenesis is known, it is best to call this disease idiopathic guttate and confluent hypermelanosis.
It was first reported in workers who were exposed to some kind of photosensitizing agent.
Understanding Diseases on Pigmentation
Colour of the skin is constituted by three components:
- Melanin which contributes black colour
- Haemoglobin which contributes red or blue colour depending upon its state of oxidation or reduction, and
- Keratin which contributes light yellow colour.
Melanin constitutes the chief pigment and is produced from the amino acid tyrosine by the action of a copper containing enzyme called tyrosinase. This enzyme converts tyrosine into dihydroxyphenylalanine (DOPA) which is further converted to dopaquinone by the same enzyme.
Both these reactions are oxidative processes which are stimulated by sunlight and oxidizing agents and are inhibited by reducing agents.
Later on, through a series of non-enzymatic chemical reactions, dopaquinone gets converted into melanin and gets bound to a protein molecule.
This entire reaction occurs in small inclusions called melanosomes present in specialised pigment-producing cells called melanocytes.
The melanocytes are dendritic cells located in the basal cell layer of the epidermis and transfer their pigment to the keratinizing cells of the epidermis by means of their dendritic processes. Each melanocyte supplies the melanin pigment to nearly 30 keratinocytes.
This pigment is ultimately lost along with the keratinized cells exfoliating from the surface of the skin.
Disorders of pigmentation can arise either due to a disturbance in the formation of melanin or in its loss from the skin, but occasionally, other causes such as incontinence of melanin towards the dermis in various disease process or deposition of other extraneous pigment may also be responsible for pigmentary disorders.
The disease has a self limiting course. Since the cause of this disease is not known, its treatment is also empirical. If the new lesions continue to appear, the patient should be treated with systemic corticosteroids in a dose of 10 to 20 mg of prednisolone a day. This dose given over a period of four to six weeks has been observed to prevent the appearance of new lesions. Then the dose of corticosteroids can be gradually reduced by 5 mg every 1-2 weeks.
The hyperpigmented lesions tend to disappear spontaneously in the course of an year or so. It is possible to decrease this period. The period can presumably be shortened by local massage with keratolytic agents, or retinoic acid, hydroquinone and fluocinolone acetonide ointments massaged one after the other at night. Vitamin C in a dose of 2.5 gm twice a day may also be given.
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