Toxic melanodermia (Rhyl’s melanosis) is a melanotic occupational dermatosis caused by the toxic effect of petroleum products, coal and photosensitization. The peculiarity of the disease is the possibility of occurrence, both in production and in everyday life, when using furnace heating, heating with kerosene, gas. Dermatosis proceeds in stages, the first manifestation of melanodermia is the reticular pigmentation of the skin of a bluish-brown hue, followed by the development of keratosis and atrophy. Pathology is diagnosed clinically with the establishment of professional harm. Treatment consists in eliminating the provoking factor with the connection of vitamin therapy, hepatoprotectors, enterosorbents, photoprotection.
Toxic melasma is one of the rare types of occupational melanosis that occurs against the background of intoxication with hydrocarbons and photosensitization. Unlike other professional dermatoses, the disease does not have an age limit due to the possibility of occurrence in everyday life. The pathological process is non-endemic, has no age and racial differences, while the cause of occurrence is always the patient’s contact with a harmful substance. Profdermatosis develops mainly in oil-producing and oil-refining countries among workers of refineries, the oil and gas industry. For the first time the description of the disease appeared in dermatology in 1917, when the Hungarian doctor G. Riel identified 17 cases of dermatosis, linking them with the hardships of wartime. Two years later, E. Hoffman suggested that the cause of pathological manifestations is associated with the contact of patients with harmful substances, a year later R. Gabermann proved that toxic melasma is the result of exposure to dust vapors saturated with acridine.
The French dermatologist A. Sivatt in 1923 described identical clinical manifestations, associating them with photosensitization. Since then, dermatologists have been unable to come to a consensus on the question of what diseases with similar symptoms are – varieties of toxic melasma or independent nosologies. The relevance of the topic is connected with the increase in morbidity as a result of the development of the oil refining complex, with the economic losses of states in cases of loss of working capacity by patients suffering from this pathology, violation of their quality of life.
Professional triggers of toxic melanodermia are known, they are substances that cause phototoxic reactions: oil refining products, substandard perfumes, hyperinsolation. The internal state of the patient’s body also matters: lack of vitamins, pathology of the digestive tract, bad habits. The mechanism of development is not fully understood. It is believed that melanogenesis is normally an adaptation of the body to changes in the environment. With the development of pathological processes of melanin formation, excessive ultraviolet radiation is important in 60% of cases, pregnancy in 20% and endocrinological disorders unrelated to pregnancy in 20%.
If the onset of pathology is associated with the transdermal penetration of a pathogenic origin into the skin, then a protective inflammation occurs at the point of contact, the immune system is activated, trying to cope with foreign elements due to the T-lymphocytic antigen-antibody reaction. Ultraviolet light acts on the melanocytes of the epidermis, which are associated with keratinocytes, other antigens destroy keratinocytes and indirectly (through the imbalance of the hormonal system) provoke the release of melanocytostimulating hormone.
In the first case, keratinocytes that have received melanin from melanocytes bring it to the surface as part of horn cells, which is visually manifested by skin pigmentation. In the second case, the hypothalamic-pituitary system stimulates the dispersion and movement of melanin from melanocytes to keratinocytes, which are themselves destroyed. Therefore, simultaneously with hyperpigmentation of the skin, hyperkeratosis and inflammation phenomena are observed.
Since the skin is hormone-dependent, disorders in the hormonal system cause hypermitotic activity of melanocytes and keratinocytes of the epidermis, which, exchanging melanin, initiate inflammation of the skin and its hyperpigmentation. At the same time, T-lymphocytes additionally sensitize the dermis, destroying its cells, provoking the release of cytokines, interleukins into the dermis, stimulating the processes of inflammation and proliferation. This is how toxic melasma develops “cascadingly”.
Classification and symptoms
There is no consensus on the classification of the pathological process in modern dermatology. According to the primary elements, nodular, bullous and mixed melasma are distinguished. As for clinical manifestations, some dermatologists consider poikiloderma of Sivatt and melanosis of Gabermann–Hoffmann to be variants, more precisely, different stages of the development of toxic melanodermia, but most authors are of the opinion that these nosologies are independent. Experts believe that, taking into account the mechanism of development, toxic melanodermia, together with Sivatt’s poikiloderma and Gabermann-Hoffmann melanosis, is included in a large group of melanosis (its toxic reticular variety), and all these pathologies should be considered as independent diseases.
The disease develops slowly. Dermatologists distinguish three stages of the clinical course of toxic melasma: erythematous, pigmented, atrophic. The primary element of the clinical manifestations of the pathological process is erythema, which transforms into a reticulated brown-cyanotic hyperpigmentation in the form of small spots that tend to grow and merge in open areas of the skin, especially in the temples. Cystic dilated capillaries appear on the surface of the spots in the form of small flaky nodules. Hyperpigmented skin thickens, the skin pattern increases, pustules form with the outcome of skin atrophy. Sometimes the mucous membranes are involved in the process. Rashes are accompanied by prodromal phenomena, due to metabolic disorders, the patient loses weight. Sometimes there is a non-intense itching.
Diagnosis and treatment
The diagnosis of the disease is made by a dermatologist on the basis of anamnesis (determination of the cause of dermatosis, detection of occupational harm), clinical and histological data: hyperkeratosis, acanthosis, accumulation of melanin in the epidermis, perivascular infiltration in the dermis. Differential diagnosis is carried out with other melasma, hemochromatosis, pellagra, pigmented photodermatitis, Addison’s disease, arsenic dyschromia. Treatment consists in eliminating the cause that caused the pathological process, course vitamin therapy using hepatoprotectors and enterosorbents, correction of metabolic processes. Externally, photoprotective agents, keratolytic, anti-inflammatory and exfoliating ointments, skin whitening preparations are used. Compliance with a special diet rich in vitamins and minerals is shown. As a preventive measure, regular occupational examinations are carried out at work, working conditions are improved, patients with identified toxic melasma are transferred to another job outside of contact with occupational hazards. Of great importance in the prevention of the disease belongs to the examination of working capacity.