[Lipids peroxidation in children with atopic dermatitis].
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Biomedical subjects
Publications and source records attributed to V G Akimov.
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Blood serum lysyl oxidase activity considerably varies, these variations correlating with the skin process dissemination, in children suffering from focal scleroderma. This enzyme was undetectable in normal subjects and patients with dermatoses whose clinical symptoms are similar to those of focal scleroderma. Blood serum lysyl oxidase activity elevation is a specific sign, characteristic of patients with focal scleroderma; it therefore may be used for the laboratory diagnosis of this dermatosis, assessment of its dissemination and severity.
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The authors have demonstrated the pathogenetic significance of elevated copper levels in the blood and involved skin in development of collagen metabolism disorders in children suffering from focal scleroderma. A correlation between elevation of blood serum copper level and the skin process dissemination and activity was revealed. Copper concentration in involved skin of these children surpassed 7-fold the normal value.
Experiments with 120 guinea pigs have revealed that skin griseofulvin levels depend on blood griseofulvin level and reduce after a prolonged (for 3-4 weeks) administration of the antibiotic in a dose of 30 mg/kg. Reduction of P-450 system enzymes activities achieved with alpha-tocopherol slows down griseofulvin biotransformation rate and significantly elevates its blood serum and skin concentrations.
Guinea pig experiments making use of spectrofluorometry have revealed reduced level of Schiff's bases in skin biopsy specimens obtained from foci of allergic contact dermatitis induced by 2,4-dinitrochlorobenzene (DNCB). Iron sulfate electrophoresis resulted in a decrease of the sensitization and of the allergic contact dermatitis intensity, as well as in enhancement of lipid peroxidation in the skin. These data permit a supposition that reduction of lipid peroxidation is one of the pathogenetic mechanisms of delayed type hypersensitivity, and that lipid peroxidation enhancement in the skin by iron sulfate electrophoresis is one of the possible mechanisms of suppressing allergic contact dermatitis.
Studies with the use of Fe2(+)-induced chemiluminescence of apo-beta-lipoproteins and electron histochemistry have revealed that PUVA therapy and vitamin A high doses enhance lipid peroxidation and activate adenylate cyclase in patients with Devergie's disease. This finding permits a conclusion on the usefulness of enhancing lipid peroxidation in order to reduce cellular mitotic activity.
Two patients with the plaque form of photodermatosis are described. Clinical manifestations of this condition are similar to those of discoid lupus erythematosus in appearance, but not to those of prurigo or eczema. The authors suggest that the term 'polymorphic photodermatosis' be used instead of 'solar prurigo' or 'solar eczema', representing, in their opinion, clinical variants of the same disease.
Symmetrical lipomatosis of the neck (Madelung's syndrome) in a 52-year-old man abusing alcohol is described.
A patient with discoid lupus erythematosus has developed porphyria cutanea tarda. The combination of these diseases may be explained by similar changes in the free-radical processes in the body, induced by sunlight.
Basing on the literature data and their own clinical experience, the authors consider atopic dermatitis as skin manifestations of hereditary atopic constitution. They distinguish 5 clinical forms of the condition, emphasizing the age succession (phase pattern) of the clinical and morphologic picture of the dermatosis. Attention is called to the fact that atopic dermatitis may be a part of the clinical picture of many syndromes. The authors hope that the present discussion will minimize the confusion in the terminology of this disease.
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