[Oxygen-dependent phagocytosis in patients with tinea pedis during treatment]. / Oksigenozavisimyi fagotsitoz u bol'nykh rubrofitiei stop v protsesse lecheniia.

Clinico-cytochemical (with the use of NBT test) studies of 27 patients with T. rubrum-induced trichophytosis of the soles has demonstrated a functional imbalance of the peripheral blood phagocytizing cells. Reduced neutrophil activity is associated with a compensatory elevation of mononuclear fungicidal potential. Chlorophyllipt administration corrected the metabolic shifts.

[Cytochemical study of the natural resistance of the body in Trichophyton rubrum-induced mycosis (tinea)]. / Tsitokhimicheskoe issledovanie estestvennoi rezistentnosti organizma pri mikoze, obuslovlennom krasnym trikhofitonom (rubrofitii).

Clinical-cytochemical examination of 27 patients with tinea has permitted estimating nonspecific immune status of an organism. The NBT-test is shown to be highly informative and active. Differences in metabolic activity of phagocytizing subpopulations of peripheral blood are revealed. The results obtained underlie the development of the pathogenetically substantiated therapy method using diucyphon and chlorophyllipt, immunomodulators of different pharmacological groups.

[The nonspecific correction of phagocytosis in patients with foot mycoses]. / Nespetsificheskaia korrektsiia fagotsitoza u bol'nykh mikozami stop.

A clinico-cytochemical examination of 47 patients with mycosis pedis is presented. The author established that these patients showed an inhibition of the phagocytic activity of neutrophils due to imbalance of acid and alkaline phosphatases. It is considered justified to use diuciphon as a means of unspecific immunocorrection.

[Oxygen-dependent indicators of phagocytosis in an infection caused by Trychophyton rubrum]. / Oksigenozavesimyi indikator fagotsitoza pri infektsii, obuslovlennoi krasnym trikhofitonom.

A clinico-cytochemical investigation of 27 patients with rubrophytia revealed a suppression of phagocytic activity of neutrophils conjugated with inhibition of the nitroblue tetrazolium test. It was confirmed that inclusion into the therapeutic complex of chlorophyllipt allows to level the intraleucocytic metabolic disbalance, to achieve enhanced regression of clinical manifestations of mycosis.

[Clinico-mycologic analysis of the effectiveness of treatment in patients with rubrophytosis of the feet]. / Kliniko-mikologicheskii analiz éffektivnosti lecheniia bol'nykh rubrofitiei stop.

The authors carried out a clinico-mycological study of an extensive method of treatment of patients with rubrophytosis pedis based on an analysis of 34 patients with different clinical forms of the disease. It was established that the complex use of different antibiotics (ketoconazole, clotrimazole, chlorhexidine) proved highly effective.

[The glycolytic status of peripheral blood phagocytes and its therapeutic correction in patients with foot mycoses]. / Glikoliticheskii status fagotsitov perifericheskoi krovi i ego terapevticheskaia korrektsiia u bol'nykh mikozami stop.

Changed glycogen levels in the neutrophils and monocytes is a pathogenetic component contributing to the development of mycoses of the soles and a characteristic feature of nonspecific immune reactivity. The neutrophilic phagocytic activity is depressed in such patients, and the monocytes are functionally inert. Furazolidonum, potassium orotate, and riboflavin are effective stimulants of the cell-mediated defense in such patients.

[The esterase activity of the peripheral blood in patients with foot mycoses]. / Aktivnost' ésteraz perifericheskoi krovi u bol'nykh mikozami stop.

Nonspecific esterase activities were measured in the peripheral blood phagocytes (neutrophils and monocytes) of 37 patients with mycoses of the soles. The measurements have revealed lowered potentials of alpha-naphthylacetate esterase, naphthol-AS-acetate esterase, and naphthol-AS-D-chloracetate esterase, which appears to be due to depressed leucocyte phagocytic activity. Diucifon therapy corrected this metabolic imbalance.