[Calcium-transporting system of erythrocytes in psoriasis]. / Kal'tsii-transportiruiushchie sistemy v éritrotsitakh pri psoriaze.

The activity of Ca-ATPase and permeability of erythrocyte membrane for calcium in patients with psoriasis were studied with the aim to reveal disturbances in the calcium membrane transport under psoriasis. In the presence of endogenic activators the mean values of the maximal Ca-ATPase activity of erythrocyte membranes in patients with psoriasis and in healthy people have no essential differences and make up 264 +/- 12 and 244 +/- 10 mumol P/1 cells per 1 min, respectively. The rate of 45Ca accumulation in erythrocytes under inhibition of Ca-ATPase in patients suffering from psoriasis is by 64% higher than in healthy people. The data obtained along with the previously revealed changes in the calcium metabolism in patients with psoriasis make it possible to suppose the presence of the system disturbance of the calcium membrane transport, in particular an increase in the plasma membrane permeability for cells of different types. Such a disturbance may distort a regulatory (messenger) function of calcium ions in the processes of proliferation, differentiation, functional activity and death of different cell types.

[Permeability for 45Ca and Ca-ATPase activity in erythrocyte membranes of patients with psoriasis]. / Izuchenie pronitsaemosti dlia 45Ca i aktivnosti Ca-ATFazy membran éritrotsitov bol'nykh psoriazom.

Accumulation of 45Ca in erythrocytes was 1.6-fold higher in presence of vanadate in patients with psoriasis as compared with healthy persons. This difference was maintained within 24 hrs of the heparinized blood storage, although penetration of Ca2+ through erythrocyte membranes was increased by about 67% both in patients and in healthy persons. Maximal activity of Ca2(+)-ATPase in erythrocyte membranes, measured in presence of endogenous regulators, was near normal values in the majority of the patients (15-300 microM P/L er. min) and above normal values--in 18% of the patients (320-420 microM P/L er. min). The data obtained suggest that systemic impairments of membrane transport of Ca2+ are of importance for pathogenesis of psoriasis.

[Disordered calcium metabolism in Reiter's disease]. / O narushenii kal'tsievogo obmena pri bolezni Reitera.

Cellular (erythrocytic) and extracellular (blood serum) calcium levels have been measured in patients with Reiter's disease and with urogenital chlamydiosis over the course of treatment. Calcium metabolism disorders depending on the disease severity have been detected in chlamydiosis patients. Calcium homeostasis imbalance manifests as a significant rise of the red cell calcium level in the presence of normal Ca ion concentration in the blood serum, which fact may result from impaired Ca ion transport through the plasma membrane. Combined therapy, including erythromycin, resulted, besides Chlamydia elimination, in normalization of Ca metabolism parameters under study.

[The state of calcium homeostasis in the blood in patients with psoriasis during a period of enhanced epidermopoiesis]. / Sostoianie kal'tsievogo gomeostaza krovi u bol'nykh psoriazom v period usilennogo épidermopoéza.

As a model of generalized impairments of the membrane structure in patients with psoriasis, an "erythrocyte-blood plasma" system was used for studies of calcium homeostasis. Distinct accumulation of Ca2+ in erythrocytes and reduction of Ca2+ content in blood plasma were observed in patients with psoriasis, thus demonstrating its redistribution between cells and medium. This Ca2+ transfer occurred due to an increase of Na+ concentration in the cells, which caused a decrease in the rate of Ca2+ excretion and led to elevation of the ion content in cytoplasmic fraction. The elevated intracellular concentration of Ca2+ in patients with psoriasis contributed to activation of lipid peroxidation as well as to selective increase in permeability of erythrocyte membranes for K+. The data obtained suggest that a number of alterations in homeostasis of calcium may be considered among the factors responsible for activation of cellular proliferation in the patients with psoriasis.