Different factors are involved in the development of thrombocytopenia in patients with lymphoproliferative disorders. Significant correlation was detected between the number of megakaryocytes in bone marrow and platelet count (r = 0.485, p = 0.002, n = 37) and significant difference between the number of megakaryocyte in patients with normal platelet count (>200000/μl) and patients with marked thrombocytopenia (platelet count < 100000/μl). All patients in the latter group (n = 15) had a relatively low number of megakaryocytes. Low but significant reverse correlation was found between the level of platelet‐associated IgG (PA‐IgG) and platelet count (r = – 0.249, p = 0.024, n = 82) and significant difference between the mean levels of PA‐IgG in the groups of patients with platelet count > 200000/μl and < 100000/μl. PA‐IgG were increased in 46% of patients in the total group and in 65% of patients with platelet count < 100000/μl. The correlation between platelet count and PA‐IgG was about 2 times higher in splenectomized (r= – 0.549, p = 0.005, n = 24) than nonsplenectomized patients. All splenectomized patients with platelet count < 100000/μl (n = 8) had a significant increase in PA‐IgG. Serum antibodies were detected in only 7% of tested patients. This group was characterized by severe thrombocytopenia (in 6 of 10 patients – platelet count <50000/μl) and a high incidence of haemorrhages (in 5 of 10 patients). Thus the depression of platelet production was suggested to be the basic cause of thrombocytopenia in lymphoproliferative disorders. Involvement of immune mechanisms was revealed in a large number of patients and correlated with a deeper and more complicated thrombocytopenia.

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The objective of this investigation was to evaluate the effect of 47 mg zinc supplementation on deficiency of zinc in rats during 98 d of restriction of motor activity (hypokinesia), which appeared by higher plasma zinc concentration. One Hundred 13-week-old Sprague-Dawley male rats weighing 360-390 g were used to perform the studies: They were equally divided into four groups: 1. Unsupplemented control animals (UCA); 2. Unsupplemented hypokinetic animals (UHA); 3. Supplemented control animals (SCA); and 4. Supplemented hypokinetic animals (SHA). For the simulation of the effect of hypokinesia (HK), the UHA and SHA were kept in small individual cages made of wood, which restricted their movements in all directions without hindering food and water intake. The SCA and SHA received daily with their food an additional amount of zinc. Before and during the experimental period of 98 d, plasma, urinary and fecal zinc, balance of zinc, food intake, and body weight were determined at different intervals. In the SHA and UHA, the concentration of zinc in plasma, and the elimination of zinc in urine and feces increased significantly when compared with the SCA and UCA, whereas the balance of zinc was negative. The body weight and food intake decreased significantly in the SHA and UHA when compared with the SCA and UCA. The increased plasma concentration of zinc in both the SHA and UHA groups was in contrast to the observed hypozincnemia during prolonged immobilization as during prolonged hospitalization. This reaction suggests that there may be some other mechanisms that are affecting the process of control and regulation of zinc metabolism during prolonged HK. It was concluded that exposure to prolonged restriction of motor activity of rats induces significant increases in plasma concentration, fecal and urinary elimination of zinc in the presence of negative zinc balance and regardless the daily intake of large amounts of zinc with their food, leading to zinc deficiency.

The work presents the indications for the choice of methods of diagnostic and surgical treatment of acute cholecystitis in patients with decompensated cardiovascular diseases. When covering the possibil- ity of diagnostic methods, their specificity and sensitivity. detailed characteristics of such instrumental techniques as ultrasonography, magnetic resonance cholangiopancreatography, magnetic tomography, echocardiography, electrocardiography, diagnostic laparoscopy has been given. The role of specific bio- chemical markers of myocardial necrosis has been showed: kretinfosfokinaza, cardiac troponin-I. Pos- sible changes on the electrocardiogram in these patients with acute cholecystitis and reasons for their appearance have been described.