Does smoking affect thrombocytopoiesis and platelet activation in women and men?

PURPOSE: Smoking is a significant risk factor of cardiac ischaemia. Changes in platelet count, morphology and platelet activation enhance the risk. MATERIAL AND METHODS: The objective of the study was to assess platelet parameters in smoking healthy subjects with reference to sex. In the group of women, 27% were smokers, in the group of men--49%. All the subjects were tested for platelet count (PLT), mean platelet volume (MPV), percentage of large platelets (L(PLT)), concentrations of beta-thromboglobulin, sP-selectin (soluble) and thrombopoietin, percentage of reticulated platelets (RP) and absolute count of reticulated platelet. RESULTS: Lower platelet count (237.00 +/- 39.52 vs 258.34 +/- 40.81 x 10(9)/l, p = 0.0002), higher percentage of reticulated platelets (1.39 +/- 0 .66 vs 1.04 +/- 0.35%, p = 0.04) and higher concentration of sP-selectin (52.66 +/- 18.54 vs 43.94 +/- 17.14 ng/ml, p = 0.03) were observed only in the group of smoking women, compared to non-smokers. In neither of the sexes smoking had an effect on the following parameters: mean platelet volume, percentage of large platelets, concentration of thrombopoietin, absolute count of reticulated platelet and concentration of beta1 -thromboglobulin. CONCLUSIONS: The results allow the hypothesis that women are more sensitive to smoking than men. Platelets in male smokers are less sensitive to smoking--the study showed no significant changes in the parameters.

Effect of tumor stage and nephrectomy on CD62P expression and sP-selectin concentration in renal cancer.

The CD62P receptor and its soluble form sP-selectin is a marker of platelet (PLT) activation, and constitutes a ligand for CD24 antigen of neoplastic cells and tumor stroma components. The aim of the study was to evaluate the relationship dynamics of the percentage of CD62P+ platelets, the level of the receptor expression and the concentration of soluble form of sP-selectin in renal cancer. Examinations were performed before and after nephrectomy in patients with renal cancer (group A - 25, T2N0M0; group B - 27, T2N1-2M0) and in control group (C - 24 subjects). The two groups A and B showed an increased subpopulation of CD62P+ platelets (p<0.01) and elevated sP-selectin concentration (p<0.001) before and after nephrectomy. Although following nephrectomy sP-selectin concentration decreased markedly, it was still higher 3 months after the procedure compared to control group (p<0.05). Following nephrectomy, however, no statistically significant differences were found in the % of CD62P+ platelets and the receptor expression. Greater dynamics of changes before and after nephrectomy in the percentage of CD62P+ platelets (B1:B2 p<0.05) and the receptor expression (B1:B3 p<0.001) was observed in patients with local lymph node involvement (group B) while sP-selectin concentration was similar in both groups. Nephrectomy did not normalize intravascular activation of PLT and TNM had no significant effect on the expression of CD62P and concentration of sP-selectin.

beta-Thromboglobulin in patients with acute myocardial infarction according to the treatment.

Many studies report on the increased activity of platelets in patients with heart disease, especially with acute myocardial infarction (MI). The aim of the present study was to evaluate dynamics of beta-thromboglobulin (beta-TG) concentration in patients with MI according to the disease duration and type of treatment. We investigated 29 patients, who were divided into two groups according to the type of treatment. beta-TG concentration was determined using the immunoenzymatic method (ELISA). Blood was taken 1st, 3rd, 5th, 8th and 11th day of infarction. Our results indicate that in the course of myocardial infarction there is a change in platelet activation. The treatment applied affects beta-TG concentration, and the thrombolytic therapy inhibits platelet activation.

Flow cytometric analysis of CD 62P expression in patients with acute myocardial infarction.

Much attention has been paid to the role of platelets in the pathogenesis of heart diseases, e.g. ischaemic disease and myocardial infarction. During platelet activation changes appear both in the internal structure and in the membrane. The release reaction is associated with the appearance of CD 62P (P-selectin). The aim of the present study was evaluate CD 62P expression in patients with acute myocardial infarction according to the disease duration and the type of treatment. We study 29 patients with acute myocardial infarction (MI). The patients were divided into two groups: group A--15 patients treated with heparin and aspirin and group B--14 patients treated with streptokinase, heparin and aspirin. The control group consisted of 21 healthy subjects. We indicated that P-selectin expression is influenced by infarction duration and type of treatment. Our study demonstrates that thrombolytic therapy inhibits platelet activation. Patients receiving streptokinase showed lower CD 62P expression than those treated only with heparin and aspirin, both before and after platelet activation with thrombin.

Platelet factor 4 as a marker of platelet activation in patients with acute myocardial infarction.

The aim of the present study was evaluate dynamics of platelet factor 4, as a marker of platelet activation, in patients with acute myocardial infarction according to the disease duration and type of treatment. In the recent years much attention has been paid to the role of platelets in the pathogenesis of ischaemic disease and myocardial infarction. Rupture or splitting of atheroma and increased platelet activation are a direct cause of acute thrombotic process in coronary vessels. During platelet activation alpha granules release proteins, e.g. platelet factor 4 (PF 4). We investigated 29 patients with acute myocardial infarction (MI); the patients were divided into two groups: group A--15 patients treated with heparin and aspirin; group B--14 patients treated with streptokinase, heparin and aspirin. Control group (C) consisted of 21 healthy subjects. PF 4 concentration was determined on the 1st, 3rd, 5th, 8th, 11th day of MI using the immunoenzymatic method. Our results indicate that in the course of myocardial infarction there is a change in the platelet factor 4 and that thrombolytic therapy inhibits platelet activation.

Phagocytic activity of platelets in patients with myocardial infarction.

The aim of our present study was to analyse the dynamics of changes in the phagocytic activity of platelets with myocardial infarction according to the treatment applied. Twenty patients with acute myocardial infarction and thirty healthy subjects were examined. Platelet count, phagocytic activity of platelets and the phagocytic index were determined. We observed reduced phagocytic activity of platelets in the first 24 hours of infarction, which may be due to exhaustion of most active platelets in a thrombus and microaggregates. A transitory increase in the phagocytosis activity of platelets observed on the third day of infarction may be caused by the release of large, more active platelets from splenic pool. On the eight day of infarction, the phagocytic activity of platelets became normalized in both experimental groups. Our study indicates that together with platelet activation the phagocytic activity gets reduced being a likely response to the thrombocytopenic factor. This can be confirmed by the increased number of platelets on the 8th day. Our results suggest a slightly attenuated phagocytic ability of platelets, irrespective of the treatment applied. The reduction seems to result from the effect of platelets exhaustion on the procoagulative activity in patients with myocardial infarction.