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We analysed 22 patients suffering from migraine to evaluate the possible activation of platelet function utilizing the following methods: platelet factor 4, thromboxane B2 and 6 - keto prostaglandin F 1 alpha levels in platelet poor plasma. Laboratory tests were performed on all patients during headache-free period and the results obtained were compared with those of a normal healthy individuals. The mean results obtained in the patients group during pain-free period indicated a significant activation of platelet function when compared with the normal group.

Platelet function was investigated in 11 healthy non-smokers, 11 medium smokers (less than 10 cigarette/day) and 11 heavy smokers (greater than 20 cigarette daily). Cigarette consumption was in medium smokers 6.2 cigarette/day, and in heavy smokers 30.7 cigarette/day. Erythrocyte count, platelet count, plasma levels of cholesterol and triglycerides, and circulating platelet aggregates showed no significant difference between smokers and non-smokers. Thromboxane B2 level in plasma was higher in heavy smokers (20.1 +/- 17.3 pg/0.1 ml) than in non-smokers (58.8 +/- 37.1 pg/0.1 ml) and medium smokers (65.4 +/- 32.1 pg/0.1 ml) (P less than 0.01). Platelet factor 4 level was high in non smokers prior to smoking 1 cigarette and normal in medium and heavy smokers. Plasma concentration of beta thromboglobulin and 6-ketoprostaglandin F1 alpha showed no significant changes between non-smokers and heavy smokers. No dependence on smoking 1 cigarette was found in any group. The data suggest that long term cigarette smoking increases platelet activity manifested by an increased activity of thromboxane A2. Cigarette smoking contributes to the development of coronary artery disease also by means of activation of platelet functions.

The method of selective decontamination of the gastrointestinal tract represents a new possibility of protection of immunocompromised patients against infectious complications with frequent lethal issue. The method is based on employment of such antibiotics and chemotherapeutical drugs that eliminate the aerobic gram-negative microflora and yeasts preserving the anaerobic portion of the bowel microflora that is responsible for the so-called colonization resistance of the intestinal tract. Such a treatment provides patients with more resistance against infection and there is no need for strict reverse isolation. The theoretical exposition of the SD mechanism is given along with instruction on how to use this method and summarizing the hitherto clinical results of its employment. The authors' proper more than 6 year experience is compared with the world literature, and the SD method is stated to be a valuable import in preventing infections in hematological patients. Some unresolved problems and future prospects are also discussed.