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Background: The clotting state of the blood changes according to the type of physical exercise to which a group of healthy subjects are subjected. We studied the behaviour of the coagulation system before and after near-maximum, specific and standardized exercise tests in three groups of males practising sports defined as demanding in terms of cardiovascular output., Methods: The study was a comparative investigation between athletes and the group of controls composed of presumably healthy males., Setting: athletes training for competitions such as marathon, rowing and weightlifting., Participants and Interventions: we tested 7 rowers using the rowing machine, 12 marathon runners using the treadmill, 7 weightlifters using their own exercise equipment, and 7 healthy subjects (controls) using the cycle ergometer., Measures: during the tests we monitored heart rates, maximal oxygen intake, anaerobic threshold, respiratory quotient, maximum ventilation, and lactic acid. The following coagulation tests were performed before and after near-maximum exercise: prothrombin time (PT), partial activated thromboplastin time (PTT), fibrinogen (FBG), antithrombin III (ATIII), protein C (PC), protein S (PS), prothrombin fragment 1 + 2 (F1 + 2), tissue activator of plasminogen (t-PA) and its inhibitor (PAI)., Results: The most significant results showed a low basal PC in the rowers which decreased further after near-maximum exercise; significantly higher basal activities of ATIII, PC and PS in the marathon runners compared to the rowers; a high proportion of weightlifters showed a reduction in t-PA after exercise and an increase of PAI; the controls were the only group in which fibrinolytic activity and all the circulating anticoagulants increased after near-maximum exercise. Thus subjects who practise aerobic sports differ principally in terms of variations in inhibitors (low PC in rowers and marathon runners, increased presence of inhibitors in controls). The weightlifters did not show any significant variations, and so the kind of exercise involved (training to increase resistance and maximum strength) and the recovery times between the exercises do not seem to trigger changes in coagulation/fibrinolysis., Conclusions: We can therefore confirm that only relatively prolonged effort can trigger a mechanism beneficial to the cardiovascular system. In conclusion, physical activity benefits the coagulation system particularly as regards fibrinolysis, but certain subjects may be at risk of thrombosis and these must be identified and followed. We suggest that fibrinolytic activity be studied in athletes who practise weightlifting and have a history of cardiovascular disease, and that inhibitors (protein C in particular) be studied in rowers with a family history of thromboembolism.

Variations of platelet aggregation and plasma levels of clotting factors V, IX, XI, and XII were studied in 5 patients with Niemann-Pick disease type Is in the course of a 3-year study of treatment with periodic subcutaneous infusions of amniotic epithelial cells. Before commencement of treatment, the concentrations of these factors were found to be abnormal in four of five patients. It was possible to complete the study protocol in only two patients. Platelet aggregation and plasma levels of V, IX, XI, and XII clotting factors had been determined before each epithelial amniotic cells implantation and after 24, 48, and 72 hours. In both patients the aggregation test and the plasma levels of coagulation factors V, IX, XI, and XII were below the normal values of reference. Results showed that the epithelial amniotic cells treatment normalized platelet aggregation after each implantation in the two studied patients, both in terms of intensity of response (increase in light transmission after addition of adenosine diphosphate up to 350%) and in terms of obtaining an irreversible aggregation with 3 and 8 microM of adenosine diphosphate. The data related to clotting factors showed an increase of these concentrations up to 60% and some of these concentrations normalized completely.

We report two cases of factor V deficiency. A 12-year-old girl with thalassemia major was admitted for bone marrow transplant (mismatched). She was found to have a heterozygous deficiency of factor V (21%), but this was considered compatible with the transplant, which was performed without the support of suppernatant cryoprecipitate. A 14-year-old girl (factor V 2%) with a negative history (menarche at age 12, menstrual cycle regular and normal in quantity and length). One year previously she had complained of menorrhagia (length of period, 9 days); tests revealed server anaemia (Hb 4.9 g/dl). We show how even severe cases of factor V deficiency may often be silent, and not require transfusion in surgical procedures, thus avoiding the risks associated with such therapy.

Background: Hematocrit (HCT) is significantly higher in newborns than in adults, but this fact is not usually considered when performing coagulation tests in newborns. We studied 71 healthy full-term newborns and compared them to 100 healthy adults to test the hypothesis that correcting the anticoagulant-to-blood ratio for neonatal HCT would reduce the differences among the two populations., Methods: PT, PTT, fibrinogen, platelets and factors II, VII, IX, X, V, VIII were measured in 71 healthy full-term newborns and 100 healthy adults. An anticoagulant-blood ratio corrected for HCT was used. In 16 newborns, a non corrected value was also used and results were compared with the corrected ratio., Results: A significant difference was observed between newborns and adults in all tests with the exceptions of fibrinogen and factor V. In the 16 newborns from whom blood was collected without correcting in the anticoagulant, a significant difference was also found in all parameters but fibrinogen. A weak correlation linked the different variables., Conclusions: After correction for HCT, neonatal PT and factors V, VII, VIII and IX were much closer to adult values; neonatal PTT and factors II and X were still definitely lower.

Platelet aggregation inhibition, induced by prostaglandin E1 (PGE1), was evaluated in 38 patients affected by migraine. Our data indicate a complete insensitivity to PGE1 in these subjects. The insensitivity to PGE1 leads to decreased cyclic-AMP (cAMP) levels, determining an imbalance in the inhibitory mechanism. From this observation we can suppose that the decreased affinity of PGE1-receptors, causing decreased cAMP levels, may be involved in pathogenesis of migraine.