SummaryPlatelet count and aggregation were assessed in 9 Finnish amateur runners aged 34 to 48, and one 65-year old taking part in a non-competitive marathon race (42.2 km).After the run the mean value of platelet count showed a very significant rise (p <0.001). The platelets were markedly more sensitive to both ADP and collagen-induced aggregation. A highly significant increase (p <0.001) was noted for both the intensity and velocity of platelet aggregation.The finding of platelet hyperaggregability after prolonged strenuous exercise even in trained subjects is discussed. It is concluded that a thorough medical examination of the haemostatic balance is recommended before a marathon race.

SummaryBlood coagulation, fibrinolysis, platelet count-aggregation and Cortisol were assessed in 35 Finnish amateur runners aged 27 to 56 years (mean 40) and three aged 65, 67, and 82 who had run a non-competitive Marathon in 1975, 1976 and 1977 over the classical itinerary. After the run, in all 3 years, APTT showed shortening (p < 0.001); prothrombin time and plasma fibrinogen were not significantly altered; euglobulin lysis time was shorter (p < 0.001) and FDP increased (p < 0.001); PSPT became positive in all subjects, whereas the ethanol gelation test remained negative; no cryofibrinogen was detected. Platelet count and aggregation showed increase (p < 0.001) in 1975 (extreme heat, 25° C) but remained unaltered in 1976, 1977 (15–18° C). Cortisol levels were always significantly increased – more markedly in 1975. Women’s responses were similar to those of men. A possible correlation between physical fitness and the responses of haemostatic balance is suggested and the influence of weather is discussed.

SummaryIn this paper, a five generation Greek family is described with haemophilia B. The disease is characterized by a normal ox-brain prothrombin time, normal levels of the vitamin-K dependent clotting factors VII and X and a proportional reduction of factor IX acttivity and antigen levels all of which is consistent with the cross-reacting material negative form of haemophilia B. However, in this family the factor IX levels in the three patients of generation V are around 1 U/dl while the three older patients in generation III have factor IX levels ranging from 28 to 44 U/dl. In the oldest patient of generation V we observed a rise of the factor IX level from 1 U/dl up to the age of 13 to 10 U/dl at age 14. In addition, the older patients have very mild bleeding symptoms or none at all, while the young ones have occasional spontaneous haemorrhages in muscles and joints, compatible with severe or moderately severe haemophilia. The disease appears to be similar to haemophilia B Leyden which has been described in a Dutch family.

In the light of our previous studies on marathon runners (Dessypris et al. 1976, Dimitriadou et al. 1977, Mandalaki et al. 1977, 1977 a) we decided to determine antithrombin III levels. Plasma AT III is known to be decreased in thrombotic or prethrombotic cases (Lane and Biggs 1977), postoperatively, and in DIC (Lane and Biggs 1977). Mandalaki et al. (1977) have demonstrated a clear-cut activation of the fibrinolytic mechanism, with increased plasma fibrinolytic activity but without any unfavourable signs of intravascular clotting (Mandalaki et al. 1977, 1977 a). Therefore, determination of AT III after such strenuous exercise might contribute to the overall picture of haemostatic balance. AT III was assessed in 9 Finnish amateur runners, aged 29 to 53, taking part in a non competitive marathon run on October 1976 and in a similar group on October 1977 (n = 14, ages 27-54). They were all in training having practiced regularly to increase their stamina. They had been medically examined some weeks before the event and declared fit for the run. Both the races were held over the classical itinerary in Athens, Greece. Venous blood was collected in siliconized glass tubes containing 3.8% trisodium citrate as anticoagulant in the ratio of one part of citrate to nine parts of blood. Supernatant plasma was collected in siliconized glass tubes and kept at-30° C until tested. Blood samples were obtained within 30 min of completion of the run. Control samples were taken 1 day before the race at 8.00 (fasting) in 1976, and 5 days after the run at 8.00 (fasting) in 1977. AT III was assayed by the enzymatic method, with a chromogenic substance (S 2160) as substrate, according to the technique of Blomback et al. (1974). Our results (expressed as a percentage of the value estimated for a normal plasma pool) are as follows:. Control (mean ± SD) Post-marathon (mean ± SD) 1976 84.4 ± 22.2 87.4 ± 1 1 .1 1977 134.5 ± 2 5 .9 134.4 ± 37.5 No change in AT III levels was provoked by either Marathon race. These findings suggest that the hypercoagulability noted after the run (Mandalaki et al. 1977, 1977 a) does not cause any AT III consumption, i.e. there is no dangerous activation of the coagulation process.