Abstract

In order to elucidate the mechanism concerning the development of arterial thrombosis, various blood coagulation factors and plasma 17-OHCS levels were determined in 18 cases of hypertension, 10 cases ob cerebromalacia, 13 cases of angina pectoris, 13 cases of myocardial infarction and 20 normal subjects simultaneously. Furthermore, effects of single or daily administration of prednisolone on the blood coagulation were observed in 17 cases with various diseases. The results obtained were as follows : 1. Shortening of prothrobinm time, increase in prothrombin concentration or factor 7 activity were observed in half of 10 patients in 69 hours after single oral dose of 25 mg of prednisolone. The daily administration of prednisolone was followed by similar changes in 6 out of 7 cases.In this case, an increase in factor 5 activity was obtained in 6 cases, although no remarakable change was found after single dose.2. Plasma 17-OHCS levels were significantly increased in patients with hypertension, angina pectoris, cerebromalacia or myocardial infarction. The levels tended to be higher in the latter two diseases, especially in fresh cases.3. Significant increase in factor 7 activity was observed in all these patients, while significant increase in factor 5 activity was seen only in patients with myocardial infarction. In patients with cerebromalacia or myocardial infarction, one stage prothrombin time was significantly shortened. No significant increase in prothrombin concentration was found in all these patients. Changes in these blood clotting factors were more remarkable in patients with arterial thrombosis. From the clinical observation, these changes seemed to be related to the development of arterial thrombosis.4. There was highly significant inverse relationship between 17-OHCS levels in plasma and one stags prothrombin time. Similarly, significant relationship was observed between 17-OHCS levels and factor 5 or 7 activity. There was no correlation between 17-OHCS levels and prothrombin concentration.From the results above described, it is concluded that adrenocotrical hyperfunction may be responsible for an increase in blood coagulability and the development of thrombosis.

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