[Studies on platelet function in toxemia of pregnancy].
This study evaluated the role of platelets in the pathogenesis of toxemia. The findings were: (1) Thrombocytopenia and macrothrombocytosis are characteristic of toxemia. (2) ADP induced platelet aggregation increases during pregnancy, but decreases in severe toxemia significantly. (3) beta-thromboglobulin levels in both plasma and urine rise during pregnancy, and are significantly high in toxemia, especially in a severe type. (4) The plasma TxB2/6-keto-PGF1 alpha ratio markedly increase in severe toxemia due to the increase in the amount of TxB2. And in the IInd trimester, the ratio in the toxemia onset group in which toxemic pregnancy occurred in the IIIrd trimester showed a significantly higher value than the control group. These findings suggest that, in toxemic patients, platelets are in a hyperactive state and there is rapid turnover caused by selective consumption in organs such as the kidneys and placenta, and that platelet aggregation decreases due to the relative increase in the number of exhausted platelets as the toxemic state is impending. Furthermore, the TxA2/PGI2 balance shifts to TxA2 dominant and measurement of the plasma TxB2/6-keto-PGF1 alpha ratio was considered to help prediction of toxemia in the latter term of pregnancy.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D001792:Blood Platelets / Q000502:physiology*; D005260:Female; D006801:Humans; D010974:Platelet Aggregation; D010976:Platelet Count; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D013929:Thromboxane B2 / Q000097:blood; D001620:beta-Thromboglobulin / Q000032:analysis
D001620:beta-Thromboglobulin; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha