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Summary: In an attempt to define the role of an altered fibrinolytic mechanism in the pathogenesis and pathology of pre‐eclampsia, a prospective study was carried out on 60 primigravidae at intervals throughout pregnancy. Forty remained normal, 11 were deemed to have excessive weight gain, and 12 developed pre‐eclampsia (including 3 from the high weight gain group). A venous stasis stress test was applied at each sampling, and plasminogen activator levels were assayed in peripheral venous and cord venous plasma. The high weight gain group showed no differences from the group whose pregnancies remained normal. Release of activator from venous endothelium under stress was significantly impaired by the 20th week of gestation in the patients who subsequently developed pre‐eclampsia. Furthermore, there was a delay in return to normal fibrinolytic activity after placental expulsion, and the mean cord activator level was lower in these patients.
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R G Condie (1976) studied this question.
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