Objective. A plasma platelet aggregating factor (PAF) has been implicated in the pathogenesis of platelet activation in thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). Similar mechanism may be operative in pre‐eclampsia. Methods. Coagulation profile and detailed in vitro platelet aggregation with various agonists were studied. PAF was demonstrated by spontaneous aggregation of normal platelets with test plasma. Non‐parametric Wilcoxon's rank sum test and Krauskal Wally's one way analysis of variance were applied.Result. Twenty‐two pre‐eclamptic patients and 20 normal pregnant controls were studied. Anti‐thrombin III levels were within normal range and fibrin degradation products were only border line raised (>10 <40 μg/ml) in 14 (65.4%) patients. In vitro platelet aggregation was abnormal in 17 (77.2%) patients. PAF was demonstrable in 10 of 22 (45.5%) patients.Conclusion. Platelet aggregation studies indicated the presence of both activated (hyperaggregable) as well as exhausted (hypoaggregable) platelets in circulation. PAF demonstrable in 45.4% pre‐eclampsia patients would suggest its role in the pathogenetic mechanism of platelet activation in this disease.