PLATELET ACTIVATION IN NORMOTENSIVE AND HYPERTENSIVE PREGNANCIES COMPLICATED BY INTRAUTERINE GROWTH-RETARDATION

Objective To study platelet function in normotensive and hypertensive intrauterine growth retardation (IUGR). Design ADP and collagen induced whole blood platelet aggregation, P-thromboglobulin release and platelet count were measured in the IUGR groups at a mean gestational age of 36 weeks (28-40), and at 1, 24, 48 h and six weeks post delivery. The normal pregnancy group were studied serially at 12, 20, 28, 32 and 36 weeks of gestation and at 1, 24, 48 h and six weeks post delivery. Setting Trinity College Medical School, St. James's Hospital, Dublin. Subjects Twenty-nine women with a fetus with diagnosed IUGR were recruited for the study. Of these, 15 were normotensive throughout their pregnancy and the remaining 14 pregnancies were complicated by both hypertension and proteinuria. Twenty healthy primigravida acted as controls. Results In the hypertensive IUGR group, levels of collagen and ADP induced aggregation were almost 50% lower before delivery than in normal pregnancy. Platelet count in the hypertensive group was decreased by 30% compared with normal pregnancy. Levels of beta-thromboglobulin were 40 to 50% higher in both the normotensive and hypertensive IUGR groups compared with normal pregnancy. Unlike the hypertensive IUGR group, the normotensive IUGR group showed similar levels of platelet count and ADP and collagen induced aggregation to those found at 36 weeks of normal pregnancy. In the early puerperium of hypertensive pregnancies, the platelet parameters measured returned gradually to normal. The normotensive IUGR group had increased levels of ADP induced aggregation in the first 24 to 48 h post delivery. The platelet count in the normotensive but not the hypertensive group correlated with birthweight. Conclusions Normotensive and hypertensive IUGR are accompanied by platelet activation. In normotensive IUGR, this activation appears to be confined to the uteroplacental circulation. In hypertensive IUGR, the results suggest that platelet activation also extends into the peripheral circulation resulting in a reduced platelet responsiveness and a lower platelet count. Release of vasoactive amines from activated platelets in the peripheral circulation may be responsible for the clinical syndrome of hypertension and proteinuria present in pregnancies complicated by pre-eclampsia and IUGR but absent in normotensive IUGR.