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Notes: Summary. Blood viscosity and several of its determinants (packed cell volume, plasma viscosity, plasma fibrinogen and erythrocyte deformability) and several haemostatic variables (platelet count, serum fibrin degradation products and plasma soluble fibrin) were measured in 106 women during normal third-trimester pregnancy, 12 patients with moderate pre-eclampsia, nine patients with severe pre-eclampsia and 16 patients with confirmed fetal growth retardation. Blood viscosity was measured at high and low shear rates (94.5 and 0.94 s−1), with and without correction to a standard packed cell volume of 0.45. In normal pregnancy low-shear blood viscosity increased significantly towards term, associated with significant increases in packed cell volume and plasma viscosity (but not fibrinogen); there was no change in high-shear blood viscosity at native packed cell volume and a decrease in viscosity after correction for packed cell volume, associated with a significant increase in erythrocyte deformability. Significant decrease in the platelet count and significant increases in serum fibrin degradation products and plasma soluble fibrin suggested a degree of haemostatic activation in normal third-trimester pregnancy. In moderate pre-eclampsia blood viscosity was significantly lower at low shear rate, due to a significantly lower packed cell volume and despite a significantly elevated plasma viscosity. In severe pre-eclampsia high-shear blood viscosity was significantly elevated after correction for packed cell volume, associated with a significantly reduced erythrocyte deformability; plasma fibrinogen levels were reduced, but other variables were not significantly abnormal. In fetal growth retardation blood viscosity was significantly increased at both shear rates, despite a reduced packed cell volume: this was also associated with a significant reduction in erythrocyte deformability. In general there was little correlation between blood viscosity factors and haemostatic variables, but in normal-term pregnancy soluble fibrin levels correlated with blood viscosity at both shear rates. We suggest that increased blood viscosity and decreased erythrocyte deformability may play a role in the placental insufficiency of severe pre-eclampsia and fetal growth retardation.

Notes: In 26 women receiving either medroxyprogesterone acetate (Depo-Provera) injections or combined oestrogen-progestogen pills for contraception, tests of coagulation and fibrinolysis were performed before treatment, and after 8, 16 and 24 weeks of therapy. In the medroxyprogesterone group no significant changes were induced in fibrinogen, the vitamin K-dependent factors, or antithrombin III. Plasminogen levels fell during therapy, and were significantly lower than pre-treatment values after 16 and 24 weeks. By contrast, the 13 women receiving oral contraceptives showed raised levels of fibrinogen and plasminogen after 8 weeks of treatment, and of factors VII and X after 24 weeks. These data suggest that medroxyprogesterone acetate injections induce fewer changes in the blood coagulation system than oral contraceptives.

Notes: The technique of plasma fibrinogen chromatography was used to study sequential changes in coagulant and fibrinolytic activity in six patients with severe pre-eclampsia. Plasma soluble fibrinogen-fibrin complex and plasma fibrinogen-fibrin degradation product levels were measured as indices of coagulant and fibrinolytic activity respectively. Clinical deterioration antenatally was accompanied by increasing coagulant and decreasing fibrinolytic activity, while a more stable clinical picture was associated with steady coagulant and increasing fibrinolytic activity. Following delivery, a surge in fibrinolytic activity accompanied or preceded clinical recovery. The pattern of increased coagulant and diminished fibrinolytic activity would seem to favour the development of disseminated intravascular coagulation in these patients and it is possible that the balance between coagulant and fibrinolytic activity may influence the clinical course and outcome of the Pregnancy

Notes: Blood viscosity (Contraves L S 30) and its determinants were measured in 23 patients with mild/moderate pre-eclampsia, 10 patients with intrauterine growth retardation and 22 control subjects, matched for age and gestation. Both abnormal groups had a significantly increased blood viscosity at high shear rate (94 s-1) associated with increased haematocrit. Fibrinogen levels were also increased, but there were no significant differences between groups in plasma viscosity, low shear viscosity (0.94s-1) or red cell deformability, measured by a low-shear washed cell system of filtration through 5-μm pore diameter Nuclepore filters. In the pre-eclamptic group, measurements were repeated after 1–2 weeks in nine patients treated with labetalol (a combined alpha and beta adrenergic blocker) and in 10 patients treated with bed rest. Labetalol reduced blood pressure but no change in rheology was seen in either group. Control of blood pressure by labetalol does not adversely affect rheology, in contrast to diuretics which are known to cause haemoconcentration and increased blood viscosity.

Notes: The effects of bromocriptine and quinestrol upon coagulation and fibrinolysis during the puerperium were studied. Quinestrol therapy was associated with increased levels of factors VII and IX and decreased antithrombin activity on the sixth postpartum day, and increased factor IX and plasminogen levels on the fourteenth postpartum day. Six weeks after delivery elevated levels of factors II and VII and of plasminogen were recorded in women given quinestrol. Bromocriptine therapy only caused an increase in the level of factor IX at six weeks after delivery. Compared to controls, patients given bromocriptine had lower prolactin and higher FSH levels during the puerperium whereas the patients given quinestrol had increased prolactin levels and a late fall in FSH levels.

Notes: In view of the association between pre-eclampsia and disseminated intravascular coagulation, three patients presenting with severe pre-eclampsia before the 28th week of pregnancy were treated with heparin. In all three patients, there was deterioration of hypertension and proteinuria that necessitated the withdrawal of treatment after five to six days. During treatment, serum and urinary fibrinolytic degradation products (FDPs) continued to rise or remained unaltered, plasminogen levels showed a steady fall, and the platelet count remained at a reduced level. These data suggest that heparin was an ineffective form of treatment and did not prevent the intravascular fibrin deposition associated with severe pre-eclampsia.

Notes: Two oestrogens, stilboestrol and quinestrol, were used to inhibit lactation and their effects upon coagulation and fibrinolysis were compared with control patients before delivery, during the puerperium and six weeks after delivery. During the first week of the puerperium, stilboestrol therapy was associated with rises of factors IX and X and quinestrol therapy with rises of factors IX and 11. Six weeks after delivery, the clotting factors were similar to the control values in those who had received stilboestrol but factor II was still raised in the quinestrol treated patients. Additionally, a significant rise of factor X in the quinestrol group was noted at this time. Plasma antithrombin levels rose during the first week of the puerperium in all three groups but, six weeks after delivery, they were lower in those who had received oestrogens. Stilboestrol and quinestrol were also associated with a rise of plasminogen and antiplasmin concentration during the first week of the puerperium. Six weeks after delivery, quinestrol treated patients still had raised levels of plasminogen and antiplasmin while the stilboestrol treated patients only had raised levels of antiplasmin. These changes in coagulation and fibrinolysis are similar to those reported during oral contraceptive therapy. The persisting changes six weeks after delivery in women who had taken quinestrol might indicate an increased thrombogenic risk when long acting oestrogen preparations are used to inhibit lactation.

Notes: Tests of coagulation, fibrinolysis and platelet function were performed in patients with normal pregnancy, severe pre-eclampsia, mild pre-eclampsia, essential hypertension and placental insufficiency.Compared with normal pregnancy, severe pre-eclampsia was associated with higher serum and urinary fibrinolytic degradation products, cryofibrinogen and factor VIII levels, lower plasminogen and antithrombin activity and diminished sensitivity to urokinase-induced fibrinolysis. In addition severely pre-eclamptic patients had reduced platelet counts, lower response to adenosine diphosphate platelet aggregation and diminished platelet factor 3 activity. These changes were present before delivery and in the immediate puerperium, but six weeks after delivery the only difference detected between severely pre-eclamptic and normal patients was reduced platelet disaggregation in the severely pre-eclamptic group. In mild pre-eclampsia the changes in coagulation and fibrinolysis were less marked but serum fibrinolytic degradation products, cryofibrinogen, factor VIII and V levels were significantly raised and the platelet count reduced.No abnormalities of coagulation, fibrinolysis or platelet function were detected in essential hypertension. In placental insufficiency there was diminished platelet disaggregation before delivery but all other tests of coagulation, fibrinolysis and platelet function were similar to normal pregnancy.These results support the hypothesis that intravascular coagulation is present in pre-eclampsia.

Notes: Factor VIII related antigen (VIIIRAg), Factor VIII coagulant activity (VIIIC), plasma uric acid, total plasma oestriol, plasma human placental lactogen (hPL) and urine oestrogen/creatinine ratio were measured in a group of 21 patients clinically suspected of fetal growth retardation and compared with normal pregnancy. Of the hormone assays, hPL was better than either oestriol or oestrogen/creatinine ratio at distinguishing between normal and growth retarded pregnancies. Uric acid levels tended to be higher than normal in patients with fetal growth retardation, but the best means of distinguishing normal from growth retarded pregnancies proved to be the VIIIRAg/VIIIC ratio. This ratio was significantly elevated in fetal growth retardation compared with normal pregnancy, and the increase was evident as early as 30 weeks gestation. Using the VIIIRAg/VIIIC ratio test, the outcome of 17 of the 21 suspect pregnancies could be correctly predicted.