SERUM-LIPOPROTEINS, INSULIN, AND URINARY PROSTANOID METABOLITES IN NORMAL AND HYPERTENSIVE PREGNANT-WOMEN

Objective: To determine if hyperinsulinemia, hypertension, hypertriglyceridemia, and low levels of high-density lipoprotein (HDL) cholesterol are present in women with pregnancy-induced hypertension or preeclampsia. Methods: Serum concentrations of insulin, uric acid, total and lipoprotein cholesterol, triglyceride, and apolipoproteins A-I and B were measured in 31 women with pregnancy-induced hypertension (eight with proteinuria) and in 21 healthy, pregnant, weight-matched controls at 30-39 weeks' gestation. The urinary excretion of the stable metabolites of prostacyclin (PGI(2)) (6-keto-prostaglandin [PG] F-1 alpha and 2,3-dinor-6-keto-PGF(1 alpha)) and thromboxane A(2) (TxA(2)) (thromboxane B-2 and 2,3-dinor-thromboxane B-2) was assessed in 17 women with pregnancy-induced hypertension and in eight controls. Results: Women with pregnancy-induced hypertension exhibited 18% lower mean serum HDL(2) cholesterol levels (0.9 versus 1.1 mmol/L, P < .05) and 65% higher mean triglyceride levels (3.3 versus 2.0 mmol/L, P < .05) compared to controls, whereas other serum lipid and apolipoprotein values did not differ significantly in the two groups. Mean serum insulin levels (13.3 versus 6.5 mU/L, P < .01) and uric acid levels (339.7 versus 232.2 mu mol/L, P < .01) in patients with pregnancy-induced hypertension were significantly higher than those in the controls. Urinary output of PGI(2) metabolites was reduced by 35-45% in patients with pregnancy-induced hypertension, whereas no differences were seen in the excretion of TxA(2) metabolites. Serum HDL(2) cholesterol concentrations correlated positively with 2,3-dinor-6-keto-PGF(1 alpha) excretion, and serum triglyceride concentrations correlated positively with 2,3-dinor-thromboxane B-2 excretion. In addition, insulin levels correlated positively with triglyceride levels but negatively with HDL(2) cholesterol concentrations. Conclusion: The metabolic characteristics (hypertriglyceridemia, hyperinsulinemia, hyperuricemia, low HDL(2) cholesterol) in pregnancy-induced hypertension resemble the main features of the ''insulin resistance syndrome.'' This may result in endothelial cell dysfunction as evidenced by PGI(2) suppression.