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 (PGI2) (6-keto-prostaglandin [PG] F1 alpha and 2,3-dinor-6-keto-PGF1 alpha) and thromboxane A2 (TxA2) (thromboxane B2 and 2,3-dinor-thromboxane B2) was assessed in 17 women with pregnancy-induced hypertension and in eight controls.


RESULTS
Women with pregnancy-induced hypertension exhibited 18% lower mean serum HDL2 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 231.2 mumol/L, P < .01) in patients with pregnancy-induced hypertension were significantly higher than those in the controls. Urinary output of PGI2 metabolites was reduced by 35-45% in patients with pregnancy-induced hypertension, whereas no differences were seen in the excretion of TxA2 metabolites. Serum HDL2 cholesterol concentrations correlated positively with 2,3-dinor-6-keto-PGF1 alpha excretion, and serum triglyceride concentrations correlated positively with 2,3-dinor-thromboxane B2 excretion. In addition, insulin levels correlated positively with triglyceride levels but negatively with HDL2 cholesterol concentrations.


CONCLUSIONS
The metabolic characteristics (hypertriglyceridemia, hyperinsulinemia, hyperuricemia, low HDL2 cholesterol) in pregnancy-induced hypertension resemble the main features of the "insulin resistance syndrome." This may result in endothelial cell dysfunction as evidenced by PGI2 suppression.
Kaaja
R
R
Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Finland.
Tikkanen
M J
MJ
Viinikka
L
L
Ylikorkala
O
O
D016632:Apolipoprotein A-I / Q000097:blood; D016633:Apolipoprotein A-II / Q000097:blood; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D011464:Epoprostenol / Q000378:metabolism / Q000652:urine*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000378:metabolism* / Q000652:urine; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000097:blood / Q000378:metabolism* / Q000652:urine; D013928:Thromboxane A2 / Q000378:metabolism / Q000652:urine*; D014280:Triglycerides / Q000097:blood; D014527:Uric Acid / Q000097:blood
D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D007328:Insulin; D008055:Lipids; D014280:Triglycerides; D014527:Uric Acid; D013928:Thromboxane A2; D002784:Cholesterol; D011464:Epoprostenol