Acid reflux drug fails to show benefit in pre-eclampsia treatment

Omeprazole falls short of improving the maternal circulating profile of sFlt-1 (soluble Fms-like tyrosine kinase-1), PlGF (placental growth factor), and ET-1 (endothelin-1) in women with established pre-eclampsia, as shown in a study.

A total of 50 women (mean age 31 years, mean body mass index 26 kg/m², median gestational age 30 weeks) with confirmed pre-eclampsia were randomly assigned to groups that did (n=24) or did not (n=26) receive 40-mg omeprazole once daily. Those in the treatment group received recommendations to continue treatment until delivery.

Researchers collected serum and EDTA plasma at baseline and days 1, 2, 4, 8, then twice weekly (during routine blood measurements) until delivery. The samples were then analysed for the changes in sFlt-1, PlGF, and CT-proET-1.

Forty out of 50 women (20 in each group) were included in the final analysis. Baseline sFlt-1, PlGF, and CT-proET-1 levels were identical in the two groups. After 4 days, the levels of the markers in the blood remained similar in women receiving and not receiving omeprazole.

The omeprazole group had a similar prolongation of pregnancy as the nonomeprazole group (median, 15 versus 14 days). Furthermore, there were no significant between-group differences detected in maternal/perinatal complications, except for a higher neonatal intubation rate in the nonomeprazole group (31 percent vs 4 percent; p=0.02).

Results of the placenta perfusion model confirmed that both omeprazole and its S-isomer, esomeprazole, when maternally applied, reached the foetal compartment (foetal-to-maternal ratio, 0.43–0.59). Meanwhile, only esomeprazole inhibited placental sFlt-1 release.

Despite the previous reports of low sFlt-1 and ET-1 in pre-eclamptic women using proton pump inhibitors, the findings argue against the role of such drugs as a potential treatment for pre-eclampsia.