The effect of glucocorticoid therapy on fetal lung maturity indices in hypertensive pregnancies

Objective: To assess fetal lung maturity tests in hypertensive pregnancies and to examine the effect of glucocorticoid therapy. Methods: In a cohort study involving 68 pregnant women with hypertension, 34 received antenatal betamethasone before amniocentesis and 34 did not. Controls were 68 women with uncomplicated pregnancies, matched for gestational age at amniocentesis and fetal gender. Amniotic fluid (AF) samples were analyzed by lamellar body count, planimetric and stechiometric lecithin-sphingomyelin ratio (L/S), and presence of phosphatidylglycerol. Results: Fetal lung maturity, as determined by lamellar body counts and by planimetric L/S, was lower in hypertensive pregnancies not treated with steroids than in controls (19,600 +/- 14,500 versus 39,800 +/- 22,700, P < .009, and 1.9 +/- 0.6 versus 3.9 +/- 1.8, P < .01, respectively). In the period of 24 to 33 weeks' gestation, the percentage of untreated pregnancies with mature lamellar body counts and mature L/S was significantly lower than that of controls (13% versus 33%, P < .001; 6% versus 40%, P < .002 and P < .003, respectively). In contrast, in patients treated with betamethasone, the percentage of cases with mature indices for both tests was not significantly different from that of controls, but was higher than that of untreated hypertensive patients (40% versus 13%, P < .001; 33% versus 6%, P < .001). Phosphatidylglycerol did not differ among groups. From 34 to 38 weeks, no difference was found in the percentage of mature cases for lamellar bodies in pregnant women with hypertension not treated with steroids in comparison with controls (68% versus 84%), nor between cases treated and controls (74% versus 84%). In the same period, no difference in L/S values was found among groups, and the percentage of cases positive for phosphatidylglycerol was lower in hypertensive pregnancies than in controls (47% versus 95%, P < .001) and was not affected by steroid treatment (37% versus 95%, P < .001). Conclusion: Fetal lung maturity, as reflected in AF tests, is delayed in hypertensive pregnant patients, and steroids increase all lung maturity indices except phosphatidylglycerol between 24 and 33 weeks' gestation. (Obstet Gynecol 1998;92:220-5. (C) 1998 by The American College of Obstetricians and Gynecologists.

The effect of glucocorticoid therapy on fetal lung maturity indices in hypertensive pregnancies

Objective: To assess fetal lung maturity tests in hypertensive pregnancies and to examine the effect of glucocorticoid therapy. Methods: In a cohort study involving 68 pregnant women with hypertension, 34 received antenatal betamethasone before amniocentesis and 34 did not. Controls were 68 women with uncomplicated pregnancies, matched for gestational age at amniocentesis and fetal gender. Amniotic fluid (AF) samples were analyzed by lamellar body count, planimetric and stechiometric lecithin-sphingomyelin ratio (L/S), and presence of phosphatidylglycerol. Results: Fetal lung maturity, as determined by lamellar body counts and by planimetric L/S, was lower in hypertensive pregnancies not treated with steroids than in controls (19,600 +/- 14,500 versus 39,800 +/- 22,700, P < .009, and 1.9 +/- 0.6 versus 3.9 +/- 1.8, P < .01, respectively). In the period of 24 to 33 weeks' gestation, the percentage of untreated pregnancies with mature lamellar body counts and mature L/S was significantly lower than that of controls (13% versus 33%, P < .001; 6% versus 40%, P < .002 and P < .003, respectively). In contrast, in patients treated with betamethasone, the percentage of cases with mature indices for both tests was not significantly different from that of controls, but was higher than that of untreated hypertensive patients (40% versus 13%, P < .001; 33% versus 6%, P < .001). Phosphatidylglycerol did not differ among groups. From 34 to 38 weeks, no difference was found in the percentage of mature cases for lamellar bodies in pregnant women with hypertension not treated with steroids in comparison with controls (68% versus 84%), nor between cases treated and controls (74% versus 84%). In the same period, no difference in L/S values was found among groups, and the percentage of cases positive for phosphatidylglycerol was lower in hypertensive pregnancies than in controls (47% versus 95%, P < .001) and was not affected by steroid treatment (37% versus 95%, P < .001). Conclusion: Fetal lung maturity, as reflected in AF tests, is delayed in hypertensive pregnant patients, and steroids increase all lung maturity indices except phosphatidylglycerol between 24 and 33 weeks' gestation. (Obstet Gynecol 1998;92:220-5. (C) 1998 by The American College of Obstetricians and Gynecologists.