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Effect of the 100‐g oral glucose tolerance test on fetal acid–base balance
Author(s) -
Weissman Amir,
Lowenstein Lior,
Drugan Arie,
Zimmer Etan Z.
Publication year - 2003
Publication title -
prenatal diagnosis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.956
H-Index - 97
eISSN - 1097-0223
pISSN - 0197-3851
DOI - 10.1002/pd.576
Subject(s) - fetus , amniotic fluid , medicine , pregnancy , acidosis , acid–base homeostasis , gestation , endocrinology , obstetrics , biology , genetics
Abstract Objective Previous studies have shown that maternal hyperglycemia may lead to fetal hypoxia and acidosis. The aim of the present study was to examine the impact of an oral 100‐g glucose tolerance test on the fetal acid–base balance at mid‐gestation. Methods The study was conducted in healthy women who were scheduled for termination of pregnancy. The study group ( n = 18) received an oral solution containing 100‐g glucose and the control group ( n = 18) received only water 1 h prior to termination of pregnancy. Termination of pregnancy was performed by fetal intracardiac injection of potassium chloride (KCl) and intraamniotic instillation of PGF2α. Acid–base variables were evaluated in the fetal blood and the amniotic fluid. Results The glucose levels differed significantly between the study group and the control group with regard to maternal blood (127 ± 28 versus 69 ± 11 mg/dL, p < 0.001), fetal blood (128 ± 24 versus 71 ± 17 mg/dL, p < 0.001) and amniotic fluid (39 ± 13 versus 28 ± 5 mg/dL, p < 0.006). A linear relationship was found between maternal, fetal and amniotic fluid levels of glucose after maternal glucose ingestion. No significant changes were observed in the acid–base balance variables (pH, base excess, bicarbonate, lactate) in the fetal blood and the amniotic fluid of the study and control groups. Conclusion The 100‐g oral glucose tolerance test has no adverse effect on the fetal acid–base balance when glucose levels reach a peak 1 h after the test in normal pregnancies. Copyright © 2003 John Wiley & Sons, Ltd.