Background Since use of non-steroidal anti-inflammatory drugs (NSAIDs) during pregnancy is common, small increases in the risk of birth defects may have significant implications for public health. Results of human studies on the teratogenic risks of NSAIDs are inconsistent. Therefore, we evaluated the risk of selected birth defects after prenatal exposure to prescribed and over-the-counter NSAIDs. Methods and Findings We used data on 69,929 women enrolled in the Norwegian Mother and Child Cohort Study between 1999 and 2006. Data on NSAID exposure were available from a self-administered questionnaire completed around gestational week 17. Information on pregnancy outcome was obtained from the Medical Birth Registry of Norway. Only birth defects suspected to be associated with NSAID exposure based upon proposed teratogenic mechanisms and previous studies were included in the multivariable logistic regression analyses. A total of 3,023 women used NSAIDs in gestational weeks 0–12 and 64,074 women did not report NSAID use in early pregnancy. No associations were observed between overall exposure to NSAIDs during pregnancy and the selected birth defects separately or as a group (adjusted odds ratio , 95% confidence interval –). Associations between maternal use of specific types of NSAIDs and the selected birth defects were not found either, although an increased risk was seen for septal defects and exposure to multiple NSAIDs based on small numbers (2 exposed cases; crude odds ratio , 95% confidence interval –). Conclusions Exposure to NSAIDs during the first 12 weeks of gestation does not seem to be associated with an increased risk of the selected birth defects. However, due to the small numbers of NSAID-exposed infants for the individual birth defect categories, increases in the risks of specific birth defects could not be excluded.
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We calculated the pooled estimates (Odds Ratio and their 95% Confidence Interval and the associated P -value) using the DerSimonian-Laird method using a random effects model. Random models take into account both the sampling variance within the studies and the variation in the underlying effect across studies. The assumption of variation in the underlying effect seems plausible given the different populations, study designs, drugs type, and exposure assessment methods used in the original studies. To assess the statistical heterogeneity of the summary measures we used the Cochran’s Q statistics and calculated I 2 . 21 We considered an I 2 value of 25% or lower as trivial heterogeneity and an I 2 of 75% or higher as important heterogeneity.