PERSISTENT PULMONARY-HYPERTENSION OF THE NEWBORN AND SMOKING AND ASPIRIN AND NONSTEROIDAL ANTIINFLAMMATORY DRUG CONSUMPTION DURING PREGNANCY

Objective. Prenatal causation of persistent pulmonary hypertension of the newborn (PPHN) is suggested by a specific pattern of pulmonary vas cular remodeling observed immediately after birth in some infants with fatal PPHN. The goal of this study was to determine whether PPHN is a ssociated with fetal exposure to: (1) tobacco and marijuana smoking (i e, contributors to fetal hypoxemia), (2) consumption of aspirin and ot her nonsteroidal antiinflammatory drugs (ie, inhibitors of prostagland in synthesis), and (3) cocaine use (ie, a contributor to vasospasm). D esign. Case-control interview study. Setting. Two Harvard-affiliated n ewborn intensive care units. Participants. Mothers of case infants who had PPHN or who met criteria for the referent group. Interventions. D uring July 1985 through April 1989, we interviewed mothers of 103 infa nts with PPHN and 298 control infants. Because of potential selection bias that might result from recruiting only inborn control infants eve n though two-thirds of cases were outborn, separate analyses compared the 103 total and 35 inborn infants with PPHN with the 298 inborn cont rol infants. Multivariate analyses were used to adjust for potential c onfounding factors, including maternal education and Medicaid health i nsurance (ie, two markers of socioeconomic status), other antenatal fa ctors found to be associated with PPHN (ie, maternal urinary tract inf ection and diabetes mellitus), and the infant's sex. Main Outcome Meas ures. Self-reported use or consumption of tobacco, marijuana, cocaine, aspirin, and other nonsteroidal antiinflammatory drugs during pregnan cy. Results. The adjusted odds ratios (and 95% confidence intervals) f or maternal pregnancy exposures to the factors of principal interest a mong the total study population were: aspirin, 4.9 (1.6-15.3); and non steroidal antiinflammatory drugs, 6.2 (1.8-21.8); for the inborn group they were: aspirin, 9.6 (2.4-39.0); and nonsteroidal antiinflammatory drugs, 17.5 (4.3-71.6). Although the association between tobacco smok ing during pregnancy and PPHN was elevated in univariate analyses, wit h odds ratios (and 95% confidence intervals) of 2.0 (1.2-3.4) and 1.3 (0.6-3.3) for total and inborn populations, respectively, the relation ship was not significant after adjustment for all other factors in the final logistic regression model. Acknowledged illicit drug use was to o infrequent (3.2%) to evaluate. Conclusion. Maternal consumption of n onsteroidal antiinflammatory drugs and aspirin during pregnancy or the reasons these drugs were ingested seem to contribute to an increased risk of PPHN.