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Few studies have assessed the risk of adverse pregnancy outcomes in women with multiple sclerosis (MS). We used 2 large US administrative databases, the Truven Health MarketScan Database (2011-2015; Truven Health Analytics Inc., Ann Arbor, Michigan) and the Nationwide Inpatient Sample (2007-2011), to identify delivery cohorts. MS and pregnancy outcomes (infections, cesarean delivery, preterm delivery, poor fetal growth, preeclampsia, chorioamnionitis, postpartum hemorrhage, stillbirth, and infant malformations) were identified during pregnancy and at delivery. We calculated adjusted risk ratios according to MS status and relapse(s) in the year before delivery. Among over 5 million pregnancies, we identified 3,875 pregnancies in women with MS. Women with MS had an increased risk of infections during pregnancy (Truven Health: adjusted risk ratio (aRR) = 1.22, 95% confidence interval (CI): 1.16, 1.27) and preterm delivery (Truven Health: aRR = 1.19 (95% CI: 1.04, 1.35); Nationwide Inpatient Sample: aRR = 1.30 (95% CI: 1.16, 1.44)). The risks of other outcomes were similar for women with and without MS. In the Truven Health database, risk ratios for the pregnancy outcomes in women experiencing relapses versus those without relapses were between 0.9 and 1.4, and confidence intervals overlapped the null. Overall, women with MS had an increased risk of infections and preterm delivery; however, their risks for other adverse pregnancy outcomes were not elevated. Disease activity before delivery was not a strong predictor of outcomes.

In a 2002-2004 prospective cohort study of deliveries of infants at <28 weeks at 14 US centers, the authors sought the antecedents of white matter damage evident in newborn cranial ultrasound scans (ventriculomegaly and an echolucent lesion) and of cerebral palsy diagnoses at age 2 years. Of the 1,455 infants enrolled, those whose mothers received an antenatal steroid tended to have lower risks of ventriculomegaly and an echolucent lesion than their peers (10% vs. 23%, P < 0.001 and 7% vs. 11%, P = 0.06, respectively). Risk of ventriculomegaly was increased for infants delivered because of preterm labor (adjusted odds ratio (OR) = 2.3, 95% confidence interval (CI): 1.1, 4.9), preterm premature rupture of fetal membranes (OR = 3.6, 95% CI: 1.5, 8.7), and cervical insufficiency (OR = 2.8, 95% CI: 1.4, 5.5) when compared with infants delivered because of preeclampsia. Risk of an echolucent lesion was increased for infants delivered because of preterm labor (OR = 2.7, 95% CI: 1.2, 5.7) and intrauterine growth retardation (OR = 3.3, 95% CI: 1.2, 9.4). The doubling of diparesis risk associated with preterm labor and with preterm premature rupture of fetal membranes did not achieve statistical significance, nor did the doubling of quadriparesis risk and the tripling of diparesis risk associated with cervical insufficiency.

Traditionally, the investigation of preterm birth has relied on diagnostic definitions derived from maternal clinical presentation. However, clinical presentation may be only tangentially related to the underlying etiology of a disease. The utilization of data derived directly from the intrauterine or maternal systemic environment would be invaluable in consideration of the causes of preterm birth. In this issue, Kelly et al. (Am J Epidemiol. 2009;170(2)148-158) contribute to our understanding of the epidemiology of the intrauterine environment by classifying the vascular biology of the maternal-placental interface in cases of preterm delivery. Their histology-based approach observes that vascular conditions may be grouped into 5 constructs with specific relations to maternal and fetal vascular pathology. The frequencies of these constructs vary with regard to delivery indication and gestational age, suggesting that the intrauterine conditions associated with preterm birth are more complicated than originally appreciated. This work is laborious, and replication of the technique will be important. However, these authors have taken a large step toward introducing an "intrauterine" perspective into perinatal epidemiology and into our understanding of the underlying etiologies of preterm birth.