Placental histopathology is not more prevalent in women with IBD: P-1.

Women with inflammatory bowel disease (IBD) are at increased risk for adverse pregnancy outcomes that include pre-term delivery, low birth weight, and small for gestational age (SGA) infants. Most recognized cases of fetal growth restriction in singleton pregnancies have underlying placental causes. To date, studies showing increased risk of poor pregnancy outcomes in IBD patients focus on maternal and fetal factors. We performed a pilot study to investigate whether there is an increase in placental histopathology in pregnant women with IBD.

We performed a retrospective observational study. Patients were identified through their enrollment in the national, multicenter Pregnancy In Inflammatory Bowel Disease And Neonatal Outcome (PIANO) study, for which Women and Infants Hospital (WIH) serves as a site. The placental tissue of 7 ulcerative colitis, 5 Crohn's, and 2 indeterminate colitis subjects who gave birth at WIH between 2008-2011 were evaluated for diffuse placental acute or chronic villitis, deciduitis, parenchymal disease, and chorioamnionitis. For all 14 subjects, the medical and obstetric history, medication list, social history, and birth outcomes were reviewed. The study subjects were matched to 26 normal healthy controls by gestational age at delivery.

The median gestational age was 38 weeks. 29% of IBD infants were preterm. SGA infants accounted for 29% of births to IBD mothers compared to 19% for controls. Six out of the fourteen IBD patients had mild-moderate flares or were diagnosed with their disease during pregnancy. Five patients required corticosteroids and one was maintained on an immunomodulator. Three other patients received at least one dose of a TNF-alpha inhibitor during their pregnancy. There was no evidence of diffuse placental villitis, deciduitis, or parenchymal disease in IBD subjects. Histological evidence of chorioamnionitis was present in 27% of control placentas and 7% of those from IBD mothers.

In this pilot study, it does not appear that placental inflammatory activation is responsible for the increase in adverse pregnancy outcome in women with IBD. Decreased rates of chorioamnionitis in IBD placentas may be due to the use of corticosteroids and immune modifying agents. Further studies with larger numbers may be needed to determine the possible association between placental histopathology and poor pregnancy outcomes in IBD.