Objective This study examined associations between maternal lipid levels at mid-pregnancy and preterm delivery, medically indicated or spontaneous. Design Prospective cohort study. Setting Women were recruited from 52 clinics in five Michigan, U.S.A communities (1998–2004). Population Pregnant women were enrolled at 15–27 weeks’ gestation and followed to delivery (n=3019). Methods A single blood sample was obtained at study enrollment. Blood lipids, i.e., total (TC), high-density lipoprotein (HDLc), low-density lipoprotein (LDLc) cholesterol, and triglycerides (TG), were measured on a subcohort (n=1,309). Main Outcome Measures There were 221 spontaneous, 100 medically indicated preterm deliveries and 988 term deliveries. Polytomous logistic regression models examined relations among cholesterol levels (Low: <10th %tile, Referent: 10th–<70th %tile, High: ≥70th %tile), quartiles of TG (Referent: first quartile) and delivery outcome (Referent: term). Results Odds of medically indicated preterm delivery were increased among women with low TC (adjusted odds ratio (aOR)= 2.04, 95% confidence interval (CI): 1.12,3.72), low HDLc (aOR=1.89, 95%CI: 1.04,3.42), or low LDLc (aOR=1.96, 95%CI: 1.09,3.54). Odds of spontaneous preterm delivery were increased among women with high TC (aOR=1.51, 95%CI: 1.06,2.15), high LDLc (aOR=1.42, 95%CI: 0.99,2.04) or high TG (aOR=1.90, 95%CI: 1.21,2.97 and aOR=1.72, 95%CI: 1.06,2.78 for third and fourth quartiles, respectively). Conclusions Extremely low TC, HDLc and LDLc were associated with a modest increase in risk of medically indicated preterm delivery, while high TC, LDLc and TG modestly increased risk of spontaneous preterm delivery. Further research is needed to uncover explanations for these associations and to identify optimal ranges for maternal lipids.

Decreased bone density and stature can occur in pediatric patients with inflammatory bowel disease (IBD). Little is known about how IBD broadly impacts the skeleton. To evaluate the influence of an acute episode of IBD on growing bone, 4-wk-old mice were administered 5% dextran sodium sulfate (DSS) for 5 days to induce colitis and their recovery was monitored. During active disease and early recovery, trabecular bone mineral density, bone volume, and thickness were decreased. Cortical bone thickness, outer perimeter, and density were also decreased, whereas inner perimeter and marrow area were increased. These changes appear to maintain bone strength since measures of moments of inertia were similar between DSS-treated and control mice. Histological (static and dynamic), serum, and RNA analyses indicate that a decrease in osteoblast maturation and function account for changes in bone density. Unlike some conditions of bone loss, marrow adiposity did not increase. Similar to reports in humans, bone length decreased and correlated with decreases in growth plate thickness and chondrocyte marker expression. During disease recovery, mice experienced a growth spurt that led to their achieving final body weights and bone length, density, and gene expression similar to healthy controls. Increased TNF-alpha and decreased IGF-I serum levels were observed with active disease and returned to normal with recovery. Changes in serum TNF-alpha (increased) and IGF-I (decreased) paralleled changes in bone parameters and returned to normal values with recovery, suggesting a potential role in the skeletal response.

This study population is unique in its size and recruitment by gestational age rather than birth weight. Inflammation occurred frequently, but not in placentas that had characteristics of vasculopathy. The prevalence of inflammation decreased with increasing gestational age, while vasculopathy increased. Funisitis need not be accompanied by chorionic inflammation.

Inconsistent findings linking placental histologic chorioamnionitis (HCA) and preterm delivery may result from variations in HCA definition, population studied, and exclusion criteria. This analysis from the 1998-2004 Pregnancy Outcomes and Community Health Study (five Michigan communities) includes the first 1,053 subcohort women (239 preterm, 814 term) with completed placental assessments. Multiple HCA definitions were constructed by 1) varying polymorphonuclear leukocytes/high-powered field thresholds and placenta components included and 2) using polymorphonuclear leukocyte characteristics to assign low/high maternal, fetal inflammation stage and grade. In African Americans, HCA was associated with preterm delivery before 35 weeks. The effect size was modest for polymorphonuclear leukocytes/high-powered field thresholds of greater than 10 and greater than 30 (odds ratios (ORs) ¼ 0.8 and 2.0); larger for greater than 100 (OR ¼ 3.2, 95% confidence interval (CI): 1.4, 7.1); strengthened after excluding medically indicated preterm deliveries (OR ¼ 4.9, 95% CI: 2.0, 11.8); and strongest for high maternal/high fetal HCA (OR ¼ 5.6, 95% CI: 1.4, 22.1). These latter HCA criteria also produced the largest effect size in Whites/others (OR ¼ 2.7, 95% CI: 0.3, 26.9). Among preterm deliveries before 35 weeks excluding those medically indicated, 12% of Whites/others and 55% of African Americans had high maternal HCA. The authors conclude that HCA definition, exclusion criteria, and race/ethnicity influence the HCA-preterm delivery association and that HCA contributes to preterm delivery-related ethnic disparity.