Influence of adolescence and obesity on the rate of stillbirth.

BACKGROUND: We hypothesise that the rate of stillbirth is increased in mothers younger than 18 years of age compared to adult mothers, and that obesity further increases the risk of stillbirth in this population. METHODS: We conducted a population-based cohort study comparing rates of stillbirth between adolescent, defined as young women under the age of 18 and adult women. We then compared the rate of stillbirth in normal weight vs. obese adolescents. These effects were stratified according to gestational age. Log-binomial regression models were used to estimate the effect of adolescence and obesity on stillbirth risk while adjusting for important confounders. Risk ratios (RR) with 95% confidence intervals [CI]were calculated. RESULTS: We reviewed data from 650 760 births in Missouri between 1998 and 2005. Stillbirth rates were 6.7 and 4.1 per 1000 in adolescents and adult women, respectively (RR 1.2, 95% CI 1.03-1.5). A higher proportion of stillbirths occurred prior to 28 weeks in adolescents vs. adults (53% vs. 37% respectively, P = 0.002). The risk of stillbirth in obese adolescents was further increased over normal weight adolescents (adjusted RR [aRR] 1.7, 95% CI 1.02-2.9). CONCLUSION: Adolescent pregnancies, particularly obese adolescents, are at an increased risk of stillbirth.

Modulation of lipopolysaccharide-induced chorioamnionitis in fetal sheep by maternal betamethasone.

OBJECTIVE: We tested the hypothesis that the order of exposure to maternal betamethasone and intra-amniotic (IA) lipopolysaccharide (LPS) will differentially modulate inflammation in the chorioamnion. STUDY DESIGN: Time-mated Merino ewes with singleton fetuses received saline alone, IA LPS alone, maternal betamethasone before LPS, or betamethasone after LPS. We assessed inflammatory markers in the chorioamnion and the amniotic fluid. RESULTS: Inflammatory cell infiltration, expression of myeloperoxidase, serum amyloid A3 (acute phase reactant) in the chorioamnion, and levels of interleukin (IL)-8 in the amniotic fluid increased 7 days after LPS exposure. Betamethasone prior to LPS decreased infiltration of the inflammatory cells, CD3+ T cells, and decreased the levels of IL-1ß and IL-8 in the amniotic fluid. CONCLUSIONS: Betamethasone 7 days prior to LPS exposure suppressed LPS-induced inflammation. The markers of inflammation largely had returned to the baseline 14 days after LPS exposure.

Modulation of lipopolysaccharide-induced chorioamnionitis by Ureaplasma parvum in sheep.

OBJECTIVE: Ureaplasma colonization in the setting of polymicrobial flora is common in women with chorioamnionitis, and is a risk factor for preterm delivery and neonatal morbidity. We hypothesized that Ureaplasma colonization of amniotic fluid would modulate chorioamnionitis induced by Escherichia coli lipopolysaccharide (LPS). STUDY DESIGN: Sheep received intraamniotic (IA) injections of media (control) or live Ureaplasma either 7 or 70 days before delivery. Another group received IA LPS 2 days before delivery. To test for interactions, U parvum-exposed animals were challenged with IA LPS, and delivered 2 days later. All animals were delivered preterm at 125 ± 1 day of gestation. RESULTS: Both IA Ureaplasma and LPS induced leukocyte infiltration of chorioamnion. LPS greatly increased the expression of proinflammatory cytokines and myeloperoxidase in leukocytes, while Ureaplasma alone caused modest responses. Interestingly, 7-day but not 70-day Ureaplasma exposure significantly down-regulated LPS-induced proinflammatory cytokines and myeloperoxidase expression in the chorioamnion. CONCLUSION: Acute (7-day) U parvum exposure can suppress LPS-induced chorioamnionitis.

The influence of hospital type on induction of labor and mode of delivery.

OBJECTIVE: The purpose of this study was to compare labor induction and cesarean delivery rates at term in community vs university hospitals. STUDY DESIGN: A population-based retrospective cohort study of births was performed. Primary outcomes were term gestation at <39 weeks, labor induction, and cesarean delivery. After we adjusted for comorbidities, malpresentation, and previous cesarean delivery, logistic regression assessed the association between hospital type and primary outcomes. RESULTS: Births occur less often in week 37 (n = 24390 [11%] vs 4006 [13%]; adjusted odds ratio [OR], 0.9; 95% confidence interval [CI], 0.8-0.9) and are similar in week 38 in community vs university hospitals. Inductions occur more commonly in community vs university settings at 37 weeks (n = 6440 [27%] vs 757 [19%]; adjusted OR, 1.7; 95% CI, 1.5-1.8) and at 38 weeks (n = 16586 [31%] vs 1530 [21%]; adjusted OR, 1.8; 95% CI, 1.7-1.9). Cesarean rates are no different between hospital types. CONCLUSION: Induction is 70-80% more likely at community vs university hospitals before the optimal gestational age of ≥ 39 weeks, but cesarean delivery rates do not differ at term.

The effect of maternal obesity on the rate of failed induction of labor.

OBJECTIVE: The purpose of this study was to quantify the relationship between class of obesity and rate of failed induction of labor. STUDY DESIGN: Using the Ohio Department of Health's birth certificate database from January 1, 2006, through December 31, 2007, we performed a population-based cohort study that compared failed induction of labor rates between obese and normal-weight women. RESULTS: The rate of induction is associated with increasing body mass index from 28% in normal-weight women to 34% in class III obese women (body mass index, ≥40 kg/m2). Induction failure rates are also associated with increasing obesity class from 13% in normal-weight women to 29% in class III obese women. Women with class III obesity without a previous vaginal delivery and a macrosomic fetus had the highest rate of failed induction at 80%. CONCLUSION: Obesity is associated with an increased risk of failed labor induction that appears to be related directly to increasing class of obesity.