Group Prenatal Care Reduces Risk of Preterm Birth and Low Birth Weight: A Matched Cohort Study.

BACKGROUND: Group prenatal care is a promising strategy to improve perinatal outcomes. Research in larger more diverse populations with attention to adherence is needed to inform clinical practice recommendations. We examined the impact of group prenatal care on preterm birth and low birth weight in a large metropolitan hospital, accounting for patient adherence, over an 8.5-year period. MATERIALS AND METHODS: We analyzed data from 9,348 pregnant women with a live, singleton birth who received group (CenteringPregnancy or Expect With Me) or individual prenatal care at Vanderbilt University Medical Center from January 2009 through June 2016. Propensity scores were used for matching based on year of delivery, age, race, pregnancy risk, and adequacy of care. The propensity score matched sample included 1,384 group and 5,055 individual prenatal care patients (total = 6,439 women). Preterm birth (<37 weeks gestation) and low birth weight (<2,500 g) were obtained from systematic medical review. Risks were estimated using Poisson regression. RESULTS: Controlling for individual visits, receiving group prenatal care resulted in significantly lower risk of having a preterm birth (Rate ratio [RR] 0.63, 95% confidence interval [CI] 0.49-0.81) and low birth weight baby (RR 0.62, 95% CI 0.47-0.81), compared to receiving individual care only. Women with ≥5 group prenatal care visits experienced even greater benefits: 68% (RR = 0.32; 95% CI 0.22-0.45) and 66% (RR = 0.34; 95% CI 0.23-0.50) risk reduction in preterm birth and low birth weight, respectively. CONCLUSIONS: Participation in group prenatal care may improve birth outcomes. Efforts to promote adoption and sustainability of group prenatal care by health systems may be warranted.

Inactivating mutation in the prostaglandin transporter gene, SLCO2A1, associated with familial digital clubbing, colon neoplasia, and NSAID resistance.

HPGDand SLCO2A1 genes encode components of the prostaglandin catabolic pathway, with HPGD encoding the degradative enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH), and SLCO2A1 encoding the prostaglandin transporter PGT that brings substrate to 15-PGDH. HPGD-null mice show increased prostaglandin E2 (PGE2), marked susceptibility to developing colon tumors, and resistance to colon tumor prevention by nonsteroidal anti-inflammatory drugs (NSAID). But in humans, HPGD and SLCO2A1 mutations have only been associated with familial digital clubbing. We, here, characterize a family with digital clubbing and early-onset colon neoplasia. Whole-exome sequencing identified a heterozygous nonsense mutation (G104X) in the SLCO2A1 gene segregating in 3 males with digital clubbing. Two of these males further demonstrated notably early-onset colon neoplasia, 1 with an early-onset colon cancer and another with an early-onset sessile serrated colon adenoma. Two females also carried the mutation, and both these women developed sessile serrated colon adenomas without any digital clubbing. Males with clubbing also showed marked elevations in the levels of urinary prostaglandin E2 metabolite, PGE-M, whereas, female mutation carriers were in the normal range. Furthermore, in the male proband, urinary PGE-M remained markedly elevated during NSAID treatment with either celecoxib or sulindac. Thus, in this human kindred, a null SLCO2A1 allele mimics the phenotype of the related HPGD-null mouse, with increased prostaglandin levels that cannot be normalized by NSAID therapy, plus with increased colon neoplasia. The development of early-onset colon neoplasia in male and female human SLCO2A1 mutation carriers suggests that disordered prostaglandin catabolism can mediate inherited susceptibility to colon neoplasia in man.

Genetics researchers' and IRB professionals' attitudes toward genetic research review: a comparative analysis.

PURPOSE: Genetic research involving human participants can pose challenging questions related to ethical and regulatory standards for research oversight. However, few empirical studies describe how genetic researchers and institutional review board (IRB) professionals conceptualize ethical issues in genetic research or where common ground might exist. METHODS: Parallel online surveys collected information from human genetic researchers (n = 351) and IRB professionals (n = 208) regarding their views about human participant oversight for genetic protocols. RESULTS: A range of opinions were observed within groups on most issues. In both groups, a minority thought it likely that people would be harmed by participation in genetic research or identified from coded genetic data. A majority of both groups agreed that reconsent should be required for four of the six scenarios presented. Statistically significant differences were observed between groups on some issues, with more genetic researcher respondents trusting the confidentiality of coded data, fewer expecting harms from reidentification, and fewer considering reconsent necessary in certain scenarios. CONCLUSION: The range of views observed within and between IRB and genetic researcher groups highlights the complexity and unsettled nature of many ethical issues in genome research. Our findings also identify areas where researcher and IRB views diverge and areas of common ground.