Influence of Medicaid expansion on short interpregnancy interval rates in the United States.

BACKGROUND: Short interpregnancy intervals have been associated with poor maternal and infant outcomes. Contraception access could affect the short interpregnancy interval rates. OBJECTIVE: To assess the influence of Medicaid on short interpregnancy intervals. We tested the hypothesis that Medicaid expansion and subsequent access to birth control would be associated with decreased short interpregnancy intervals. STUDY DESIGN: Using the United States birth certificate data, we performed a population-based retrospective cohort study including multiparous women who had live births in 2012 and 2016, which is before and after Medicaid expansion had been implemented in 2014. Multivariate logistic regression estimated the influence of Medicaid expansion on short interpregnancy intervals (<12 months). The rate differences of short interpregnancy intervals in 2012 and 2016 were compared between Medicaid expansion vs non-Medicaid expansion states. RESULTS: There were a total of 7,916,908 live births in 2012 and 2016 in the United States, of which 3,362,904 (42.5%) were in multiparous women with data on interpregnancy intervals (n=1,961,683 [58.3%]) in Medicaid expansion states and in non-Medicaid expansion states (n=1,401,221 [41.7%]). The rate of short interpregnancy intervals in the United States was slightly lower in 2016 (17.3%) than in 2012 (17.4%), P=.0006; rate difference 0.13% (95% confidence interval, 0.05-0.20). Short interpregnancy intervals occurred more frequently in non-Medicaid expansion states than in Medicaid expansion states in both 2012 (18.1% vs 16.6%, respectively; P<.001) and 2016 (18.1% vs 16.4%, respectively; P<.001). The rate of short interpregnancy intervals decreased by 0.11% (95% confidence interval, 0.01-0.22) in Medicaid expansion states and increased by 0.04% (95% confidence interval, 0.09-0.17) in non-Medicaid expansion states. In 2016, living in a Medicaid expansion state was associated with a modestly decreased risk of short interpregnancy intervals (adjusted relative risk, 0.97; 95% confidence interval, 0.97-0.98), even after adjustment for coexisting risks. CONCLUSION: The risk of short interpregnancy intervals decreased in the Medicaid expansion states even after adjusting for risk factors. Moreover, the short interpregnancy interval rates increased in nonexpansion states but decreased in Medicaid expansion states. If non-Medicaid expansion states had experienced the same rate of decrease in short interpregnancy intervals as Medicaid expansion states, 1122 fewer women would have had a short interpregnancy interval in 2016. Considering the known association between short interpregnancy intervals and adverse maternal and infant outcomes, these findings indicate that Medicaid expansion could improve perinatal outcomes.

Generation and validation of a conditional knockout mouse model for desmosterolosis.

The enzyme 3ß-hydroxysterol-Δ24 reductase (DHCR24, EC 1.3.1.72) catalyzes the conversion of desmosterol to cholesterol and is obligatory for post-squalene cholesterol synthesis. Genetic loss of this enzyme results in desmosterolosis (MIM #602398), a rare disease that presents with multiple congenital anomalies, features of which overlap with subjects with the Smith-Lemli-Opitz syndrome (another post-squalene cholesterol disorder). Global knockout (KO) of Dhcr24 in mice recapitulates the biochemical phenotype, but pups die within 24 h from a lethal dermopathy, limiting its utility as a disease model. Here, we report a conditional KO mouse model (Dhcr24flx/flx) and validate it by generating a liver-specific KO (Dhcr24flx/flx,Alb-Cre). Dhcr24flx/flx,Alb-Cre mice showed normal growth and fertility, while accumulating significantly elevated levels of desmosterol in plasma and liver. Of interest, despite the loss of cholesterol synthesis in the liver, hepatic architecture, gene expression of sterol synthesis genes, and lipoprotein secretion appeared unchanged. The increased desmosterol content in bile and stool indicated a possible compensatory role of hepatobiliary secretion in maintaining sterol homeostasis. This mouse model should now allow for the study of the effects of postnatal loss of DHCR24, as well as role of tissue-specific loss of this enzyme during development and adulthood.