The Association Between Medicaid Expansion and Disparities in Vestibular Schwannoma Incidence.

OBJECTIVES: The effect of Medicaid expansion as a part of the Affordable Care Act on vestibular schwannoma (VS) incidence overall and in marginalized populations has not yet been elucidated. The goal of this study was to determine if Medicaid expansion was associated with increases in VS incidence overall, as well as in patients of non-white race or in counties of low socioeconomic status (SES). METHODS: We performed a difference-in-difference (DiD) analysis from January 1st 2010-December 31st 2017 utilizing the Surveillance, Epidemiology, and End Results (SEER) database. Our DiD method compared the change in VS rate between counties that did and did not expand Medicaid among patients of white and non-white race, in low and high SES counties, before and after expansion. RESULTS: The study included 17,312 cases across 1020 counties. Medicaid expansion was associated with a 15% increase (incidence rate ratio 95% CI: [11%, 19]) in VS incidence. White populations saw a 10% increase (CI: [1.06, 1.19]), Black populations saw a 20% increase (CI: [1.10, 1.29]), and patients of other races saw a 44% increase in incidence associated with expansion (CI: [1.21, 1.70]). Low SES counties saw an increase in incidence 1.12 times higher than that of high SES counties (CI:[1.04, 1.20]). CONCLUSION: Medicaid expansion was associated with increases in VS incidence across populations. Furthermore, this increase was more evident in disadvantaged populations, such as patients of non-white race and those from low SES counties. These findings emphasize the impact of Medicaid expansion on healthcare utilization for VS diagnosis. LEVEL OF EVIDENCE: Step/Level 3-Retrospective Cohort Study Laryngoscope, 2024.

Role of Chitinase 3-Like 1 Protein in the Pathogenesis of Hepatic Insulin Resistance in Nonalcoholic Fatty Liver Disease.

A recently discovered human glycoprotein, chitinase 3-like 1 (Chi3L1), may play a role in inflammation, tissue remodeling, and visceral fat accumulation. We hypothesize that Chi3L1 gene expression is important in the development of hepatic insulin resistance characterized by the generation of pAKT, pGSK, and pERK in wild type and Chi3L1 knockout (KO) murine liver following insulin stimulation. The Chi3L1 gene and protein expression was evaluated by Real Time PCR and ELISA; lipid accumulation in hepatocytes was also assessed. To alter Chi3L1 function, three different anti-Chi3L1 monoclonal antibodies (mAbs) were administered in vivo and effects on the insulin signaling cascade and hepatic lipid deposition were determined. Transmission of the hepatic insulin signal was substantially improved following KO of the CHi3L1 gene and there was reduced lipid deposition produced by a HFD. The HFD-fed mice exhibited increased Chi3L1 expression in the liver and there was impaired insulin signal transduction. All three anti-Chi3L1 mAbs partially restored hepatic insulin sensitivity which was associated with reduced lipid accumulation in hepatocytes as well. A KO of the Chi3L1 gene reduced lipid accumulation and improved insulin signaling. Therefore, Chi3L1 gene upregulation may be an important factor in the generation of NAFLD/NASH phenotype.