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Objectives: Coronavirus disease 2019 (COVID‐19) is associated with mortality in persons with comorbidities. The aim of this study was to evaluate in‐hospital outcomes in patients with COVID‐19 with and without epilepsy. Methods: We conducted a retrospective study of patients with COVID‐19 admitted to a multicenter health system between March 15, 2020, and May 17, 2021. Patients with epilepsy were identified using a validated International Classification of Diseases, Ninth Revision, Clinical Modification (ICD‐9‐CM)/ICD‐10‐CM case definition. Logistic regression models and Kaplan–Meier analyses were conducted for mortality and non‐routine discharges (i.e., not discharged home). An ordinary least‐squares regression model was fitted for length of stay (LOS). Results: We identified 9833 people with COVID‐19 including 334 with epilepsy. On univariate analysis, people with epilepsy had significantly higher ventilator use (37.70% vs 14.30%, p <.001), intensive care unit (ICU) admissions (39.20% vs 17.70%, p <.001) mortality rate (29.60% vs 19.90%, p <.001), and longer LOS (12 days vs 7 days, p <.001). and fewer were discharged home (29.64% vs 57.37%, p <.001). On multivariate analysis, only non‐routine discharge (adjusted odds ratio [aOR] 2.70, 95% confidence interval [CI] 2.00–3.70; p <.001) and LOS (32.50% longer, 95% CI 22.20%–43.60%; p <.001) were significantly different. Factors associated with higher odds of mortality in epilepsy were older age (aOR 1.05, 95% CI 1.03–1.08; p <.001), ventilator support (aOR 7.18, 95% CI 3.12–16.48; p <.001), and higher Charlson comorbidity index (CCI) (aOR 1.18, 95% CI 1.04–1.34; p =.010). In epilepsy, admissions between August and December 2020 or January and May 2021 were associated with a lower odds of non‐routine discharge and decreased LOS compared to admissions between March and July 2020, but this difference was not statistically significant. Significance: People with COVID‐19 who had epilepsy had a higher odds of non‐routine discharge and longer LOS but not higher mortality. Older age (≥65), ventilator use, and higher CCI were associated with COVID‐19 mortality in epilepsy. This suggests that older adults with epilepsy and multimorbidity are more vulnerable than those without and should be monitored closely in the setting of COVID‐19. [ABSTRACT FROM AUTHOR]

Adolescents living with HIV (ALWH) are particularly susceptible to disruptions in care, which may lead to poor HIV-related health outcomes. Here, we report the results of a longitudinal phone-based study investigating impacts of the COVID-19 pandemic on ALWH in New York City. Participants (N = 10, mean age 21.2 years, 50% female) demonstrated substantial COVID-19 knowledge and identified Instagram as their primary source of COVID-19 information. Nearly all participants reported loss of income, and 50% reported experiencing food insecurity as a result of the pandemic. These findings highlight existing vulnerabilities among ALWH that may threaten the continuum of care. [ABSTRACT FROM AUTHOR]

Background:Signaling through the endothelin receptor B (EDNRB) is critical for the development of the enteric nervous system (ENS) and mutations in endothelin system genes cause Hirschsprung’s aganglionosis in humans. Penetrance of the disease is modulated by other genetic factors. Mutations affecting retinoic acid (RA) signaling also produce aganglionosis in mice. Thus, we hypothesized that RA and endothelin signaling pathways may interact in controlling development of the ENS. Methods:Rat immunoselected ENS precursor cells were cultured with the EDNRB ligand endothelin-3, an EDNRB-selective antagonist (BQ-788), and/or RA for 3 or 14 days. mRNA levels of genes related to ENS development, RA- and EDNRB-signaling were measured at 3 days. Proliferating cells and cells expressing neuronal, glial, and myofibroblast markers were quantified. Results:Culture of isolated ENS precursors for 3 days with RA decreases expression of the endothelin-3 gene and that of its activation enzyme. These changes are associated with glial proliferation, a higher percentage of glia, and a lower percentage of neurons compared to cultures without RA. These changes are independent of EDNRB signaling. Conversely, EDNRB activation in these cultures decreases expression of RA receptors β and γ mRNA and affects the expression of the RA synthetic and degradative enzymes. These gene expression changes are associated with reduced glial proliferation and a lower percentage of glia in the culture. Over 14 days in the absence of EDNRB signaling, RA induces the formation of a heterocellular plexus replete with ganglia, glia and myofibroblasts. Conclusions:A complex endothelin-RA interaction exists that coordinately regulates the development of rat ENS precursors in vitro. These results suggest that environmental RA may modulate the expression of aganglionosis in individuals with endothelin mutations. [ABSTRACT FROM AUTHOR]