Introduction:The impact of the COVID-19 pandemic on the incidence of pediatric type 1 (T1D) and type 2 diabetes (T2D) and severity of presentation at diagnosis is unclear. Methods: A retrospective comparison of 737 youth diagnosed with T1D and T2D during the initial 12 months of the CO-VID-19 pandemic and in the preceding 2 years was conducted at a pediatric tertiary care center. Results: Incident cases of T1D rose from 152 to 158 in the 2 years before the pandemic (3.9% increase) to 182 cases during the pandemic (15.2% increase). The prevalence of diabetic ketoacidosis (DKA) at T1D diagnosis increased over 3 years (41.4%, 51.9%, and 57.7%, p = 0.003); severe DKA increased during the pandemic as compared to the 2 years before (16.8% vs. 28%, p = 0.004). Although there was no difference in the mean hemoglobin A1c (HbA1c) between racial and ethnic groups at T1D diagnosis in the 2-years pre-pandemic (p = 0.31), during the pandemic HbA1c at T1D diagnosis was higher in non-Hispanic Black (NHB) youth (11.3 ± 1.4%, non-Hispanic White 10.5 ± 1.6%, Latinx 10.8 ± 1.5%, p = 0.01). Incident cases of T2D decreased from 54 to 50 cases (7.4% decrease) over the 2-years pre-pandemic and increased 182% during the pandemic (n = 141, 1.45 cases/month, p < 0.001). As compared to the 2-years pre-pandemic, cases increased most among NHB youth (56.7% vs. 76.6%, p = 0.001) and males (40.4% vs. 58.9%, p = 0.005). Cases of DKA (5.8% vs. 23.4%, p < 0.001) and hyperosmolar DKA (0 vs. 9.2%, p = 0.001) increased among youth with T2D during the pandemic. Conclusions: During the pandemic, the incidence and severity of presentation of T1D increased modestly, while incident cases of T2D increased 182%, with a nearly 6-fold increase in DKA and nearly a 10% incidence of hyperosmolar DKA. NHB youth were disproportionately impacted, raising concern about worsening of pre-existing health disparities during and after the pandemic.

BackgroundThe period following hospital discharge is a vulnerable time for patients when errors and poorly coordinated care are common. Suboptimal care transitions for patients admitted with cardiovascular conditions can contribute to readmission and other adverse health outcomes. Little research has examined the role of health literacy and other social determinants of health in predicting post-discharge outcomes.MethodsThe Vanderbilt Inpatient Cohort Study (VICS), funded by the National Institutes of Health, is a prospective longitudinal study of 3,000 patients hospitalized with acute coronary syndromes or acute decompensated heart failure. Enrollment began in October 2011 and is planned through October 2015. During hospitalization, a set of validated demographic, cognitive, psychological, social, behavioral, and functional measures are administered, and health status and comorbidities are assessed. Patients are interviewed by phone during the first week after discharge to assess the quality of hospital discharge, communication, and initial medication management. At approximately 30 and 90 days post-discharge, interviewers collect additional data on medication adherence, social support, functional status, quality of life, and health care utilization. Mortality will be determined with up to 3.5 years follow-up. Statistical models will examine hypothesized relationships of health literacy and other social determinants on medication management, functional status, quality of life, utilization, and mortality. In this paper, we describe recruitment, eligibility, follow-up, data collection, and analysis plans for VICS, as well as characteristics of the accruing patient cohort.DiscussionThis research will enhance understanding of how health literacy and other patient factors affect the quality of care transitions and outcomes after hospitalization. Findings will help inform the design of interventions to improve care transitions and post-discharge outcomes.

Rationale: In black women, triglycerides are paradoxically normal in the presence of insulin resistance. This relationship may be explained by race-related differences in central adiposity and SCD (stearoyl-CoA desaturase)-1 enzyme activity index. Objective: In a cross-sectional study, to compare fasting and postprandial triglyceride-rich lipoprotein particle (TRLP) concentrations and size in black compared with white pre- and postmenopausal women and determine the relationship between TRLP subfractions and whole-body insulin sensitivity, hepatic and visceral fat, and SCD-1 levels. Methods and Results: In 122 federally employed women without diabetes mellitus, 73 black (58 African American and 15 African immigrant) and 49 white; age, 44±10 (mean±SD) years; body mass index, 30.0±5.6 kg/m 2 , we measured lipoprotein subfractions using nuclear magnetic resonance. Hepatic fat was measured by proton magnetic resonance spectroscopy, insulin sensitivity index calculated by minimal modeling from a frequently sampled intravenous glucose test, and red blood cell fatty acid profiles were measured by gas chromatography and were used to estimate SCD-1 indices. Hepatic fat, insulin sensitivity index, and SCD-1 were similar in black women and lower than in whites, regardless of menopausal status. Fasting and postprandial large, medium, and small TRLPs, but not very small TRLPs, were lower in black women. Fasting large, medium, and very small TRLPs negatively correlated with insulin sensitivity index and positively correlated with visceral and hepatic fat and SCD-1 activity in both groups. In multivariate models, visceral fat and SCD-1 were associated with total fasting TRLP concentrations (adjR2, 0.39; P =0.001). Black women had smaller postprandial changes in large ( P =0.005) and medium TRLPs ( P =0.007). Conclusions: Lower visceral fat and SCD-1 activity may contribute to the paradoxical association of lower fasting and postprandial TRLP subfractions despite insulin resistance in black compared with white pre- and postmenopausal women. Similar concentrations of very small TRLPs are related to insulin resistance and could be important mediators of cardiometabolic disease risk in women. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique identifier: NCT01809288.