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Background: The telementoring Project ECHO (Extension for Community Healthcare Outcomes) model has been shown to improve disease management in diabetes in many underserved communities. The authors aim to evaluate if ECHO could also be an effective tool for quality improvement (QI) of diabetes care in these communities., Methods: Thirteen clinics in underserved communities in California and Florida participating in Project ECHO Diabetes were recruited for a 12-month QI program. The program provided weekly tele-education sessions, including a didactic presentation and case-based discussion. In addition, clinics chose their own set of quality measures to improve and met remotely to discuss their efforts, successes, and setbacks every quarter with mentorship from QI experts., Results: Of the 31 QI initiatives attempted by different clinics, all had either made improvements (25 initiatives, 80.6%) or were in the process of making improvements (6 initiatives, 19.4%) in structural, process, and outcome measures. Examples of these measures include whether clinics have protocols to identify high-risk patients (structure), numbers of continuous glucose monitor prescriptions submitted by the clinics (process), and percentage of patients with diabetes whose most recent HbA1c are > 9% (outcome). For one measure, 40.0% of the clinics had achieved a higher percentage of cumulative HbA1c measurement in the third quarter of the year, compared to the fourth quarter in the previous year. The cost of QI implementation varied widely due to different number of personnel involved across sites., Conclusion: A QI program delivered via Project ECHO Diabetes can facilitate quality improvements in underserved communities., (Copyright © 2023 The Joint Commission. Published by Elsevier Inc. All rights reserved.)

Diabetes is a serious chronic disease with high associated burden and disproportionate costs to communities based on socioeconomic, gender, racial, and ethnic status. Addressing the complex challenges of global inequity in diabetes will require intentional efforts to focus on broader social contexts and systems that supersede individual-level interventions. We codify and highlight best practice approaches to achieve equity in diabetes care and outcomes on a global scale. We outline action plans to target diabetes equity on the basis of the recommendations established by The Lancet Commission on Diabetes, organising interventions by their effect on changing the ecosystem, building capacity, or improving the clinical practice environment. We present international examples of how to address diabetes inequity in the real world to show that approaches addressing the individual within a larger social context, in addition to addressing structural inequity, hold the greatest promise for creating sustainable and equitable change that curbs the global diabetes crisis., Competing Interests: Declaration of interests AFW is supported by The Leona M and Harry B Helmsley Charitable Trust (2005-03934) and the National Institutes of Health-National Institute of Diabetes and Digestive Kidney Disease (5P30DK111024-07). LM-B is supported by an Australian National Health and Medical Research Council (NHMRC) investigator grant (1194698), and leads projects that are funded by NHMRC, the Australian Department of Health, and the Australian Medical Research Future Fund. LEE and JAC are supported by the National Institutes of Health-National Institute of Diabetes and Digestive Kidney Disease (R01DK118038 and R01DK120861, awarded to LEE; K01DK131319, awarded to JAC). LEE and RJW are supported by the National Institute on Minority Health and Health Disparities (R01MD013826, awarded to LEE and RJW; R01MD017574, awarded to LEE). RJW is supported by the American Diabetes Association (1-19-JDF-075). ANW is supported by the National Institutes of Health-Fogarty International Centre (K43TW010698). ANW declares an honorarium received from Sanofi for serving as a panel member at an educational event on thyroid cancer. JCM receives honorarium from Servier Laboratories for serving on the advisory committee at educational events. OE is a health-care disparities adviser (on a temporary advisory board role) for Medtronic. OE has received research support through his organisation T1D Exchange from Medtronic, Vertex, Dexcom, and Eli Lilly. Medtronic supports components of T1DX-QI health equity work. The T1DX-QI is funded by The Leona M and Harry B Helmsley Charitable Trust. LAD has received research support to her institution from Dompé, Lilly, MannKind, Medtronic, Provention, and Zealand Pharma; and served as a consultant for Abata Therapeutics and Vertex. SA is supported by the National Institutes of Health-National Institute of Diabetes and Digestive Kidney Disease (R01DK132302, K23115896, and P30DK111022-07), JDRF, and The Leona M and Harry B Helmsley Charitable Trust. SA receives research devices, but not salary support from Dexcom and Abbott, and is a health-care disparities adviser (on a temporary advisory board role) for Medtronic and Beta Bionics. All other authors declare no competing interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: Cytomegalovirus (CMV) continues to be a major problem post-transplantation; early markers for predicting patients at risk of CMV disease are needed. Peak CMV load in the blood correlates with CMV disease but frequently occurs too late to provide prognostic information., Methods: 359 transplant recipients (162 liver, 87 renal, and 110 bone marrow) were prospectively monitored for CMV DNA in the blood with qualitative and quantitative PCR. 3873 samples were analysed. The CMV load in the first PCR-positive sample and the rate of increase in CMV load in blood during the initial phase of replication were assessed as risk factors for CMV disease using logistic regression., Findings: 127 of the 359 patients had CMV DNA in the blood and 49 developed CMV disease. Initial viral load correlated significantly with peak CMV load (R2=0.47, p=<0.001) and with CMV disease (odds ratio 1.82 [95% CI 1.11-2.98; p=0.02; 1.34 [1.07-1.68], p=0.01, and 1.52 [1.13-2.05], p=0.006, per 0.25 log10 increase in viral load for liver, renal, and bone-marrow patients, respectively). The rate of increase in CMV load between the last PCR-negative and first PCR-positive sample was significantly faster in patients with CMV disease (0.33 log10 versus 0.19 log10 genomes/mL daily, p<0.001). In multivariate-regression analyses, both initial CMV load and rate of viral load increase were independent risk factors for CMV disease (1.28 [1.06-1.52], p=0.01, per 0.25 log10 increase in CMV load and 1.52 [1.06-2.17], p=0.02, per 0.1 log10 increase in CMV load/mL daily, respectively)., Interpretation: CMV load in the initial phase of active infection and the rate of increase in viral load both correlate with CMV disease in transplant recipients; in combination, they have the potential to identify patients at imminent risk of CMV disease.

Background: Despite ample food supplies, the incidence of childhood underweight and stunting remains high in Uganda. Many factors contribute to this situation, but the role of low zinc intakes has not been adequately explored., Objective: Our objective was to study the effect of zinc supplementation on growth and body composition of preschool children by using the outcome measures of weight, height, and midupper arm circumference (MUAC)., Design: The study was randomized, double-blind, placebo-controlled, parallel, and 8 mo long, and incorporated 6 mo of zinc supplementation. Children (n = 153) aged 55.8 +/- 11.2 mo from 3 randomly selected nursery schools of medium, low, and very low socioeconomic status in a suburb of Kampala took part. The intervention comprised 10 mg Zn (as ZnSO4) or placebo daily in freshly prepared fruit juice, Monday to Friday inclusive., Results: Zinc supplementation increased MUAC by the end of the study (P = 0.029) and led to greater weight gain in children from the school of medium socioeconomic status at 3 and 8 mo (P = 0.019 and P = 0.038, respectively). There was no effect on weight gain of the children from the other schools. Zinc supplementation had no influence on height. Infection rates (of which 82% were recorded as malaria) were lower in the zinc-supplemented group than in control subjects (P = 0.063)., Conclusions: Zinc supplementation may counter the age-related decrease in MUAC often observed in preschool children in developing countries. The study provides evidence that zinc may not be the most limiting nutrient for weight gain in children of poor nutritional status, but may become so as nutritional status improves.