Evidence relating to the impact of COVID-19 in people with diabetes (PWD) is limited but continuing to emerge. PWD appear to be at increased risk of more severe COVID-19 infection, though evidence quantifying the risk is highly uncertain. The extent to which clinical and demographic factors moderate this relationship is unclear, though signals are emerging that link higher BMI and higher HbA 1c to worse outcomes in PWD with COVID-19. As well as posing direct immediate risks to PWD, COVID-19 also risks contributing to worse diabetes outcomes due to disruptions caused by the pandemic, including stress and changes to routine care, diet, and physical activity. Countries have used various strategies to support PWD during this pandemic. There is a high potential for COVID-19 to exacerbate existing health disparities, and research and practice guidelines need to take this into account. Evidence on the management of long-term conditions during national emergencies suggests various ways to mitigate the risks presented by these events.People with diabetes (PWD) have been identified as being at increased risk of serious illness from COVID-19. COVID-19 also presents substantial indirect risks to PWD through disruptions in health care and lifestyle factors. Understanding these risks and best ways to mitigate them in the short and longer term is key to facilitating informed decision-making during and after the COVID-19 pandemic.Evidence relating to COVID-19 and diabetes is limited but continuing to emerge. In this Perspective, we summarize evidence identified through rapid reviews. We consider direct and indirect risks posed to PWD by COVID-19 and management considerations for PWD both with and without COVID-19 infection. Recognizing limitations in evidence related to COVID-19, we also bring together leaders in diabetes care from countries with high rates of COVID-19, highlighting experiences from the most affected countries including Italy, France, China, the U.K., and the U.S.

IMPORTANCE Nonalcoholic fatty liver disease (NAFLD) affects about 25% of adults worldwide and is associated with obesity. Weight loss may improve biomarkers of liver disease, but its implications have not been systematically reviewed and quantified. OBJECTIVE To estimate the association of weight loss interventions with biomarkers of liver disease in NAFLD. DATA SOURCES MEDLINE, Embase, PsycINFO, CINAHL, Cochrane, and Web of Science databases along with 3 trial registries were searched from inception through January 2019. STUDY SELECTION Randomized clinical trials of people with NAFLD were included if they compared any intervention aiming to reduce weight (behavioral weight loss programs [BWLPs], pharmacotherapy, and surgical procedures) with no or lower-intensity weight loss intervention. The review followed the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. DATA EXTRACTION AND SYNTHESIS Two independent reviewers screened the studies, extracted the data, and assessed the risk of bias using the Cochrane tool. Pooled mean differences or odds ratios (ORs) were obtained from random-effects meta-analyses. MAIN OUTCOMES AND MEASURES Blood, radiologic, and histologic biomarkers of liver disease. RESULTS Twenty-two studies with 2588 participants (with a mean [SD] age of 45 [14] years and with approximately 66% male) were included. Fifteen studies tested BWLPs, 6 tested pharmacotherapy, and 1 tested a surgical procedure. The median (interquartile range) intervention duration was 6 (3-8) months. Compared with no or lower-intensity weight loss interventions, more-intensive weight loss interventions were statistically significantly associated with greater weight change (-3.61 kg; 95% CI,-5.11 to-2.12; I 2 = 95%). Weight loss interventions were statistically significantly associated with improvements in biomarkers, including alanine aminotransferase (-9.81 U/L; 95% CI,-13.12 to-6.50; I 2 = 97%), histologically or radiologically measured liver steatosis (standardized mean difference:-1.48; 95% CI,-2.27 to-0.70; I 2 = 94%), histologic NAFLD activity score (-0.92; 95% CI,-1.75 to-0.09; I 2 = 95%), and presence of nonalcoholic steatohepatitis (OR, 0.14; 95% CI, 0.04-0.49; I 2 = 0%). No statistically significant change in histologic liver fibrosis was found (-0.13; 95% CI,-0.54 to 0.27; I 2 = 68%). Twelve studies were at high risk of bias in at least 1 domain. In a sensitivity analysis of the 3 trials at low risk of bias, the estimates and precision of most outcomes did not materially change. CONCLUSIONS AND RELEVANCE The trials, despite some heterogeneity, consistently showed evidence of the association between weight loss interventions and improved biomarkers of liver disease in NAFLD in the short to medium term, although evidence on long-term health outcomes was limited. These findings appear to support the need to change the clinical guidelines and to recommend formal weight loss programs for people with NAFLD.

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