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. 2021 Jun;23(6):1397-1401.
doi: 10.1111/dom.14329. Epub 2021 Feb 16.

Comparable COVID-19 outcomes with current use of GLP-1 receptor agonists, DPP-4 inhibitors or SGLT-2 inhibitors among patients with diabetes who tested positive for SARS-CoV-2

Affiliations

Comparable COVID-19 outcomes with current use of GLP-1 receptor agonists, DPP-4 inhibitors or SGLT-2 inhibitors among patients with diabetes who tested positive for SARS-CoV-2

Simone Bastrup Israelsen et al. Diabetes Obes Metab. 2021 Jun.

Abstract

Incretin-based therapies, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dipeptidyl peptidase-4 inhibitors (DPP-4i), have been hypothesized to exert beneficial effects on COVID-19 outcomes due to anti-inflammatory properties. In this population-based cohort study, we retrieved data from nationwide registries on all individuals diagnosed with severe acute respiratory syndrome coronavirus 2 infection up to 1 November 2020. For individuals with diabetes, we examined the impact of use of GLP-1 RAs (n = 370) and DPP-4i (n = 284) compared with sodium-glucose cotransporter-2 inhibitors (SGLT-2i) (n = 342) on risk of hospital admission and severe outcomes. Relative risks (RRs) were calculated after applying propensity score weighted methods to control for confounding. Current users of GLP-1 RAs had an adjusted RR of 0.89 (95% confidence interval 0.34-2.33), while users of DPP-4i had an adjusted RR of 2.42 (95% confidence interval 0.99-5.89) for 30-day mortality compared with SGLT-2i use. Further, use of GLP-1 RAs or DPP-4i compared with SGLT-2i was not associated with decreased risk of hospital admission. Thus, use of incretin-based therapies in individuals with diabetes and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was not associated with improved clinical outcomes.

Keywords: DPP-4 inhibitor; GLP-1 analogue; SGLT-2 inhibitor; antidiabetic drug; population study.

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Conflict of interest statement

T.B. reports grants from Pfizer, Novo Nordisk Foundation, Simonsen Foundation, Lundbeck Foundation and Kai Hansen Foundation, grants and personal fees from GSK, Pfizer and Gilead, and personal fees from Boehringer Ingelheim and MSD, with no relation to the work reported in this paper. A.P. reports grants from Alcon, Almirall, Astellas, Astra‐Zeneca, Boehringer‐Ingelheim, Novo Nordisk, Servier and LEO Pharma, with no relation to the work reported in this paper. R.W.T. reports that the Department of Clinical Epidemiology is involved in studies with funding from various companies as research grants to and administered by Aarhus University. None of these studies have relation to the present study. S.M. reports grants and personal fees from Novo Nordisk A/S and Boehringer‐Ingelheim, and personal fees from MSD and Sanofi, with no relation to the work reported in this paper. S.B.I. and H.S. report no conflicts of interest.

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