Keywords
Diabetes mellitus
Hyperglycemia
SARS-CoV-2
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Abstract
Objective: To synthesize epidemiological evidence and pathophysiological mechanisms associated with the development of diabetes mellitus (DM) following SARS-CoV-2 infection. Methods: An integrative review guided by the PECO strategy. Searches were conducted in PubMed, Scopus, SciFinder, and LILACS databases up to March 2026, with screening performed on the Rayyan platform. Original articles (2021–2026) in Portuguese, English, and Spanish were included. Selection followed the PRISMA structure, and the level of evidence was categorized according to Melnyk and Fineout-Overholt. Results: Twenty studies were selected, with a predominance of cohort studies (70%). A higher risk of incident DM and persistent glycometabolic alterations was observed in patients affected by COVID-19, particularly in severe and hospitalized cases. Pathophysiological mechanisms include beta-cell dysfunction and transdifferentiation via ACE2, systemic inflammatory response with oxidative stress, insulin resistance (via IRF1 and blockage of the PI3K/Akt pathway), molecular mimicry, and metabolic disturbances in adipose and hepatic tissues. Conclusion: There is an association between COVID-19 and post-acute glycemic alterations. However, methodological heterogeneity and the difficulty of distinguishing new-onset DM from transient hyperglycemia limit definitive causal inferences.
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