Resumo
Objetivo: Sintetizar as evidências epidemiológicas e os mecanismos fisiopatológicos associados ao desenvolvimento de diabetes mellitus (DM) após infecção por SARS-CoV-2. Métodos: Revisão integrativa orientada pela estratégia PECO. As buscas ocorreram nas bases PubMed, Scopus, SciFinder e LILACS até março de 2026, com triagem na plataforma Rayyan. Incluíram-se artigos originais (2021–2026) em português, inglês e espanhol. A seleção seguiu a estrutura do PRISMA e o nível de evidência foi categorizado por Melnyk e Fineout-Overholt. Resultados: Selecionaram-se 20 estudos, com predomínio de coortes (70%). Observou-se maior risco de DM incidente e alterações glicometabólicas persistentes em pacientes acometidos por COVID-19, sobretudo em casos graves e hospitalizados. Os mecanismos fisiopatológicos incluem disfunção e transdiferenciação das células beta via ACE2, resposta inflamatória sistêmica com estresse oxidativo, resistência à insulina (via IRF1 e bloqueio da via PI3K/Akt), mimetismo molecular e distúrbios metabólicos no tecido adiposo e hepático. Considerações finais: A associação entre COVID-19 e alterações glicêmicas pós-agudas é plausível. Contudo, a heterogeneidade metodológica e a dificuldade de diferenciar DM de início recente de hiperglicemia transitória limitam inferências causais definitivas.
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