Palabras clave
Diabetes mellitus
Hiperglucemia
SARS-CoV-2
Cómo citar
Copyright © | Todos los derechos reservados.
La revista posee los derechos de autor exclusivos para la publicación de este artículo en los términos de la ley brasileña 9610/98.
Reproducción parcial
El uso de partes de los textos, figuras y cuestionario del artículo es libre, siendo obligatoria la citación de los autores y revista.
Reproducción total
Está expresamente prohibido y debe ser autorizado por la revista.
Resumen
Objetivo: Sintetizar la evidencia epidemiológica y los mecanismos fisiopatológicos asociados al desarrollo de diabetes mellitus (DM) tras la infección por SARS-CoV-2. Métodos: Revisión integrativa guiada por la estrategia PECO. Las búsquedas se realizaron en las bases de datos PubMed, Scopus, SciFinder y LILACS hasta marzo de 2026, con cribado en la plataforma Rayyan. Se incluyeron artículos originales (2021–2026) en portugués, inglés y español. La selección siguió la estructura PRISMA y el nivel de evidencia se categorizó según Melnyk y Fineout-Overholt. Resultados: Se seleccionaron 20 estudios, con predominio de estudios de cohorte (70%). Se observó un mayor riesgo de DM incidente y alteraciones glicometabólicas persistentes en pacientes afectados por COVID-19, sobre todo en casos graves y hospitalizados. Los mecanismos fisiopatológicos incluyen disfunción y transdiferenciación de las células beta vía ECA2 (ACE2), respuesta inflamatoria sistémica con estrés oxidativo, resistencia a la insulina (vía IRF1 y bloqueo de la vía PI3K/Akt), mimetismo molecular y trastornos metabólicos en el tejido adiposo y hepático. Conclusión: Existe una asociación entre la COVID-19 y las alteraciones glucémicas posagudas. Sin embargo, la heterogeneidad metodológica y la dificultad para diferenciar la DM de inicio reciente de la hiperglucemia transitoria limitan las inferencias causales definitivas.
Referencias
AAMODT KI, POWERS AC. The pathophysiology, presentation and classification of Type 1 diabetes. Diabetes, Obesity and Metabolism, 2025; 27(S6): 15-27.
ABRAMCZYK U, et al. Consequences of COVID-19 for the Pancreas. International Journal of Molecular Sciences, 2022; 23(2): 864.
BARRETO EA, et al. COVID-19-related hyperglycemia is associated with infection of hepatocytes and stimulation of gluconeogenesis. PNAS, 2023; 120(21).
CHEN M, et al. COVID-19 May Increase the Risk of Insulin Resistance in Adult Patients Without Diabetes: A 6-Month Prospective Study. Endocrine Practice, 2021; 27(8): 834-841.
EKEZIE J, HADDAD D. New Onset Type-1 Diabetes Mellitus in a Toddler with Sars-Cov-2 Infection Presenting In Diabetic Ketoacidosis: A Case Report. Journal of Scientific Innovation in Medicine, 2021; 2(5): 01-03.
EMRANI J, et al. SARS-COV-2, infection, transmission, transcription, translation, proteins, and treatment: A review. International Journal of Biological Macromolecules, 2021; 193: 1249-1273.
GOJDA J, et al. Severe COVID-19 associated hyperglycemia is caused by beta cell dysfunction: a prospective cohort study. Nutrition & Diabetes, 2023; 13(1): 1-11.
GUO Z, et al. Effectiveness of nirmatrelvir/ritonavir and molnupiravir on post-COVID diabetes risk among an older adult cohort: a target trial emulation study. BMC Medicine, 2026; 24(1): 1–14.
HUSSEIN M, et al. SARS-CoV-2 outbreak: role of viral proteins and genomic diversity in virus infection and COVID-19 progression. Virology Journal, 2024; 21(1).
FATOKE B, et al. Type 2 diabetes mellitus as a predictor of severe outcomes in COVID-19 — a systematic review and meta-analyses. BMC Infectious Diseases, 2025; 25(1): 405.
LU JY, et al. Incidence of new-onset in-hospital and persistent diabetes in COVID-19 patients: comparison with influenza. eBioMedicine, 2023; 90.
LUI DTW, et al. A Prospective 1-Year Follow-up of Glycemic Status and C-Peptide Levels of COVID-19 Survivors with Dysglycemia in Acute COVID-19 Infection. Diabetes & Metabolism Journal, 2024; 48(4): 763-770.
MCVOY MA, KUMMARAPURUGU AB. The Role of ACE2 in SARS-CoV-2 Infection, Pathogenesis, and Antiviral Interventions. Journal of Medical Virology, 2025; 97(12).
MENDES KDS,et al. Revisão integrativa: método de pesquisa para a incorporação de evidências na saúde e na enfermagem. Texto & Contexto - Enfermagem, 2008; 17(4): 758-764.
MILLER MG, et al. SARS-CoV-2 Infection and New-Onset Type 2 Diabetes Among Pediatric Patients, 2020 to 2022. JAMA Network Open, 2024; 7(10): e2439444.
MOHAMED AH, et al. Prevalence and short-term clinical impacts of new-onset diabetes mellitus among patients with COVID-19 in jazan region, Saudi Arabia. BMC Endocrine Disorders, 2024; 24(1).
MONTEFUSCO L, et al. Acute and long-term disruption of glycometabolic control after SARS-CoV-2 infection. Nature Metabolism, 2021; 3(6): 774-785.
MŁYNARSKA E, et al. Type 2 Diabetes Mellitus: New Pathogenetic Mechanisms, Treatment and the Most Important Complications. International Journal of Molecular Sciences, 2025; 26(3): 1094.
OUZZANI M. et al. Rayyan—a Web and Mobile App for Systematic Reviews. Systematic Reviews, v. 5, n. 1, dez. 2016.
PAGE MJ, et al. The PRISMA 2020 statement: An updated guideline for reporting systematic reviews. British Medical Journal, 2021; 372: 71.
PEREIRA MG, GALVÃO TF. Etapas de busca e seleção de artigos em revisões sistemáticas da literatura. Epidemiologia e Serviços de Saúde, 2014; 23(2): 369-371.
QIAN J et al. New-onset diabetes following SARS-CoV-2 infection in the Omicron era: a matched cohort study. International Journal of Epidemiology, 2026; 55(2): dyag009.
QUEIRÓS-REIS L, et al. Disrupting SARS-CoV-2 Spike Protein Activity: A Virtual Screening and Binding Assay Study. International Journal of Molecular Sciences, 2024; 26(1): 151.
REITERER EA, et al. Hyperglycemia in acute COVID-19 is characterized by insulin resistance and adipose tissue infectivity by SARS-CoV-2. Cell Metabolism, 2021.
SANTOS LM, et al. Diabetes e COVID-19: Uma Interseção Bidirecional entre Comorbidades e Desafios. Brazilian Journal of Implantology and Health Sciences, 2025; 7(1): 1798-1808.
SHIN J, et al. SARS-CoV-2 infection impairs the insulin/IGF signaling pathway in the lung, liver, adipose tissue, and pancreatic cells via IRF1. Metabolism, 2022; 133: 155236.
SOTO ME, et al. Hyperglycemia and Loss of Redox Homeostasis in COVID-19 Patients. Cells, 2022; 11(6): 932.
STEENBLOCK C, et al. Viral infiltration of pancreatic islets in patients with COVID-19. Nature Communications, 2021; 12(1): 3534.
TANG X, et al. SARS-CoV-2 infection induces beta cell transdifferentiation. Cell Metabolism, 2021; 33(8): 1577-1591.e7.
TIMOFEEVA AM, et al. SARS-CoV-2 Spike Protein and Molecular Mimicry: An Immunoinformatic Screen for Cross-Reactive Autoantigen Candidates. International Journal of Molecular Sciences, 2025; 26(18): 8793.
TSVETKOVA VT, et al. Link Between Immune Dysregulation in COVID- 19 and Beta-Cell Dysfunction. Journal of Endocrinology and Metabolism, 2025; 15(4): 161-180.
WARD JL, et al. SARS-CoV-2 infection and new-onset type 1 diabetes in the post-acute period among children and young people in England. Diabetic Medicine, 2025.
WEE LE, et al. Risk of New-Onset Type 2 Diabetes Among Vaccinated Adults After Omicron or Delta Variant SARS-CoV-2 Infection. JAMA Network Open, 2025; 8(4): e252959.
WONG R, et al. Effect of SARS-CoV-2 Infection on Incident Diabetes by Viral Variant: Findings From the National COVID Cohort Collaborative (N3C). Diabetes Care, 2024; 47(10): 1846-1854.
WU CT, et al. SARS-CoV-2 infects human pancreatic β cells and elicits β cell impairment. Cell Metabolism, 2021; 33(8): 1565-1576.e5.
ZHANG X, et al. SARS-CoV-2: An Updated Review Highlighting Its Evolution and Treatments. Vaccines, 2022; 10(12): 2145.
ZHAO X, et al. Understanding the interplay between COVID-19 and diabetes: insights for the postpandemic era. Frontiers in Endocrinology, 2025; 16.