Covid-19 is a recently-emerged infectious disease caused by the novel severe acute respiratory syndrome coronavirus SARS-CoV2. SARS-CoV2 differs from previous coronavirus infections (SARS and MERS) due to its high infectivity (reproduction value, R 0 , typically 2–4) and pre- or asymptomatic transmission, properties that have contributed to the current global Covid-19 pandemic. Identified risk factors for disease severity and death from SARS-Cov2 infection include older age, male sex, diabetes, obesity and hypertension. The reasons for these associations are still largely obscure. Evidence is also emerging that SARS-CoV2 infection exacerbates the underlying pathophysiology of hyperglycemia in people with diabetes. Here, we discuss potential mechanisms through which diabetes may affect the risk of more severe outcomes in Covid-19 and, additionally, how diabetic emergencies and longer term pathology may be aggravated by infection with the virus. We consider roles for the immune system, the observed phenomenon of microangiopathy in severe Covid-19 infection and the potential for direct viral toxicity on metabolically-relevant tissues including pancreatic beta cells and targets of insulin action.
【저자키워드】 COVID-19, diabetes, management, microangiopathy, ketoacidosis, 【초록키워드】 pathology, Coronavirus infection, coronavirus, SARS-CoV2, pandemic, obesity, disease severity, Infection, risk, Transmission, Infectious disease, immune system, outcome, MERS, risk factor, virus, hypertension, SARS-CoV2 infection, Asymptomatic, pathophysiology, Older age, death, target, hyperglycemia, association, Male sex, Diabetic, acute respiratory syndrome, potential mechanism, tissue, Affect, Cell, caused, include, contributed, diabete, Identified, exacerbate, viral toxicity, insulin action, pancreatic, 【제목키워드】 relationship,