Increased Risk of Diabetes and Diabetic Ketoacidosis Associated With COVID-19

It is known that pancreatic β-cells are permissive to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection through the expression of ACE receptor 2 (1) and that the infection may also induce indirect β-cell damage through a cytokine storm and a proinflammatory milieu (2). It has also been shown that inflammatory and immunological alterations (3) following a coronavirus disease 2019 (COVID-19) infection may lead to acute and long-term disruption of glucose metabolism (4–6). A recent study showed that the combination of augmented circulating inflammatory factors that exert toxic effects on human pancreatic islets and SARS-CoV-2 –specific viral RNA in pancreatic tissues, together with the alteration of secretory granules, promotes glucose metabolism alterations (7). Despite the increasing number of observations, the complex pathogenic model that links COVID-19 and new-onset diabetes has not been fully clarified yet. Many retrospective studies, systematic reviews, and meta-analyses reported an increase in new-onset diabetes associated with COVID-19 (8). A recent meta-analysis by Banerjee et al. (9) showed 59% higher risk of individuals developing diabetes in the postacute COVID-19 phase versus the risk for healthy control individuals (hazard ratio [HR] 1.59) and versus the risk for severity-matched non –COVID-19 respiratory tract infections (moderate-severe/hospitalized cases, HR 1.52; mild cases, HR 1.22), while a role for steroid use was excluded (ster...
Source: Diabetes - Category: Endocrinology Source Type: research