Figure 1.

Diabetes/Hyperglycemia and Possible Outcomes in COVID-19 Patients.

SARS-CoV-2 infection causes activation of RAAS that can result in a ‘cytokine storm’ via the AngII/AT1R axis, resulting in the synthesis and secretion of proinflammatory cytokines/chemokines such as tumor necrosis factor-α (TNFα), interleukins (ILs)1/2/6, interferon-γ (IFNγ), and monocyte chemoattractant protein-1 (MCP1). In SARS-CoV-2-infected individuals with pre-existing diabetes, the diabetes-associated proinflammatory status and endothelial dysfunction, and the incidence of one or more comorbidities – such as obesity, hypertension, CVD, NAFLD, and CKD, and the hyperglycemia-induced DKA and HHS – can lead to an increase in disease severity, higher rates of intensive care unit (ICU) admissions, and may be responsible for the poor prognosis and higher mortality rates in diabetic COVID-19 patients. Interestingly, reports also suggest that SARS-CoV-2 infects the β-islets of the pancreas, causing β-cell damage and subsequent new-onset diabetes, severe hyperglycemia and DKA in COVID-19 patients. Treatment using appropriate glucose-lowering agents and proper management of blood glucose levels aids recovery and survival among affected diabetic COVID-19 patients. Various aspects – such as benefits, contraindications, and limitations of using certain combinations of glucose-lowering agents and antiviral treatments that could affect the outcome of the disease in a diabetic COVID-19 patient – must be carefully analyzed. Abbreviations: ACE2, angiotensin-converting enzyme 2; AngII, angiotensin II; AT1R, angiotensin II type I receptor; CKD, chronic kidney disease, COPD, chronic obstructive pulmonary disorder; COVID-19, coronavirus disease 2019; CVD, cardiovascular disease; DKA, diabetic ketoacidosis; HHS, hyperglycemic hyperosmolar syndrome; NAFLD, nonalcoholic fatty liver disease; RAAS, renin–angiotensin–aldosterone system; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2. Created with BioRender.com.