COVID Impacts

Up to 50% of the people who have died from COVID-19 had metabolic and vascular disorders. Notably, there are many direct links between COVID-19 and the metabolic and endocrine systems. Thus, not only are patients with metabolic dysfunction (eg, obesity, hypertension, non-alcoholic fatty liver disease, and diabetes) at an increased risk of developing severe COVID-19 but also infection with SARS-CoV-2 might lead to new-onset diabetes or aggravation of pre-existing metabolic disorders. 

Following infection with SARS-CoV-2, toll-like receptors 2, 3, and 4 are activated, and IL-1β and IL-6 are released. The metaflammation observed in patients with metabolic disorders allows for a hyperimmune response, which reaches pathogenic levels. This cytokine release provokes fever, systemic inflammation, and subsequent sepsis.

In terms of the pathophysiology, endocrine and metabolic organs (including the brain, pancreas, liver, skeletal muscle, and adipose tissue) might be damaged either directly or indirectly by viral infection and contribute to the development of new-onset hyperglycaemia or insulin resistance in survivors of COVID-19. Based on experiments in islets isolated from human donors and infected with SARS-CoV-2, and on data from post-mortem tissue from patients who died due to COVID-19, SARS-CoV-2 can infect and replicate in cells of the endocrine and exocrine pancreas.

New-onset hyperglycaemia, ketoacidosis, diabetes, and severe metabolic complications of pre-existing diabetes have been frequently observed in patients with COVID-19.

Evidence from the outbreak of the closely related SARS-CoV in 2002–03 suggests that there is a likelihood of long-term metabolic sequelae from COVID-19. Long-term metabolic abnormalities have been observed for up to 12 years in survivors of severe acute respiratory syndrome. These abnormalities included dyslipidaemia and cardiovascular disease, as well as signs of abnormal glucose metabolism with insulin resistance, hyperglycaemia, and diabetes.