This excerpt is a preprint and has not been copyedited or certified by peer review. It should not be used to guide clinical practice, or be reported as conclusive or established information.
In this chapter we summarise the endocrine manifestations reported so far in COVID-19 disease and explore mechanisms to decipher how SARS-CoV-2 may affect various endocrine organs. Direct viral infection of multiple organs by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) seems to be due to the widespread presence of angiotensin converting enzyme-2 (ACE-2) viral receptors in various tissues. Along with other major organ-systems, multiple reports demonstrate that the endocrine system is also involved in many cases of COVID-19. The current general pathogenic hypothesis is that inflammatory and immune mediators are key elements in the endocrine system injury attributable to COVID-19. COVID-19 may injure the endocrine system at multiple levels. Hypopituitarism may result from direct viral mediated and indirect inflammatory effects of the disease. Thyroid hypofunction may be due to immune-mediated damage to thyroid glands that seems similar to the well-recognized pattern seen in cases of antibody mediated subacute thyroiditis. COVID-19 precipitates hyperglycaemia in some patients known to have diabetes and appears to evoke new diagnoses of diabetes during acute illness, likely due to increased insulin resistance caused by the systemic inflammatory response. COVID-19 has also been shown to trigger Type 1 diabetes with ketoacidosis. Systemic and direct viral effects may be important in exacerbation of diabetes since SARS-CoV-2 induced beta cell apoptosis and immune mediated beta cell destruction have both been demonstrated in vitro. Gonadal effects of COVID-19 remains somewhat unclear although the presence of virus in semen has been reported.
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