Endocrine Abstracts

SARS-CoV-2 infection produces greater morbidity and mortality in people with cardiovascular disease, diabetes, and obesity, raising the possibility that the consequences of viral infection are modulated directly and indirectly by the endocrine system. Hospitalization and severity of illness is more common in males, further suggesting that sex, possibly male and female sex hormones, modifies the host response to coronavirus infection. SARS-Co-V-2 cellular infection requires ACE2, as well as associated proteases, including TMPRSS2. These molecules are widely expressed in cardiometabolic organs, and the gastrointestinal tract, and to a lesser extent, in the endocrine and exocrine pancreas. Notably, TMPRSS2 is regulated by sex steroids, and clinical trials are examining whether disruption of steroid control of TMPRSS2 expression might be therapeutically useful in SARS-CoV-2 infection, Viral infection may also modify the host susceptibility to autoimmune disease, through dysregulation of humoral and cellular immunity and cytokine expression. Although SARS-CoV-2 infection has not been associated with widespread endocrine dysfunction beyond that commonly seen with critical illness, case reports of automimmune endocrine disease, including type 1 diabetes, have been described. The use of dexamethasone in severely ill individuals with SARS-CoV-2 prompts evaluation of potential endocrine consequences ensuing from sustained high dose glucocorticoid administration. Herein I will review the endocrine consequences of SARS-CoV-2 infection, highlight key knowns and unknowns, and discuss principles for linking coronavirus infection to disorders of the endocrine system.