COVID-19, hypothalamo-pituitary-adrenal axis and clinical implications

Excerpt

A novel coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected over 1,000,000 individuals, claiming more than 56,000 lives in over 200 countries worldwide ever since its mysterious outbreak in Wuhan, China in December 2019. The largest case series from China had shown that majority of the patients belonged to the age group of 30–79 years. Most of the cases were mild (81%), while 14% cases were severe and only 5% critical. The overall case-fatality rate was 2.3% [1]. SARS-CoV-2 primarily affects the lungs, resulting in viral pneumonia often complicated by acute respiratory distress syndrome and sepsis. The virus is able to evade the host immune system by avoiding detection of their dsRNA and by inhibiting the host interferon-I pathway [2]. The pathogen enters the pneumocyte using the host angiotensin-converting enzyme 2 (ACE2) as a receptor. In addition, the enzyme is expressed on the arterial and venous endothelial cells of many organs including the adrenal glands. Autopsy studies on patients who died from SARS (the original outbreak in 2003) had shown degeneration and necrosis of the adrenal cortical cells. The SARS-CoV (the ‘cousin’ of SARS-CoV-2) was in fact identified in the adrenal glands, hinting towards a direct cytopathic effect of the virus. Hence it is likely that cortisol dynamics may be altered in patients with SARS (and COVID-19). However, the literature is scarce is this regard. …