The paper presents the theoretical considerations on the role of endocrine and metabolic alterations accompanying
COVID-19 infection. These alterations may be presumed on the basis of the following two observations. Firstly, the virus SARS-CoV-2 responsible for the
COVID-19 infection uses an important renin-angiotensin system (RAS)
element -
angiotensin-converting enzyme 2 (ACE2) - as a receptor
protein for entry into target cells and, in consequence, disturbs the function of the main (circulating) renin-angiotensin-aldosterone system (RAAS) and of the local renin-angiotensin system localized in different tissues and organs. The binding of SARS-CoV-2 to ACE2 leads to the downregulation of this
enzyme and, in the aftermath, to the excess of
angiotensin II and
aldosterone. Thus, in the later stage of
COVID-19 infection, the beneficial effects of ACEI and ARB could be presumed. It is hypothesized that the local RAS dysregulation in the adipose tissue is the main cause of the negative role of
obesity as a risk factor of severe outcome of the
COVID-19 infection. Secondly, the outcome of
COVID-19 strongly depends on the age of the patient. Age-related hormonal deficiencies, especially those of
melatonin and
dehydroepiandrosterone, may contribute to morbidity/mortality in older people. The usefulness of
melatonin and
angiotensin converting enzyme inhibitors/
angiotensin receptor 1 blockers (the latter only in later phases of the
infection) as adjuvant drugs is probable but needs thorough clinical trials.