SARS-CoV-2 Targets And Causes Cellular Damage To Adrenal Glands

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A new study by researchers from Germany and Switzerland has found that (SARS-CoV-2) infection can directly target and cause cellular damage to the human host adrenal glands.

The researchers from Technische Universität Dresden-Germany, University of Regensburg-Germany, University Hospital Zurich-Switzerland and the University of Zurich-Switzerland found that by targeting and causing damage to the adrenal glands, the SARS-CoV-2 virus causes adrenal dysfunction which explains the manifestation of adrenal insufficiency in several patients infected with severe coronavirus disease 2019 (COVID-19) infection, along with some of the complications associated with long COVID.

The study findings were published in the peer reviewed journal: Diabetes And Endocrinology (By Lancet) https://www.thelancet.com/journals/landia/article/PIIS2213-8587(21)00291-6/fulltext

COVID-19 develops due to infection with SARS-CoV-2, which particularly in elderly with certain comorbidities (eg, metabolic syndrome)1 can cause severe pneumonia and acute respiratory distress syndrome.

Some patients with severe COVID-19 will develop a life-threatening sepsis with its typical manifestations including disseminated intravascular coagulation and multiorgan dysfunction.2

Latest evidence suggests that even early treatment with inhaled steroids such as budesonide might prevent clinical deterioration in patients with COVID-19.3 This evidence underlines the potentially important role for adrenal steroids in coping with COVID-19.

The adrenal gland is an effector organ of the hypothalamic–pituitary–adrenal axis and the main source of glucocorticoids, which are critical to manage and to survive sepsis.

Therefore, patients with pre-existing adrenal insufficiency are advised to double their doses of glucocorticoid supplementation after developing moderate to more severe forms of COVID-19.4

Adrenal glands are vulnerable to sepsis-induced organ damage and their high vascularisation and blood supply makes them particularly susceptible to endothelial dysfunction and haemorrhage. Accordingly, adrenal endothelial damage, bilateral haemorrhages, and infarctions have been already reported in patients with COVID-19.5

Adrenal glands contain the highest concentration of antioxidants to compensate enhanced generation of reactive oxygen species, side products of steroidogenesis, which together with elevated intra-adrenal inflammation can contribute to adrenocortical cell death.6

Furthermore, sepsis-associated critical illness-related corticosteroid insufficiency, which describes coexistence of the hypothalamic–pituitary–adrenal dysfunction, reduced cortisol metabolism, and tissue resistance to glucocorticoids, was reported in critically ill patients with COVID-19.7

Low cortisol and adrenocorticotropic hormone (ACTH) responses during acute phase of infections consistent with critical illness-related corticosteroid insufficiency diagnosis (random plasma cortisol level lower than 10 μg/dL) were reported in one study with patients suffering from mild to moderate COVID-19 manifestations.8

It is however possible those other factors triggered by COVID-19 such as hypothalamic or pituitary damage, adrenal infarcts, or previously undiagnosed conditions, such as antiphospholipid syndrome, might be responsible for reduced function of adrenal glands.

However, contrary to this observation, a study with patients with moderate to severe COVID-19 revealed a very high cortisol response with values exceeding 744 nmol/L, which were positively correlated with severity of disease.9

In this clinical study,9 highly elevated cortisol concentrations showed an adequate adrenal cortisol production possibly reflecting the elevated stress level of those severely affected patients.9

However, since ACTH measurements were not done, it is impossible to verify whether high concentrations of cortisol in those patients resulted from an increment of cortisol, or were confounded by reduced glucocorticoid metabolism.9

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Adrenal gland is frequently targeted by bacteria and viruses, including SARS-CoV,10 which was responsible for the 2002–04 outbreak of SARS in Asia. Considering that SARS-CoV-2 shares cellular receptors with SARS-CoV, including angiotensin-converting enzyme 2 and transmembrane protease serine subtype 2, its tropism to the adrenal gland is therefore conceivable.

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