Covid-19 Hard Copy

R250.00

The hyperinflammatory and the fibrotic changes observed in COVID-19 clinical complications resemble those associated with diseases of deficiency of the ACE-2 enzyme system.

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Description

The hyperinflammatory and the fibrotic changes observed in COVID-19 clinical complications resemble those associated with diseases of deficiency of the ACE-2 enzyme system.

COVID-19-linked comorbidities can be associated with increased output levels of aldosterone outside of the classical regulatory renin-angiotensin-system (RAS). This increased aldosterone is from the HPAaxis output, the primary and secondary hyper-aldosteronism outputs. Aldosterone has the potential to suppress the ACE-2 enzyme.

It is the suppression of the ACE-2 enzyme system, and the extent thereof, in people with comorbidities, that accounts for the unchecked angiotensin II-mediated hyperinflammation, fibrosis and thrombotic phenomena seen in complicated SARS-CoV-2 infection.

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