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As observed with SARS-CoV responsible for SARS 2003, the new coronarovirus SARS-CoV-2 uses the angiotensin converting enzyme type 2 (ACE2) as cellular receptor to infect cells. The renin aldosterone angiostensin system (RAAS) has known effects in the lungs: some receptors are pro-inflammatory, others are anti-inflammatory. Thus the deregulation of the RAAS induced by the SARS-CoV-2 could explain the inflammatory response of Covid-19 infection and be a modulator of the severity of its course.
Furthermore, the SARS 2003 experience suggests that there may be others endocrine involvment, particularly an failure on the hypothalamus-pituitary and adrenal axis. Indeeed, cases of hypocorticism and hypothyroidism of central origin were described.
Altogether, the endocrine system might play a role both in the pathophysiology of Covid-19 infection and in the activity and severity of the disease.
In this study, the investigators proposed to explore endocrine functions on biological samples in a series of patients admitted for Covid-19 in our clinic.
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Data sourced from clinicaltrials.gov
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