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.
Study Type
OBSERVATIONAL
Enrollment
50
Uhmontpellier
Montpellier, France
Plasma aldosterone levels
Plasma aldosterone levels
Time frame: 1 day (at inclusion)
Plasma renin levels
Plasma renin levels
Time frame: 1 day (at inclusion)
covid-19 infection severity
covid-19 infection severity : Ordinal scale of 7 values from 1 to 7 (1- not hospitalized, no limitation on activities; 2- not hospitalized, limitations on activities; 3- hospitalized, not requiring supplemental oxygen; 4- hospitalized, requiring supplemental oxygen; 5- hospitalized, on non-invasive ventilation or high flow oxygen devices; 6- hospitalized, on invasive mechanical ventilation or ECMO and 7- death).
Time frame: 1 day (at inclusion)
Maximum severity of Covid-19 infection
Maximum severity of Covid-19 infection using a seven-category ordinal scale at at the end of hospitalization : Ordinal scale of 7 values from 1 to 7 (1- not hospitalized, no limitation on activities; 2- not hospitalized, limitations on activities; 3- hospitalized, not requiring supplemental oxygen; 4- hospitalized, requiring supplemental oxygen; 5- hospitalized, on non-invasive ventilation or high flow oxygen devices; 6- hospitalized, on invasive mechanical ventilation or ECMO and 7- death).
Time frame: 1 day (at inclusion)
Plasma aldosterone level
Plasma aldosterone level
Time frame: 1 day (at the end of hospitalization)
Plasma ACTH level
Plasma ACTH level
Time frame: 1 day (at the end of hospitalization)
Plasma cortisol level
Plasma cortisol level
Time frame: 1 day (at inclusion)
Plasma cortisol level
Plasma cortisol level
Time frame: 1 day (at the end of hospitalization)
Plasma T3l level
Plasma T3l level
Time frame: 1 day (at the end of hospitalization)
Plasma T3l level
Plasma T3l level
Time frame: 1 day (at inclusion)
Plasma ACTH level
Plasma ACTH level
Time frame: 1 day (at inclusion)
Plasma LH level
Plasma LH level
Time frame: 1 day (at inclusion)
Plasma LH level
Plasma LH level
Time frame: 1 day (at the end of hospitalization)
Plasma DHEA level
Plasma DHEA level
Time frame: 1 day (at the end of hospitalization)
Plasma DHEA level
Plasma DHEA level
Time frame: 1 day (at inclusion)
Plasma estradiol (female) or testosterone (male) level
Plasma estradiol (female) or testosterone (male) level
Time frame: 1 day (at the end of hospitalization)
Plasma estradiol (female) or testosterone (male) level
Plasma estradiol (female) or testosterone (male) level
Time frame: 1 day (at inclusion)
Plasma FSH level
Plasma FSH level
Time frame: 1 day (at the end of hospitalization)
Plasma FSH level
Plasma FSH level
Time frame: 1 day (at inclusion)
type of treatments
type of treatments
Time frame: 1 day
Clinical characteristics
Clinical characteristics extracted from electronic medical
Time frame: 1 day
radiological characteristics
radiological characteristics : quantification of the percentage of lesional damage to the pulmonary parenchyma
Time frame: 1 day
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