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Département de Métabolomique Clinique, Hôpital Saint-Antoine, AP-HP Sorbonne Université, Paris, France
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Sorbonne Université, INSERM, Centre de Recherche Saint-Antoine, Paris, France
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critical for boys and girls whose signs of virilization at birth are mild, or that may be missed. The conversion of 17-hydroxyprogesterone (17-OHP) to 11-deoxycortisol and of progesterone to 11-deoxycorticosterone, which are precursors of cortisol and
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vasopressin. ACTH then acts on the adrenal glands to produce glucocorticoids and cortisol in humans. Cortisol negatively feeds back at the level of the pituitary gland and hypothalamus to inhibit further production and release ACTH. The melanocortins act
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, 9 , 10 , 11 ). In the authors’ experience, 4 out of 11 patients with EAS showed cortisol suppression after high-dose dexamethasone and 3 out of 12 showed ACTH and/or cortisol response to CRH stimulation according to current response criteria. The
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or surgical treatment. Secondary adrenal insufficiency (SAI) was defined as basal 07:00–09:00 h cortisol (AM cortisol) below 100 nmol/L, or 1-µ cosyntropin stimulated cortisol below 400 nmol/L or peak cortisol during insulin-induced hypoglycemia test
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Primary adrenal insufficiency (PAI) or Addison’s disease is an uncommon disorder resulting from deficiency of cortisol and aldosterone due to the destruction of adrenal cortices ( 1 , 2 ). Early diagnosis and prompt institution of treatment is
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development of corticosteroid side effects between patients ( 7 ). Interestingly, when the endogenous glucocorticoid, cortisol (hydrocortisone), is compared with prednisolone at the isolated human glucocorticoid receptor (GR), the transactivation activity of
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
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Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
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Medical Research Laboratories, Department of Endocrinology and Diabetes, Department of Pediatrics, Department of Endocrinology and Diabetes, Institute of Clinical Medicine, Aarhus University, Norrebrogade 44, DK-8000 Aarhus C, Denmark
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recorded no concomitant increase in serum concentrations of GH or cortisol. Ghrelin-induced hyperglycemia: 5.9±0.2 mmol/l (ghrelin) vs 5.4±0.1 mmol/l (saline), P =0.009, in the basal period and insulin resistance during the clamp period, where ghrelin
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histories were analysed. All patients were assessed for adrenal function, including (i) serum potassium; (ii) plasma adrenocorticotropic hormone and cortisol (08:00, 16:00 and 12:00 h); (iii) 24-h urinary free cortisol; (iv) plasma renin and aldosterone
National Center for Neurological Disorders, Shanghai, China
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National Center for Neurological Disorders, Shanghai, China
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evaluation in our center before and after surgery. Patients with a morning cortisol level <3 mg/dL were deemed to have central adrenal insufficiency, and a morning cortisol level >15 mg/dL were regarded as normal. Patients whose morning cortisol levels were
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, preferably at every infusion for at least 6 months and less frequently thereafter, is generally recommended ( 45 ). Initial tests should include fasting glucose, electrolytes, thyroid stimulating hormone (TSH) and free T4 (fT4), and early morning cortisol