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Wellcome–MRC Institute of Metabolic Science, University of Cambridge and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK
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inhibition. The uninhibited AngII may then play a role in the pathogenesis of observed hypertension ( 6 ), inflammation, immunothrombosis and possible fibrosis in COVID-19. Whilst elevated serum cortisol has been identified as a marker of poor prognosis in
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Introduction Subclinical Cushing's syndrome (SCS) is defined as autonomous cortisol secretion in patients without typical signs and symptoms of hypercortisolism, as in the classic Cushing's syndrome (CS) (1) . Screening for a rare disorder like SCS
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Department of Endocrinology, Diabetes and Metabolic Disease, University Medical Center Ljubljana, Ljubljana, Slovenia
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-up ( 4 , 5 ), increases in NFAIs’ size and development of mild autonomous cortisol excess (MACE) over time have also been reported for this clinical entity ( 6 , 7 , 8 , 9 ). Currently, adequate long-term follow-up strategies of NFAIs after the
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quantitative importance of other factors, such as inhibition by insulin and stimulation by amino acids, is disputed ( 8 , 9 ). Hypoglycemia also triggers the release of other counter-regulatory hormones such as catecholamines, cortisol, and growth hormone
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glucocorticoid and mineralocorticoid biosynthesis ( 10 ). Both are typically at risk for adrenal crises in stress episodes. Interestingly, rare genetic subtypes of CAH like 11β hydroxylase deficiency (11βOHD) and 17 alpha/17–20 lyase deficiency block cortisol
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Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
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additional cortisol if needed ( 14 ). In accordance with this, a 30-day treatment protocol with a starting dose of 24 mg/day of methylprednisolone (MPSL) as the initial treatment for ST and tapered by 4 mg every 5 days is employed in our center. The
Assistance Publique Hôpitaux de Paris (APHP), Department of Endocrinology and Diabetes for Children, Bicêtre Paris-Sud, Le Kremlin Bicêtre, France
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Introduction Cushing’s disease (CD) is characterized by adrenocorticotropin (ACTH)-dependent cortisol excess originating from a pituitary adenoma and accounts for approximately 85% of cases of pediatric Cushing’s syndrome ( 1 , 2 , 3 , 4
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assess the pattern of ACTH/cortisol responses to desmopressin in the years following transsphenoidal surgery in patients with Cushing’s disease on long-term remission and to establish whether changes in the response to desmopressin in patients during
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Hormonology Department, Cochin Hospital, Paris, France
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series) but they can be responsible for autonomous cortisol secretion in about 12% of cases (1–29% among series) and for aldosterone secretion in 2.5% of cases (1.6–3.3% among series) ( 5 ). Primary bilateral macronodular adrenal hyperplasia (PBMAH) is
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, 21-deoxycorticosterone, deoxycorticosterone, corticosterone, 11-deoxycortisol, cortisol, cortisone, androstenedione, testosterone, dehydroepiandrostenedione sulfate (DHEA-S), estrone (E1), estradiol (E2), luteinizing hormone (LH), follicle