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Department of Clinical Biochemistry, Imperial College Healthcare NHS Trust, London, UK
Department of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK
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Department of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK
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which treatment with supraphysiological doses of exogenous steroid is required. The aim of glucocorticoid replacement therapy in adrenal failure is to reverse the deficiency using only physiological doses of steroids. Reproducing the diurnal cortisol
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Introduction Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders caused by enzyme defects in the steroid biosynthesis of the adrenal cortex. In approximately 95% of cases, the disorder is caused by a pathogenic
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androgen receptor (AR) modulators (SARMs) rather than testosterone may be used to treat AR-positive BC. CR1447 (4-hydroxytestosterone (4-OHT)) is a steroidal small molecule with two distinct properties, acting as a steroidal aromatase inhibitor (AI) and
Department of Pediatrics, St. Anna Kinderspital, Medical University of Vienna, Vienna, Austria
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Introduction Congenital adrenal hyperplasia (CAH; incidence 1 in 10–15,000) due to 21-hydroxylase deficiency (21-OH) ( CYP21A2 ; OMIM 201910) is an autosomal recessive disorder resulting in a deficient production of the steroid hormones
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large multicentre study comparing the efficacy of intratympanic vs systemic steroid therapy demonstrated the same level of hearing improvement between the two groups (9) . However, for the time being, there is no consensus regarding the dose and
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ovary syndrome. Competency 11 : Steroid replacement therapy for disorders of the pituitary and adrenal glands. Competency 12 : Thyroid disease. Competency 13 : Transition. Competency 1 Acromegaly. Competent Proficient Expert As competent plus As
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, 5 ). As steroid hormones are synthesised on demand, the availability of intramitochondrial cholesterol initiates steroidogenesis by providing substrate for the first rate-limiting enzyme in the steroidogenic pathway ( 6 ). Long-term exposure to ACTH
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Department of Endocrinology, Suichang County Hospital of Traditional Chinese Medicine, Lishui, China
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evidence-based researches were insufficient ( 3 ). Several studies have focused on the optimal doses of steroids ( 8 , 9 , 10 ). Some scholars have recommended an initial treatment with lower doses of prednisolone daily ( 8 , 9 ). One study has shown
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oestradiol as feminising gender-affirming hormone therapy ( 3 ). Goals of therapy are generally to increase serum oestradiol concentrations and lower serum total testosterone concentrations to achieve sex steroid concentrations in the female reference range
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, 21 ) (e.g. BrdU incorporation lymphocyte steroid sensitivity assay (BLISS) and measuring the GC-responsive gene expression) are required to determine the GC responsiveness of specific tissues and/or cells. Although GC response can be determined, an