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Glucocorticoid therapy in classic congenital adrenal hyperplasia: traditional and new treatment paradigms.
Expert Rev Endocrinol Metab
January 2025
Neurocrine Biosciences, Inc, San Diego, CA, USA.
Introduction: Classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CAH) is a rare genetic condition characterized by cortisol deficiency and excess adrenal androgens. CAH treatment is a lifelong balancing act between the need to reduce excess androgens, typically with supraphysiologic glucocorticoid (GC) doses, and concerns about potentially serious GC-related adverse events. Tradeoffs between the consequences of excess androgens versus GCs must be constantly reassessed throughout each patient's lifetime, based on current clinical needs and treatment goals.
View Article and Find Full Text PDFNeonatal pseudo-hypoaldosteronism type 1 with a novel gene variant.
Sudan J Paediatr
January 2024
Department of Paediatrics, South West Acute Hospital, Enniskillen, UK.
Pseudohypoaldosteronism (PHA) is a rare disorder that mimics congenital adrenal hyperplasia (CAH). Renal type A1A of the disorder has a known gene mutation (NR3C2) and parents may be asymptomatic despite biochemical abnormalities. Meticulous interpretation of hormonal and biochemical data, and early liaison with endocrinology and renal teams are key in diagnosis.
View Article and Find Full Text PDFSemaglutide and laparoscopic sleeve gastrectomy in an adolescent with congenital adrenal hyperplasia due to 21-hydroxylase: a case report.
J Med Case Rep
January 2025
Department of Surgery, Center for Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles and Keck School of Medicine of USC, Los Angeles, CA, USA.
Background: Classic congenital adrenal hyperplasia, primarily due to 21-hydroxylase deficiency, leads to impaired cortisol and aldosterone production and excess adrenal androgens. Lifelong glucocorticoid therapy is required, often necessitating supraphysiological doses in youth to manage androgen excess and growth acceleration. These patients experience higher obesity rates, hypertension, and glucose metabolism issues, complicating long-term health management.
View Article and Find Full Text PDF[A case of 11β-hydroxylase deficiency complicated with bilateral adrenal myelolipoma].
Zhonghua Nei Ke Za Zhi
February 2025
Department of Endocrinology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou450003, China.
Increased Oxidative and Nitrative Stress and Decreased Sex Steroid Relaxation in a Vitamin D-Deficient Hyperandrogenic Rodent Model-And a Validation of the Polycystic Ovary Syndrome Model.
Nutrients
January 2025
Department of Obstetrics and Gynaecology, Semmelweis University, Üllői Street 78/a, 1082 Budapest, Hungary.
Background/objectives: Both hyperandrogenism (HA) and vitamin D deficiency (VDD) can separately lead to impaired vascular reactivity and ovulatory dysfunction in fertile females. The aim was to examine the early interactions of these states in a rat model of PCOS.
Methods: Four-week-old adolescent female rats were divided into four groups: vitamin D (VD)-supplemented ( = 12); VD-supplemented and testosterone-treated ( = 12); VDD- ( = 11) and VDD-and-testosterone-treated ( = 11).
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