The differential diagnosis between malignant and benign adrenal cortical tumors is challenging, and concurrent androgen and cortisol production should raise suspicion of a malignant tumor. We present the case of a 36-year-old woman who exhibited pronounced hirsutism, clitoromegaly, and secondary amenorrhea. A contrast-enhanced computed tomography (CT) scan revealed a 35 × 27 mm right adrenal mass with unenhanced CT attenuation of 40 Hounsfield units (HUs). The mass exhibited absolute and relative washout rates of 50% and 28%, respectively, and was accompanied by a 25 × 20 mm adenopathy located in the hepatogastric space. Total testosterone was elevated by 247 ng/dL (8.56 nmol/L) (normal reference range, 10-75 ng/dL; 0.34-2.6 nmol/L). A 1-mg dexamethasone suppression test revealed an elevated serum morning cortisol concentration of 10.57 μg/dL (291.58 nmol/L) (reference range, <1.8 μg/dL; < 49.66 nmol/L). A fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) scan revealed increased uptake in both the adrenal mass and the adenopathy. Subsequently, the patient underwent an open right adrenalectomy and lymphadenectomy. Histological examination revealed the presence of an adrenal adenoma with myelolipomatous metaplasia, as well as a positive polymerase chain reaction (PCR) for in the adenopathy.
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http://dx.doi.org/10.1210/jcemcr/luae171 | DOI Listing |
Front Pediatr
December 2024
Pediatric Department, Buzzi Children's Hospital, Milan, Italy.
In patients affected by anorexia nervosa (AN) different endocrine abnormalities have been described, but, among them, hypothalamic-pituitary-adrenal (HPA) dysfunction, although associated to important side effects, is underestimated and has no therapeutical options. We present a narrative literature review to investigate the HPA axis in patients with AN, in order to highlight HPA dysfunction and its effects. We also described the crucial role of HPA monitoring, and to consider eventual therapeutic and preventive strategies in AN patients.
View Article and Find Full Text PDFPhysiol Rep
December 2024
SHAPE Research Centre, Department of Sport Science, Nottingham Trent University, Nottingham, UK.
Overreaching, a consequence of intensified training, is used by athletes to enhance performance. A blunted hormonal response to a 30-min interval exercise stress test (55/80) has been shown in males after intensified training, highlighting cortisol and testosterone as potential biomarkers of overreaching. Despite accounting for ~50% of the population, studies into hormonal responses to exercise in females are lacking.
View Article and Find Full Text PDFClin Endocrinol (Oxf)
December 2024
Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Objective: Many review articles have explored data regarding the coexistence of specific types of pituitary adenomas (PAs) and polycystic ovary syndrome (PCOS), particularly focusing on the potential pathogenesis of this intersection and overlapping features. However, a comprehensive evaluation encompassing the full spectrum of PAs and their association with PCOS remains lacking. This review aims to provide a broad assessment of the interactions between these entities, emphasizing pathophysiological mechanisms, clinical presentations, diagnostic challenges and therapeutic implications.
View Article and Find Full Text PDFJ Clin Res Pediatr Endocrinol
December 2024
University of Health Science, Dr Sami Ulus Child Health and Diseases Health Implementation and Research Center, Clinics of Pediatric Endocrinology, Ankara, Türkiye.
Although the most common cause of congenital adrenal hyperplasia (CAH) worldwide is 21-hydroxylase deficiency (21OHD), which accounts for more than 95% of cases, other rare causes of CAH such as 11 beta-hydroxylase deficiency (11βOHD), 3 beta-hydroxy steroid dehydrogenase (3β-HSD) deficiency, 17 hydroxylase deficiency and lipoid CAH may also be encountered in clinical practice. 11βOHD is the most common type of CAH after 21OHD, and CYP11B1 deficiency in adrenal steroidogenesis causes the inability to produce cortisol and aldosterone and the excessive production of adrenal androgens. Although the clinical and laboratory features are similar to 21OHD, findings of mineralocorticoid deficiency are not observed.
View Article and Find Full Text PDFJ Clin Res Pediatr Endocrinol
December 2024
Department of Pediatric Endocrinology, Ankara University Faculty of Medicine, Ankara, Turkiye.
Congenital adrenal hyperplasia (CAH) is an autosomal recessive disease caused by the deficiency of one of the enzymes involved in cortisol synthesis. Between 90% and 99% of cases of CAH are caused by 21-hydroxylase deficiency (21OHD) caused by mutations in CYP21A2. Although 21OHD has been historically divided into classical and non-classical forms, it is now thought to show a continuous phenotype.
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