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Giuseppe Grande, Andrea Graziani, Antonella Di Mambro, Riccardo Selice, and Alberto Ferlin

Low bone mass is common in men with Klinefelter syndrome (KS), with a prevalence of 6-15% of osteoporosis and of 25-48% of osteopenia. Reduced bone mass has been described since adolescence and it might be related to both reduced bone formation and higher bone resorption. Although reduced testosterone levels are clearly involved in the pathogenesis, this relation is not always evident. Importantly, fracture risk is increased independently from bone mineral density (BMD) and testosterone levels. Here we discuss the pathogenesis of osteoporosis in patients with KS, with a particular focus on the role of testosterone and testis function. In fact, other hormonal mechanisms, such as global Leydig cell dysfunction, causing reduced Insulin-like factor 3 (INSL3) and 25-OH vitamin D levels, and high FSH and estradiol levels, might be involved. Furthermore, genetic aspects related to the supernumerary X chromosome might be involved, as well as androgen receptor expression and function. Notably, body composition, skeletal mass and strength, and age at diagnosis are other important aspects. Although Dual-Energy X-ray Absorptiometry (DXA) is recommended in the clinical workflow for patients with KS to measure BMD, recent evidence suggests that alterations in the microarchitecture of the bones and vertebral fractures might be present even in subjects with normal BMD. Therefore, analysis of trabecular bone score (TBS), high resolution peripheral quantitative CT and vertebral morphometry seem promising tools to better estimate the fracture risk of patents with KS. This review also summarizes the evidence on the best available treatments for osteoporosis in men with KS, with or without hypogonadism.

Open access

Trine Holm Johannsen, Jakob Albrethsen, Vassos Neocleous, Federico Baronio, Martine Cools, Lise Aksglaede, Niels Jørgensen, Peter Christiansen, Meri Toumba, Pavlos Fanis, Marie Lindhardt Ljubicic, and Anders Juul

Congenital adrenal hyperplasia (CAH) is a recessive condition that affects the adrenal glands. Despite life-long replacement therapy with glucocorticoids and mineralocorticoids, adult patients with CAH often experience impaired gonadal function. In pubertal boys and in men with CAH, circulating testosterone is produced by the adrenal glands as well as the testicular, steroidogenic cells. In this European two-center study, we evaluated the function of Leydig and Sertoli cells in 61 boys and men with CAH, primarily due to 21-hydroxylase deficiency. Despite conventional hormone replacement therapy, our results indicated a significant reduction in serum concentrations of both Leydig cell-derived hormones (i.e., insulin-like factor 3 [INSL3] and testosterone) and Sertoli cell-derived hormones (i.e., inhibin B and anti-Müllerian hormone) in adult males with CAH. Serum concentrations of INSL3 were particularly reduced in those with testicular adrenal rest tumors. To our knowledge, this is the first study to evaluate circulating INSL3 as a candidate biomarker to monitor Leydig cell function in patients with CAH.

Open access

Willem de Ronde and Diederik L Smit

experience, we discuss the management of steroid abuse and give treatment recommendations for the clinical endocrinologist. What are AAS? AAS comprise a group of compounds that are structurally similar to testosterone and have similar actions when

Open access

Alessandra Gambineri and Carla Pelusi

androgens, in both sexes, there are different synthesis pathways; a classic pathway where testosterone is synthesized directly in testicular Leydig cells in men and ovarian theca cells in women. Androgens are parallel produced from Δ5- and Δ4-precursors, and

Open access

Miranda Scharff, Chantal Maria Wiepjes, Maartje Klaver, Thomas Schreiner, Guy T’Sjoen, and Martin den Heijer

oral estradiol valerate a day or 100 µg/24 h estradiol patch twice a week. People older than 40 years were advised to be treated with transdermal estrogens, because of thrombosis risk ( 12 ). Transmen were treated with testosterone. They could choose

Open access

Christos Tsatsanis, Angel Elenkov, Irene Leijonhufvud, Katerina Vaporidi, Åsa Tivesten, and Aleksander Giwercman

to be regulated by sex hormones. BAFF suppression by testosterone has been demonstrated in animal studies and indirectly in humans when comparing men with high and low testosterone levels ( 4 ). In contrast, estrogens have been demonstrated to induce

Open access

Andre Madsen, Anders Juul, and Lise Aksglaede

the study period as previously described ( 19 ). Serum concentrations of total testosterone, dehydroepiandrosterone sulfate (DHEAS), 17-hydroxyprogesterone (17-OHP), androstenedione (4A), SHBG, follicle-stimulating hormone (FSH), luteinizing hormone

Open access

Yael Sofer, Nava Nevo, Michal Vechoropoulos, Gabi Shefer, Etty Osher, Nathan Landis, Karen Tordjman, Geoffrey L Hammond, and Naftali Stern

glucose, insulin, lipids, liver enzymes and testosterone levels. A glucose tolerance test (GTT) was done after an overnight fast with an intra-peritoneal injection of glucose (2 mg/kg). Glucose was measured at the following time points: 0, 15, 30, 60, 90

Open access

Lukas Ochsner Ridder, Agnethe Berglund, Kirstine Stochholm, Simon Chang, and Claus H Gravholt

(follicle-stimulating hormone, luteinizing hormone) and 65–85% of KS patients having decreased testosterone levels ( 6 ). KS patients may have signs of hypogonadism regardless of testosterone levels within the normal range. Even though current guidelines

Open access

Dorte Glintborg, Hanne Mumm, Jens Juul Holst, and Marianne Andersen

free testosterone ( 14 ). OCP may increase body weight ( 15 ) and insulin resistance ( 14 , 16 ), which could be associated with decreased GLP-1 levels. In contrast, animal studies suggested that estradiol and progesterone treatment could increase the