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Thozhukat Sathyapalan Department of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, UK

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Anne-Marie Coady Department of Obstetric Ultrasound, Hull and East Yorkshire Women’s and Children’s Hospital, Hull, UK

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Eric S Kilpatrick Department of Clinical Biochemistry, Sidra Medical and Research Center, Doha, Qatar

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Stephen L Atkin Department of Medicine, Weill Cornell Medical College, Doha, Qatar

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.7 92.6 ± 3.2 0.67 0.03 ± 0.02 0.12 Testosterone (nmol/L) 4.1 ± 0.2 2.9 ± 0.1 2.7 ± 0.1 <0.01 −24.6 ± 2.6 <0.01 4.4 ± 0.2 4.3 ± 0.2 4.2 ± 0.8 0.73 −0.1 ± 1.5 0.18 SHBG (nmol/L) 31.1 ± 1.0 35.3 ± 1.2 36

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Dorte Glintborg Department of Endocrinology, Odense University Hospital, Odense, Denmark
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark

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Katrine Hass Rubin OPEN – Odense Patient data Explorative Network, Department of Clinical Research, University of Southern Denmark and Odense University Hospital, Odense, Denmark

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Mads Nybo Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Odense, Denmark

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Bo Abrahamsen OPEN – Odense Patient data Explorative Network, Department of Clinical Research, University of Southern Denmark and Odense University Hospital, Odense, Denmark
Department of Medicine, Holbæk Hospital, Holbæk, Denmark

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Marianne Andersen Department of Endocrinology, Odense University Hospital, Odense, Denmark
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark

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analyzed at Odense University hospital. We have published details regarding assays recently ( 10 , 16 ). Serum total testosterone and SHBG were analyzed using a specific RIA after extraction as previously described ( 18 ). This method shows close

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Rohit Barnabas R Barnabas, Endocrinology, Seth GS Medical College and KEM Hospital, Mumbai, 400012, India

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Swati Jadhav S Jadhav, Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, India

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Anurag Ranjan Lila A Lila, Department of Endocrinology, Seth GS Medical College and KEM Hospital, Mumbai, India

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Sirisha Kusuma Boddu S Boddu, Endocrinology, Rainbow Children's Hospital Banjara Hills, Hyderabad, India

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Saba Samad Memon S Memon, Endocrinology, Seth GS Medical College and KEM Hospital, Mumbai, India

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Sneha Arya S Arya, Endocrinology, Seth GS Medical College and KEM Hospital, Mumbai, India

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Samiksha Chandrashekhar Hegishte S Hegishte, Endocrinology, Seth GS Medical College and KEM Hospital, Mumbai, India

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Manjiri Karlekar M Karlekar, Department of Endocrinology, KEM Hospital and Seth G S Medical College, Mumbai, India

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Virendra A Patil V Patil, Endocrinology, Seth GS Medical College and KEM Hospital, Mumbai, 400012, India

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Vijaya Sarathi V Sarathi, Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, India

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Nalini S Shah N Shah, Mumbai, 400012, India

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Tushar Bandgar T Bandgar, Endocrinology , Seth Gordhandas Sunderdas Medical College, Mumbai, India

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Background: The data on Leydig cell hypoplasia (LCH) resulting from biallelic Luteinizing hormone/chorionic gonadotropin receptor (LHCGR) inactivating variants is limited to case series.

Methods: We aim to describe our patients and perform systematic review of the patients with LHCGR inactivating variants in the literature. Detailed phenotype and genotype data of 3 patients from our centre and 85 (46,XY: 67; 46,XX: 18) patients from 59 families with LHCGR-inactivating variants from literature were described.

Results: Three 46,XY patients(age 6-18 years) from our centre, with two reared as females, had two novel variants in LHCGR. Systematic review (including our patients) revealed 72 variants in 88 patients. 46,XY patients (n=70, 56 raised as females) presented with pubertal delay (n=41) or atypical genitalia(n=17). Sinnecker score ≥3 (suggesting antenatal hCG inaction) was seen in 80% (56/70), and hCG-stimulated testosterone was low (<1.1 ng/ml) in 77.4% (24/31), whereas puberty/postpubertal age, high LH (97.6%, 41/42) and low (<1.0 ng/ml) basal testosterone (94.9%, 37/39) was observed in most. FSH was elevated in 21/51 of these patients. Variants with <10% receptor function were exclusively seen in cohorts with Sinnecker 4/5 (10/15 vs. 0/5, p=0.033). 46,XX patients (n=18) presented with oligo/amenorrhea and/or anovulatory infertility and had polycystic ovaries (7/9) with median LH of 10 IU/L (1.2-38).

Conclusion: In summary, this study comprehensively characterizes LHCGR variants, revealing genotype-phenotype correlations and informing clinical management of LCH. In 46,XY LCH patients, pubertal LH inaction is uniform with variable severity of antenatal hCG inaction. Few mutant LHCGR have differential action for LH and hCG.

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Willem de Ronde Department of Internal Medicine, Spaarne Gasthuis, Haarlem, the Netherlands

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Diederik L Smit Department of Internal Medicine, Spaarne Gasthuis, Haarlem, the Netherlands

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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

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Alessandra Gambineri Endocrinology Unit, Department of Medical and Surgical Sciences, St Orsola-Malpighi Hospital, Alma Mater University of Bologna, Bologna, Italy

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Carla Pelusi Endocrinology Unit, Department of Medical and Surgical Sciences, St Orsola-Malpighi Hospital, Alma Mater University of Bologna, Bologna, Italy

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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

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Miranda Scharff Department of Endocrinology and Center of Expertise on Gender Dysphoria, Amsterdam University Medical Center, Vrije Universiteit, Amsterdam, the Netherlands

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Chantal Maria Wiepjes Department of Endocrinology and Center of Expertise on Gender Dysphoria, Amsterdam University Medical Center, Vrije Universiteit, Amsterdam, the Netherlands

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Maartje Klaver Department of Endocrinology and Center of Expertise on Gender Dysphoria, Amsterdam University Medical Center, Vrije Universiteit, Amsterdam, the Netherlands

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Thomas Schreiner Department of Endocrinology, Oslo University Hospital, Oslo, Norway

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Guy T’Sjoen Department of Endocrinology & Center for Sexology and Gender, Ghent University Hospital, Ghent, Belgium

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Martin den Heijer Department of Endocrinology and Center of Expertise on Gender Dysphoria, Amsterdam University Medical Center, Vrije Universiteit, Amsterdam, the Netherlands

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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

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Christos Tsatsanis Department of Clinical Chemistry, School of Medicine, University of Crete, Heraklion, Crete, Greece
Molecular Reproductive Research Group, Department of Translational Medicine, Lund University, Malmö, Sweden
Institute of Molecular Biology and Biotechnology, FORTH, Heraklion, Greece

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Angel Elenkov Molecular Reproductive Research Group, Department of Translational Medicine, Lund University, Malmö, Sweden
Reproductive Medicine Centre, Skåne University Hospital Malmö, Malmö, Sweden

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Irene Leijonhufvud Reproductive Medicine Centre, Skåne University Hospital Malmö, Malmö, Sweden

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Katerina Vaporidi Molecular Reproductive Research Group, Department of Translational Medicine, Lund University, Malmö, Sweden

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Åsa Tivesten Wallenberg Laboratory for Cardiovascular and Metabolic Research, Institute of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden

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Aleksander Giwercman Molecular Reproductive Research Group, Department of Translational Medicine, Lund University, Malmö, Sweden
Reproductive Medicine Centre, Skåne University Hospital Malmö, Malmö, Sweden

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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

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Rebeca Esquivel-Zuniga Department of Pediatrics, University of Virginia, Charlottesville, Virginia, USA

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Alan D Rogol Department of Pediatrics, University of Virginia, Charlottesville, Virginia, USA

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concentrations of total and free testosterone. Moreover, those males with type 2 diabetes mellitus (T2DM) and obesity or other components of the metabolic syndrome are more likely to have diminished testosterone levels than those with isolated obesity ( 19

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Andre Madsen Hormone Laboratory, Department of Medical Biochemistry and Pharmacology, Haukeland University Hospital, Bergen, Norway
Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Anders Juul Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark

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Lise Aksglaede Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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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

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Yael Sofer Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Nava Nevo Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel

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Michal Vechoropoulos Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Gabi Shefer Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Etty Osher Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Nathan Landis Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Karen Tordjman
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Geoffrey L Hammond Departments of Cellular & Physiological Sciences and Obstetrics & Gynaecology, University of British Columbia, Vancouver, British Columbia, Canada

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Naftali Stern Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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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

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