The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Department of Environmental Medicine, Institute of Public Health, University of Southern Denmark, Odense, Denmark
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The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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The International Research Centre in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Introduction Testosterone in serum is primarily bound to proteins with only a minor fraction circulating as free unbound testosterone. The major high-affinity binding protein is sex hormone-binding globulin (SHBG) ( 1 ). Because of the short
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Introduction Testosterone is the primary sex hormone and anabolic steroid in men. It is secreted primarily by the Leydig cells of the testicles and, to a much lesser extent, by the adrenal glands. Testes produce 3–10 mg of testosterone daily
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus N, Denmark
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Department of Molecular Medicine, Aarhus University Hospital, Aarhus N, Denmark
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Introduction Men with 47,XXY Klinefelter syndrome (KS) commonly present hypergonadotropic hypogonadism and are commonly treated with testosterone supplementation therapy ( 1 ). However, this treatment is almost entirely based on our knowledge
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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
Department of Endocrinology, St James’s Hospital, Dublin, Ireland
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Department of Endocrinology, University of Manchester, Manchester, UK
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Department of Paediatric Endocrinology & Diabetes, Newcastle-upon-Tyne Hospitals, Newcastle upon Tyne, UK
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Endocrine Research Group, Institute of Genetic Medicine, University of Newcastle-upon-Tyne, Newcastle upon Tyne, UK
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remainder being identifiable later during the process of pubertal induction through failure to normalise testicular volume with testosterone therapy ( 1 ). Given the aforementioned factors, the diagnostic evaluation and management of pubertal delay should
International Centre 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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International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Section of Biostatistics, University of Copenhagen, Copenhagen, Denmark
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International Centre for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Fertility, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
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International Centre 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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International Centre 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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International Centre 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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International Centre 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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International Centre 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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International Centre 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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International Centre 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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International Centre 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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International Centre 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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International Centre 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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well as an increased risk of developing insulin resistance, metabolic syndrome, and osteoporosis ( 1 ). Low to low-normal serum concentrations of testosterone are seen in most adults with KS, but nearly all have highly elevated concentrations of
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Erythrocytosis, or elevated hematocrit, is a common side effect of testosterone therapy (TTh) in male hypogonadism. Testosterone stimulates erythropoiesis through an initial rise in erythropoietin (EPO), establishment of a new EPO/hemoglobin ‘set point’, and a parallel decrease in the master iron regulator protein hepcidin, as well as several other potential mechanisms. Evidence shows an increased thrombotic risk associated with TTh–induced erythrocytosis. Several guidelines for the treatment of male hypogonadism by endocrine organizations recommend against starting TTh in patients presenting with elevated hematocrit at baseline or to stop TTh when its levels cannot be controlled by dose-adjustments. Importantly, therapeutic phlebotomy or venesection is mentioned as a means of reducing hematocrit in these patients. However, evidence supporting the efficacy or safety of therapeutic phlebotomy in lowering hematocrit in TTh–induced erythrocytosis is lacking. In light of this dearth of evidence, the recommendation to lower hematocrit using therapeutic phlebotomy is notable, as phlebotomy lowers tissue oxygen partial pressure (pO2) and, eventually, depletes iron stores, thereby triggering various biological pathways which might also increase thrombotic risk. The potential pros and cons should therefore be carefully weighed against each other and shared decision making is recommended for initiating therapeutic phlebotomy as a treatment in patients on TTh who present with increased hematocrit.
Department of Gynecology and Reproductive Medicine, Karolinska University Hospital, Stockholm, Sweden.
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estradiol, progesterone and testosterone, as well as subsequent anovulation and amenorrhea ( 3 ). Several mechanisms underlie such inhibition of the HPG axis ( Fig. 1 ), including exercise-induced activation of the hypothalamic-pituitary-adrenal axis and a
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testosterone secretion. FSH primarily stimulates Sertoli cells adjacent to germ cells within the seminiferous tubules. Intratesticular testosterone stimulated by LH, and stimulation of Sertoli cells by FSH seems both important for induction of spermatogenesis
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Section of Biostatistics, Department of Public Health, University of Copenhagen, Copenhagen, Denmark
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due to increasing survival rates and longer follow-up time ( 1 ). HSCT interferes with the male reproductive axis, potentially causing testosterone deficiency and impaired spermatogenesis due to the detrimental effects of high-dose chemotherapy and