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  • Abstract: adrenarche x
  • Abstract: amenorrhoea x
  • Abstract: fertility x
  • Abstract: Gender x
  • Abstract: Hypogonadism x
  • Abstract: infertility x
  • Abstract: menarche x
  • Abstract: menopause x
  • Abstract: testes x
  • Abstract: transsexual x
  • Abstract: Turner x
  • Abstract: sperm* x
  • Abstract: ovary x
  • Abstract: follicles x
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Ping Li Department of Endocrinology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China

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Fei Cheng Department of Endocrinology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China

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Lei Xiu Department of Endocrinology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China

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Objective

This study sought to determine the effect of the recombinant human growth hormone (rhGH) treatment of Turner syndrome (TS) on height outcome.

Methods

We searched in MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews. A literature search identified 640 records. After screening and full-text assessment, 11 records were included in the systematic review. Methodological quality was assessed using the Cochrane Risk of Bias tool. RevMan 5.3 software was used for meta-analysis. We also assessed the quality of evidence with the GRADE system.

Results

Compared with controls, rhGH therapy led to increased final height (MD = 7.22 cm, 95% CI 5.27–9.18, P < 0.001, I2 = 4%; P = 0.18), height standard deviation (HtSDS) (SMD = 1.22, 95% CI 0.88–1.56, P < 0.001, I2 = 49%; P = 0.14) and height velocity (HV) (MD 2.68 cm/year; 95% CI 2.34, 3.02; P < 0.001, I2 = 0%; P = 0.72). There was a small increase in bone age (SMD 0.32 years; 95% CI 0.1, 0.54; P = 0.004, I2 = 73%; P = 0.02) after rhGH therapy for 12 months. What is more, the rhGH/oxandrolone combination therapy suggested greater final height (MD 2.46 cm; 95% CI 0.73, 4.18; P = 0.005, I2 = 32%; P = 0.22), increase and faster HV (SMD 1.67 cm/year; 95% CI 1.03, 2.31; P < 0.03, I2 = 80%; P < 0.001), with no significant increase in HtSDS and bone maturation compared with rhGH therapy alone.

Conclusions

For TS patients, rhGH alone or with concomitant use of oxandrolone treatment had advantages on final height.

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D Santi Unit of Endocrinology, Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy
Unit of Endocrinology, Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy

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A R M Granata Unit of Endocrinology, Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy

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M Simoni Unit of Endocrinology, Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy
Unit of Endocrinology, Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy

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Introduction

The aim of this study is to comprehensively evaluate whether FSH administration to the male partner of infertile couples improves pregnancy rate, spontaneously and/or after assisted reproductive techniques (ART).

Methods

Meta-analysis of controlled clinical trials in which FSH was administered for male idiopathic infertility, compared with placebo or no treatment. Randomization was not considered as an inclusion criterion.

Results

We found 15 controlled clinical studies (614 men treated with FSH and 661 treated with placebo or untreated). Concerning the type of FSH, eight studies used recombinant FSH, whereas seven studies used purified FSH. Nine studies evaluated spontaneous pregnancy rate, resulting in an overall odds ratio (OR) of about 4.5 (CI: 2.17–9.33). Eight studies evaluated pregnancy rate after ART, showing a significant OR of 1.60 (CI: 1.08–2.37). Sub-dividing studies according to the FSH preparations (purified/recombinant), pregnancy rate improvement remained significant for each preparation. Eleven studies considered sperm quality after FSH treatment, finding a significant improvement of sperm concentration (2.66×106/ml, CI: 0.47–4.84), but not of concentration of sperm with progressive motility (1.22×106/ml, CI: −0.07 to 2.52). Three trials evaluated testicular volume, showing a non-significant increase in men treated (1.35 ml, CI: −0.44 to 3.14).

Conclusion

The results of controlled clinical trials available in the literature indicate an improvement of pregnancy rate after FSH administration to the male partner of infertile couples, both spontaneously and after ART. However, the heterogeneity of studies, the high risk of bias and the lack of precise criteria to guide FSH administration limit the strength of these results. Future studies should be designed to identify the markers of FSH response which are helpful in the decision-making process. Meanwhile, the use of FSH in the treatment of male infertility should be cautious.

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Pravik Solanki Faculty of Medicine, Nursing and Health Sciences, Monash University, Victoria, Australia
Alfred Health, Melbourne, Victoria, Australia

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Beng Eu Prahran Market Clinic, Victoria, Australia
Department of General Practice, Melbourne Medical School, The University of Melbourne, Victoria, Australia

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Jeremy Smith Faculty of Science, University of Western Australia, Perth, Australia

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Carolyn Allan Hudson Institute of Medical Research, Melbourne, Victoria, Australia

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Kevin Lee Faculty of Medicine, Nursing and Health Sciences, Monash University, Victoria, Australia

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Hypogonadism can result following anabolic steroid abuse. The duration and degree of recovery from anabolic steroid-induced hypogonadism (ASIH) is immensely variable, and there is a paucity of prospective controlled data characterising the trajectory of natural recovery following cessation. This poses difficulties for users trying to stop androgen abuse, and clinicians wanting to assist them. The objective of this paper was to synthesise evidence on the physical, psychological and biochemical patterns of ASIH recovery. We present the pathophysiology of ASIH through a literature review of hypothalamic–pituitary–testosterone axis recovery in supraphysiological testosterone exposure. This is followed by a scoping review of relevant observational and interventional studies published on PubMed and finally, a conclusion that is an easy reference for clinicians helping patients that are recovering from AAS abuse. Results indicate that ASIH recovery depends on age and degree of androgen abuse, with physical changes like testicular atrophy expected to have near full recovery over months to years; spermatogenesis expected to achieve full recovery over months to years; libido returning to baseline over several months (typically less potent than during AAS use); and recovery from gynaecomastia being unlikely. For psychological recovery, data are insufficient and conflicting, indicating a transient withdrawal period which may be followed by persisting longer-term milder symptoms. For biochemical recovery, near complete recovery of testosterone is seen over months, and complete gonadotropin recovery is expected over 3–6 months. Further prospective studies are indicated to more closely describe patterns of recovery.

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Jan-Bernd Stukenborg NORDFERTIL Research Lab Stockholm, Pediatric Endocrinology Unit, Department of Women’s and Children’s Health, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Kirsi Jahnukainen NORDFERTIL Research Lab Stockholm, Pediatric Endocrinology Unit, Department of Women’s and Children’s Health, Karolinska Institutet and University Hospital, Stockholm, Sweden
Division of Haematology-Oncology and Stem Cell Transplantation, Children’s Hospital, University of Helsinki, Helsinki University Central Hospital, Helsinki, Finland

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Marsida Hutka MRC Centre for Reproductive Health, The Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, UK

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Rod T Mitchell MRC Centre for Reproductive Health, The Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, UK
Edinburgh Royal Hospital for Sick Children, Edinburgh, UK

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Testicular function and future fertility may be affected by cancer treatment during childhood. Whilst survival of the germ (stem) cells is critical for ensuring the potential for fertility in these patients, the somatic cell populations also play a crucial role in providing a suitable environment to support germ cell maintenance and subsequent development. Regulation of the spermatogonial germ-stem cell niche involves many signalling pathways with hormonal influence from the hypothalamo-pituitary-gonadal axis. In this review, we describe the somatic cell populations that comprise the testicular germ-stem cell niche in humans and how they may be affected by cancer treatment during childhood. We also discuss the experimental models that may be utilized to manipulate the somatic environment and report the results of studies that investigate the potential role of somatic cells in the protection of the germ cells in the testis from cancer treatment.

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Rossella Cannarella Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy

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Andrea Crafa Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy

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Sandro La Vignera Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy

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Rosita A Condorelli Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy

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Aldo E Calogero Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy

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Background

Animal studies suggest that insulin-like growth factor 1 (IGF1) may influence the function of the hypothalamus–pituitary–testicular axis, especially in childhood, but the evidence in humans is scanty. Laron syndrome, a human model of IGF1 deficiency, may help to solve this issue.

Purpose

This systematic review aims to analyze puberty onset and progression, testicular volume, gonadotropin, and total testosterone serum levels, sperm parameters and fertility, and penile length in patients with Laron syndrome.

Methods

Specific keywords were used. All data on male patients with Laron syndrome were included.

Results

Seventeen articles matched the inclusion criteria and were entered in the analysis, for a total of 125 male patients. Puberty was absent in 8.9% and delayed in 35.6% of untreated patients of pubertal age. After onset, the duration of the pubertal process was prolonged in 76.9% of untreated patients. The growth spurt was absent in 52.6% and delayed in 31.6% of untreated patients. The testicular volume was small in the two patients who did not receive any treatment. Treatment with IGF1 increased gonadotropin and testosterone serum levels in five out of five patients of pubertal age. No effect was found in four out of four patients younger than 5 years. No study reported data on sperm parameters and fertility. Micropenis occurred in 67.2% of patients.

Conclusion and future perspectives

Delayed puberty is common in patients with Laron syndrome. The growth hormone–IGF1 axis may influence the time of puberty onset. Serum levels of IGF1 should be investigated in children with delayed puberty, scarce progression of testicular growth, and/or micropenis. IGF1 levels might be measured in children with delayed puberty, poor testicular growth, and/or micropenis.

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Jens F Rehfeld Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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The birth certificate for endocrinology was Bayliss’ and Starling’s demonstration in 1902 that regulation of bodily functions is not only neuronal but also due to blood-borne messengers. Starling named these messengers hormones. Since then transport via blood has defined hormones. This definition, however, may be too narrow. Thus, today we know that several peptide hormones are not only produced and released to blood from endocrine cells but also released from neurons, myocytes, immune cells, endothelial cells, spermatogenic cells, fat cells, etc. And they are often secreted in cell-specific molecular forms with more or less different spectra of activity. The present review depicts this development with the story about cholecystokinin which was discovered in 1928 as a hormone and still in 1976 was conceived as a single blood-borne peptide. Today’s multifaceted picture of cholecystokinin suggests that time may be ripe for expansion of the hormone concept to all messenger molecules, which activate their target cells – irrespective of their road to the target (endocrine, neurocrine, neuronal, paracrine, autocrine, etc.) and irrespective of their kind of activity as classical hormone, growth factor, neurotransmitter, adipokine, cytokine, myokine, or fertility factor.

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A Rehfeld Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Denmark
Department of Cellular and Molecular Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), University of Copenhagen, Rigshospitalet, Denmark

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

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

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J H Petersen Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Denmark
International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), University of Copenhagen, Rigshospitalet, Denmark
Department of Biostatistics, University of Copenhagen, Copenhagen, Denmark

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S Dissing Department of Cellular and Molecular Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

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

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Human sperm cell function must be precisely regulated to achieve natural fertilization. Progesterone released by the cumulus cells surrounding the egg induces a Ca2+ influx into human sperm cells via the CatSper Ca2+-channel and thereby controls sperm function. Multiple chemical UV filters have been shown to induce a Ca2+ influx through CatSper, thus mimicking the effect of progesterone on Ca2+ signaling. We hypothesized that these UV filters could also mimic the effect of progesterone on sperm function. We examined 29 UV filters allowed in sunscreens in the US and/or EU for their ability to affect acrosome reaction, penetration, hyperactivation and viability in human sperm cells. We found that, similar to progesterone, the UV filters 4-MBC, 3-BC, Meradimate, Octisalate, BCSA, HMS and OD-PABA induced acrosome reaction and 3-BC increased sperm penetration into a viscous medium. The capacity of the UV filters to induce acrosome reaction and increase sperm penetration was positively associated with the ability of the UV filters to induce a Ca2+ influx. None of the UV filters induced significant changes in the proportion of hyperactivated cells. In conclusion, chemical UV filters that mimic the effect of progesterone on Ca2+ signaling in human sperm cells can similarly mimic the effect of progesterone on acrosome reaction and sperm penetration. Human exposure to these chemical UV filters may impair fertility by interfering with sperm function, e.g. through induction of premature acrosome reaction. Further studies are needed to confirm the results in vivo.

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Pamela Stratton Office of the Clinical Director, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA

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Neelam Giri Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Sonia Bhala Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Martha M Sklavos Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA

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Blanche P Alter Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Sharon A Savage Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Ligia A Pinto Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA

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Fanconi anemia (FA), dyskeratosis congenita-related telomere biology disorders (DC/TBD), and Diamond–Blackfan anemia (DBA) are inherited bone marrow failure syndromes (IBMFS) with high risks of bone marrow failure, leukemia, and solid tumors. Individuals with FA have reduced fertility. Previously, we showed low levels of anti-Müllerian hormone (AMH), a circulating marker of ovarian reserve, in females with IBMFS. In males, AMH may be a direct marker of Sertoli cell function and an indirect marker of spermatogenesis. In this study, we assessed serum AMH levels in pubertal and postpubertal males with FA, DC/TBD, or DBA and compared this with their unaffected male relatives and unrelated healthy male volunteers. Males with FA had significantly lower levels of AMH (median: 5 ng/mL, range: 1.18–6.75) compared with unaffected male relatives (median: 7.31 ng/mL, range: 3.46–18.82, P = 0.03) or healthy male volunteers (median: 7.66 ng/mL, range: 3.3–14.67, P = 0.008). Males with DC/TBD had lower levels of AMH (median: 3.76 ng/mL, range: 0–8.9) compared with unaffected relatives (median: 5.31 ng/mL, range: 1.2–17.77, P = 0.01) or healthy volunteers (median: 5.995 ng/mL, range: 1.57–14.67, P < 0.001). Males with DBA had similar levels of AMH (median: 3.46 ng/mL, range: 2.32–11.85) as unaffected relatives (median: 4.66 ng/mL, range: 0.09–13.51, P = 0.56) and healthy volunteers (median: 5.81 ng/mL, range: 1.57–14.67, P = 0.10). Our findings suggest a defect in the production of AMH in postpubertal males with FA and DC/TBD, similar to that observed in females. These findings warrant confirmation in larger prospective studies.

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Sakina Kherra CHU Parnet Hopital, Algiers, Algeria

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Wendy Forsyth Paterson Royal Hospital for Sick Children, Yorkhill, Glasgow, UK

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Filiz Mine Cizmecioglu Paediatric Endocrinology and Diabetes Department, Kocaeli University, Kocaeli, Turkey

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Jeremy Huw Jones Department of Pediatric Endocrinology, Royal Hospital for Children Glasgow, NHS Greater Glasgow and Clyde, Glasgow, UK

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Mariam Kourime Abderrahim Harouchi Hôpital, Casablanca, Morocco

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Heba Hassan Elsedfy Pediatrics Department, Ain Shams University, Cairo, Egypt

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Sameh Tawfik Department of Pediatrics, Maadi Hospital, Cairo, Egypt

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Andreas Kyriakou Department of Pediatric Endocrinology, Royal Hospital for Children Glasgow, NHS Greater Glasgow and Clyde, Glasgow, UK

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Mohamad Guftar Shaikh Department of Pediatric Endocrinology, Royal Hospital for Children Glasgow, NHS Greater Glasgow and Clyde, Glasgow, UK

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Malcolm David Cairns Donaldson Section of Child Health, Glasgow University School of Medicine, Glasgow, UK

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Background

Hypogonadism is a key feature of Prader–Willi syndrome (PWS) but clear strategies for hormone replacement are lacking.

Objective

To evaluate the gonadal status and outcome in patients attending a Scottish PWS clinic from 1991 to 2019.

Methods

In 93 (35F:56M) patients, median follow-up 11.2 years, gonadal and pubertal status were assessed clinically. Pelvic ultrasound findings and basal/stimulated gonadotrophins were compared with age-matched controls.

Results

Females:of 22 patients aged > 11, 9 had reached B4–5, while 5 were still at B2–3, and 6 remained prepubertal. Eight patients experienced menarche aged 9.8–21.4 years, none with a normal cycle. Uterine length and ovarian volumes were normal but uterine configuration remained immature, with low follicular counts. Gonadotrophins were unremarkable, serum oestradiol 129 (70–520) pmol/L. Only 5 patients received oestrogen replacement. Males:fifty-four (96%) patients were cryptorchid (9 unilateral). Weekly hCG injections resulted in unilateral/bilateral descent in 2/1 of 25 patients. Of 37 boys aged > 11, 14 (9 with failed/untreated bilateral cryptorchidism) failed to progress beyond G1, 15 arrested at G2–3 (testes 3–10 mL), and 8 reached G4–5. Gonadotrophins were unremarkable except in boys at G2–5 in whom FSH was elevated: 12.3/27.3 vs 3.25/6.26 U/L in controls (P < 0.001). In males aged > 13, testosterone was 3.1 (0.5–8.4) nmol/L. Androgen therapy, given from 13.5 to 29.2 years, was stopped in 4/24 patients owing to behavioural problems.

Conclusion

Despite invariable hypogonadism, few females and only half the males with PWS in this study received hormone replacement. Double-blind placebo-controlled crossover trials of sex steroids are required to address unproven behavioural concerns.

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Shuang Ye Department of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China

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Yuanyuan Xu Department of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China

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Jiehao Li Department of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China

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Shuhui Zheng Research Center for Translational Medicine, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China

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Peng Sun Department of Pathology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China

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Tinghuai Wang Department of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China

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The role of G protein-coupled estrogen receptor 1 (GPER) signaling, including promotion of Ezrin phosphorylation (which could be activated by estrogen), has not yet been clearly identified in triple-negative breast cancer (TNBC). This study aimed to evaluate the prognostic value of GPER and Ezrin in TNBC patients. Clinicopathologic features including age, menopausal status, tumor size, nuclear grade, lymph node metastasis, AJCC TNM stage, and ER, PR and HER-2 expression were evaluated from 249 TNBC cases. Immunohistochemical staining of GPER and Ezrin was performed on TNBC pathological sections. Kaplan–Meier analyses, as well as logistic regressive and Cox regression model tests were applied to evaluate the prognostic significance between different subgroups. Compared to the GPER-low group, the GPER-high group exhibited higher TNM staging (P = 0.021), more death (P < 0.001), relapse (P < 0.001) and distant events (P < 0.001). Kaplan–Meier analysis showed that GPER-high patients had a decreased OS (P < 0.001), PFS (P < 0.001), LRFS (P < 0.001) and DDFS (P < 0.001) than GPER-low patients. However, these differences in prognosis were not statistically significant in post-menopausal patients (OS, P = 0.8617; PFS, P = 0.1905; LRFS, P = 0.4378; DDFS, P = 0.2538). There was a significant positive correlation between GPER and Ezrin expression level (R = 0.508, P < 0.001) and the effect of Ezrin on survival prognosis corresponded with GPER. Moreover, a multivariable analysis confirmed that GPER and Ezrin level were both significantly associated with poor DDFS (HR: 0.346, 95% CI 0.182–0.658, P = 0.001; HR: 0.320, 95% CI 0.162–0.631, P = 0.001). Thus, overexpression of GPER and Ezrin may contribute to aggressive behavior and indicate unfavorable prognosis in TNBC; this may correspond to an individual’s estrogen levels.

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