Subclinical male hypogonadism

2021 ◽  
Vol 46 (3) ◽  
Author(s):  
Giovanni CORONA ◽  
Giulia RASTRELLI ◽  
Mauro DICUIO ◽  
Sergio CONCETTI ◽  
Marianna MINNETTI ◽  
...  
Keyword(s):  
Male Hypogonadism

Male hypogonadism: therapeutic choices and pharmacological management

2020 ◽  
Vol 45 (3) ◽  
Author(s):  
Sandro La Vignera ◽  
Giulia Izzo ◽  
Gian Pietro Emerenziani ◽  
Rossella Cannarella ◽  
Rosita A. Condorelli ◽  
...  
Keyword(s):  
Male Hypogonadism ◽  
Pharmacological Management

Testosterone-dependent changes in neurons of hypothalamic arcuate nucleus and reversibility of these changes by modeled male hypogonadism

2017 ◽  
pp. 21-30
Author(s):  
А.В. Дробленков ◽  
Л.Г. Прошина ◽  
Ю.Н. Юхлина ◽  
А.А. Байрамов ◽  
П.Д. Шабанов ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Nerve Cell ◽  
Arcuate Nucleus ◽  
Degenerative Changes ◽  
Control Group ◽  
Male Hypogonadism ◽  
Nissl Staining ◽  
Neuron Body ◽  
Androgen Synthesis ◽  
Reactive Changes

Актуальность. Значение недостаточности тестостерона для структурного гомеостазиса нейронов, регулирующих выработку гонадотропин-рилизинг гормона (ГнРГ) и синтезирующих данный гормон, мало изучены. Цель. Установить реактивные изменения, количество рецепторов к андрогенам (АР) и особенности их распределения в нейронах медиального аркуатного ядра гипоталамуса (МАЯ) при экспериментальном гипогонадизме, а также обратимость этих изменений после восстановительной терапии тестостероном. Методы. У самцов крыс Вистар (16 особей) моделировали гипогонадизм путем удаления одной гонады на 2-3 день постнатальной жизни и исследовали гистологические срезы каудальной части МАЯ у молодых животных (4 мес.) при отсутствии и осуществлении заместительной терапии. Контрольную группу составляли интактные самцы аналогичного возраста (8 особей). В середине левосторонней части МАЯ на площади 0,01 мм определяли реактивные изменения клеток и площадь тел малоизмененных нейронов (после окрашивания срезов методом Ниссля), а также число и долю тел нервных клеток, различавшихся по степени экспрессии АР. Результаты. Установлено, что нейроны МАЯ содержат большое количество АР, распределенных в различных частях их тела. При гипогонадизме происходит перераспределение АР и снижение степени их экспрессии (количества). Сгущение АР в области оболочки ядра и плазмолеммы, образование конгломератов в ядре и цитоплазме было характерно для нейронов с умеренной экспрессией. В цитоплазме и в области плазматической мембраны рецепторы отсутствовали у клеток со слабой и очень низкой экспрессией. Снижение степени экспрессии АР при гипогонадизме сопряжено с уменьшением площади тела и гибелью части нейронов. Заключение. Выявленные дегенеративные тестостерон-зависимые изменения нейронов МАЯ, которые синтезируют ГнРГ или пептиды, влияющие на его выработку, могут обусловить уменьшение высвобождения гонадолиберина, вторичное снижение синтеза андрогенов и реализацию морфофункциональных проявлений его вторичного дефицита. Заместительная терапия частично компенсирует дегенеративные изменения нейронов, восстанавливает интенсивность экспрессии АР, однако не влияет на процесс гибели нервных клеток. Background. Importance of testosterone deficiency for structural homeostasis of the neurons regulating production of gonadotropin-releasing hormone (GnRH) and synthesizing this hormone is insufficiently understood. Aim. To determine reactive changes, quantity of androgens receptors (AR), and features of their distribution in neurons of hypothalamic medial arcuate nucleus (MAN) in experimental hypogonadism and reversibility of these changes by restorative therapy with testosterone. Methods. Hypogonadism was modeled in 16 Wistar rats by removing one gonad on postnatal days 2-3, and histological sections of caudal MAN were examined in young, 4-month old animals with and without a replacement therapy. The control group consisted of 8 age-matched intact males. Cell reactive changes, areas of slightly changed neuron bodies (Nissl staining of sections), and the number and proportion of nerve cell bodies differing in the degree of AR expression were determined in the middle left-sided part of MAN, on an area of 0.01 mm. Results. MAN neurons contained a large quantity of AR distributed in different parts of the neuron body. In hypogonadism, AR redistributed and their expression (quantity) decreased. Condensation of AR in the region of nucleo- and plasmolemma and formation of conglomerates in the nucleus and cytoplasm were characteristic of neurons with moderate expression. In the regions of cytoplasm and plasma membrane, the receptors were absent in cells with low and very low expression. The reduced AR expression in hypogonadism was associated with a decreased neuron body area and death of a part of neurons. Conclusions. The identified degenerative changes in the testosterone-dependent neuronal MAN that synthesize GnRH or peptides affecting the GnRH production may decrease the release of GnRH, cause a secondary decrease in the androgen synthesis, and mediate morphological and functional manifestations of GnRH secondary deficit. The replacement therapy partially compensated for degenerative changes in neurons and restored the intensity of AR expression, however, it did not influence the process of nerve cell death.

Clinical and Biochemical Study of Hypoandrogenic Metabolic Syndrome in the Cardiovascular Risk Content of Male Patients

2017 ◽  
Vol 54 (1) ◽  
pp. 137-140
Author(s):  
Ana Minodora Grozdan ◽  
Oana Paduraru ◽  
Rodica Ghiuru ◽  
Costinela Georgescu ◽  
Letitia Duceac
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Biochemical Study ◽  
Male Hypogonadism ◽  
Male Patients

The aim of this study was to determine the incidence of hypoandrogenenic to male patients with S.Met., in the context of cardiovascular risk factors. It performed description of a correlation with diagnostic components of S.Met., and specifying an interrelated male hypogonadism with each of the major cardiovascular risk factors.

Why Do We Need New Markers for Male Hypogonadism and How Seminal Proteomics Might Solve the Problem?

2020 ◽  
Vol 27 (12) ◽  
pp. 1186-1191
Author(s):  
Giuseppe Grande ◽  
Domenico Milardi ◽  
Silvia Baroni ◽  
Andrea Urbani ◽  
Alfredo Pontecorvi
Keyword(s):  
Serum Testosterone ◽  
Clinical Syndrome ◽  
Testosterone Replacement ◽  
Total Testosterone ◽  
Male Hypogonadism ◽  
Grey Zone ◽  
Testosterone Levels ◽  
Normal Number ◽  
Replacement Treatment

Male hypogonadism is “a clinical syndrome that results from failure of the testis to produce physiological concentrations of testosterone and/or a normal number of spermatozoa due to pathology at one or more levels of the hypothalamic– pituitary–testicular axis”. The diagnostic protocol of male hypogonadism includes accurate medical history, physical exam, as well as hormone assays and instrumental evaluation. Basal hormonal evaluation of serum testosterone, LH, and FSH is important in the evaluation of diseases of the hypothalamus-pituitary-testis axis. Total testosterone levels < 8 nmol/l profoundly suggest the diagnosis of hypogonadism. An inadequate androgen status is moreover possible if the total testosterone levels are 8-12 nmol/L. In this “grey zone” the diagnosis of hypogonadism is debated and the appropriateness for treating these patients with testosterone should be fostered by symptoms, although often non-specific. Up to now, no markers of androgen tissue action can be used in clinical practice. The identification of markers of androgens action might be useful in supporting diagnosis, Testosterone Replacement Treatment (TRT) and clinical follow-up. The aim of this review is to analyze the main findings of recent studies in the field of discovering putative diagnostic markers of male hypogonadism in seminal plasma by proteomic techniques. The identified proteins might represent a “molecular androtest” useful as a seminal fingerprint of male hypogonadism, for the diagnosis of patients with moderate grades of testosterone reduction and in the follow-up of testosterone replacement treatment.

scholarly journals EAU-verslag Andrologie

2020 ◽  
Vol 10 (S2) ◽  
pp. 20-22
Author(s):  
Marij Dinkelman-Smit
Keyword(s):  
Sexual Dysfunction ◽  
Reproductive Health ◽  
Male Infertility ◽  
Sexual And Reproductive Health ◽  
Male Hypogonadism ◽  
Male Sexual Dysfunction

Samenvatting De EAU guidelines ‘Male infertility, male sexual dysfunction en male hypogonadism’ zijn ondergebracht onder een nieuw panel dat dit jaar de eerste ‘Sexual and Reproductive Health’ richtlijn presenteerde: zeer de moeite waard om te bekijken. Hierna volgt een samenvatting ‘Andrologie en testiculaire kiemceltumor’ uit de EAU20 Virtual.

scholarly journals Rapid Differentiation of Human Embryonic Stem Cells into Testosterone-Producing Leydig Cell-Like Cells In vitro

2021 ◽  
Author(s):  
Eun-Young Shin ◽  
Seah Park ◽  
Won Yun Choi ◽  
Dong Ryul Lee
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Male Hypogonadism ◽  
Testosterone Levels ◽  
Sequence Of Events ◽  
Short Period ◽  
Molecular Compounds

Abstract Background: Leydig cells (LCs) are testicular somatic cells that are the major producers of testosterone in males. Testosterone is essential for male physiology and reproduction. Reduced testosterone levels lead to hypogonadism and are associated with diverse pathologies, such as neuronal dysfunction, cardiovascular disease, and metabolic syndrome. LC transplantation is a promising therapy for hypogonadism; however, the number of LCs in the testis is very rare and they do not proliferate in vitro. Therefore, there is a need for an alternative source of LCs. Methods: To develop a safer, simple, and rapid strategy to generate human LC-like cells (LLCs) from stem cells, we first performed preliminary tests under different conditions for the induction of LLCs from human CD34/CD73 double positive-testis-derived stem cells (HTSCs). Based on the embryological sequence of events, we suggested a 3-step strategy for the differentiation of human ESCs into LLCs. We generated the mesendoderm in the first stage and intermediate mesoderm (IM) in the second stage and optimized the conditions for differentiation of IM into LLCs by comparing the secreted testosterone levels of each group. Results: HTSCs and human embryonic stem cells can be directly differentiated into LLCs by defined molecular compounds within a short period. Human ESC-derived LLCs can secrete testosterone and express steroidogenic markers. Conclusion: We developed a rapid and efficient protocol for the production of LLCs from stem cells using defined molecular compounds. These findings provide a new therapeutic cell source for male hypogonadism.

The pharmacotherapy of male hypogonadism besides androgens

2014 ◽  
Vol 16 (3) ◽  
pp. 369-387 ◽  
Author(s):  
Giovanni Corona ◽  
Giulia Ratrelli ◽  
Mario Maggi
Keyword(s):  
Male Hypogonadism
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