{"id":1838,"date":"2024-04-21T20:38:51","date_gmt":"2024-04-21T20:38:51","guid":{"rendered":"https:\/\/blog.antoniolamarca.it\/?p=1838"},"modified":"2024-04-21T20:38:51","modified_gmt":"2024-04-21T20:38:51","slug":"lazoospermia","status":"publish","type":"post","link":"https:\/\/blog.antoniolamarca.it\/en\/lazoospermia\/","title":{"rendered":"Azoospermia"},"content":{"rendered":"Reading Time: <\/span> 4<\/span> minutes<\/span><\/span>

Spermatogenesis is an extraordinarily complex process. The differentiation of spermatogonia into spermatozoa requires the participation of various cell types, hormones, paracrine factors, genes and epigenetic regulators. Spermatogenesis comprises a complex network of processes that occur in the seminiferous tubules and culminate in the production of the mature male gamete. The processes are: proliferation of spermatogonia; differentiation of spermatogonia into spermatocytes; meiotic division of spermatocytes producing spermatids; maturation of round spermatids; and the release of highly specialised mature spermatozoa into the lumen of the testicular tubule. The entire spermatogenic process is thought to take about 74 days while the estimated daily sperm production per man ranges from 150 to 275 million spermatozoa. Various testicular structures and cells play an important role during spermatogenesis, while a wide range of factors can influence its quality and quantity.<\/p>\n

Azoospermia is defined as the absence of spermatozoa in the ejaculate. It affects approximately 1% of all men and is the most severe manifestation of testicular failure. Azoospermia can be divided into three main categories:<\/p>\n

- dysfunction of the hypothalamus-pituitary axis<\/p>\n

- primary quantitative spermatogenic disorders<\/p>\n

- urogenital duct obstruction<\/p>\n

All these subgroups may be related to congenital and\/or acquired factors. In the case of bilateral distal or proximal obstruction of the ejaculatory ducts, the spermatogenic process is not affected and this pathological condition is called obstructive azoospermia (OA), which leads to a measurable lack of sperm in the ejaculate. On the other hand, primary or secondary testicular insufficiency leads to non-obstructive azoospermia (NOA), which is not caused by blocked testicles, but rather by poor sperm production within the testicles. Non-obstructive azoospermia accounts for 70 % of total azoospermia cases and most of them show primary testicular failure due to defective spermatogenesis. There are currently three recognised phenotypes of NOA: Sertoli cell syndrome (SCOS), maturation arrest (MA) and hypospermatogenesis.<\/p>\n

A number of acquired conditions such as orchitis, cytotoxic treatments, ejaculatory duct obstruction, central nervous system tumours, systemic diseases, etc. can lead to azoospermia and may account for about 35-40% of cases. However, one study found that about 30-40% of patients had azoospermia, but no cause was found to explain why they were infertile; these patients were defined as idiopathic non-obstructive azoospermia. Numerous theories are still being investigated that attempt to explain the differences between normal individuals and patients with idiopathic non-obstructive azoospermia from the testicular microenvironment, the patient's metabolic profile, the Sertoli cells themselves or immune profiles. In particular, interest seems to be directed at the macrophage component; macrophages are involved in various processes, their distinguishing feature being their participation in inflammation and immune regulation. By maintaining a balance between proinflammatory and anti-inflammatory cytokines, testicular macrophages help create a favourable environment for spermatogenesis and support the development of healthy spermatozoa. Therefore, testicular macrophages play a crucial role in regulating the testicular environment and maintaining the homeostasis of spermatogenesis in the testes. However, if the balance of the testicular microenvironment is disturbed, testicular macrophages present in the testes of infertile individuals can have a significant impact on the overall testicular environment. Testicular inflammation can lead to histopathological changes, such as thickening of the lamina propria, fibrosis and granuloma-like changes, which can further damage the testicular blood barrier and disrupt normal spermatogenesis, eventually leading to the arrest of spermatogenesis.<\/p>\n

 <\/p>\n

As far as congenital forms are concerned, genetic factors play a role in all the aetiological categories mentioned above and some of them are tested as part of the routine diagnostic procedure of infertile men. Genetic screening is relevant for its diagnostic value, clinical decision-making and appropriate genetic counselling. Over the past 40 years, the diagnostic armamentarium for the detection of genetic factors involved in azoospermia has been restricted to a few routine tests such as karyotype analysis, Y-chromosome microdeletions and the search for certain monogenic causes in selected cases of testicular pre- and post-azoospermia. Screening for genetic mutations based on target gene panels should be recommended when bilateral congenital absence of the vas deferens (CBAVD) or congenital hypogonadotropic hypogonadism (CHH) is suspected. The most common genetic disorder causing non-obstructive azoospermia is Klinefelter syndrome, characterised by the presence of an extra X chromosome: genotype 47XXY. Its prevalence is 1 in 600 (0.1-0.2%) in male infants, rising to 3-4% among infertile males and 10-12% in azoospermic individuals. However, the vast majority of patients, approximately 64% are still misdiagnosed or remain undiagnosed for life, due to the appearance of mild forms characterised by paucisymptomatic manifestations. This syndrome presents a broad spectrum of clinical manifestations, including classic features such as eunuchoid habitus, hypergonadotropic hypogonadism, gynaecomastia, small testes (volume < 4 ml), azoospermia and pervasive neurocognitive deficits.<\/p>\n

Spermatogenesis is indeed a complex process, regulated by various factors such as hormones and genes. Recent animal and human research has deepened our understanding of male gamete differentiation and improved clinical tools for better management of male infertility. There is still much to learn about this intricate process.<\/p>\n

 <\/p>\n

References<\/p>\n

Filipe Tenorio Lira Neto, et al. Spermatogenesis in humans and its affecting factors. Semin Cell Dev Biol. 2016 Nov:59:10-26. doi: 10.1016\/j.semcdb.2016.04.009. Epub 2016 Apr 30.<\/p>\n

Francesca Cioppi, et al. Genetics of Azoospermia. Int J Mol Sci. 2021 Mar 23;22(6):3264. doi: 10.3390\/ijms22063264.<\/p>\n

Peng Xia, et al. Macrophage-Related Testicular Inflammation in Individuals with Idiopathic Non-Obstructive Azoospermia: A Single-Cell Analysis. Mol Sci. 2023 May 16;24(10):8819. doi: 10.3390\/ijms24108819.<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>","protected":false},"excerpt":{"rendered":"

Reading Time: <\/span> 4<\/span> minutes<\/span><\/span> La spermatogenesi \u00e8 un processo straordinariamente complesso. La differenziazione degli spermatogoni in spermatozoi richiede la partecipazione di diversi tipi cellulari, ormoni, fattori paracrini, geni e regolatori epigenetici. La spermatogenesi comprende una complessa rete di processi che si verificano nei tubuli seminiferi e culmina nella produzione del gamete maschile maturo. I processi sono: proliferazione degli spermatogoni; …<\/p>","protected":false},"author":2,"featured_media":1839,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"om_disable_all_campaigns":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-1838","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorized"],"aioseo_notices":[],"_links":{"self":[{"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/posts\/1838","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/comments?post=1838"}],"version-history":[{"count":1,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/posts\/1838\/revisions"}],"predecessor-version":[{"id":1840,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/posts\/1838\/revisions\/1840"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/media\/1839"}],"wp:attachment":[{"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/media?parent=1838"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/categories?post=1838"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blog.antoniolamarca.it\/en\/wp-json\/wp\/v2\/tags?post=1838"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}