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Fetal programming
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Katherine E. Pelch, Jana L. Allison, Susan C. Nagel
The incidence of male reproductive tract disorders, including cryptorchidism, hypospadias, testicular cancer, and low sperm count, has increased over the last 30 to 50 years (168–174). It has been postulated that these disorders comprise a testicular dysgenesis syndrome (TDS) and may have a common etiology of deficient androgen production or action during development of the testes in fetal life (175).
The urinary tract and male reproductive system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Luis Beltran, Daniel M. Berney
The association of germ cell tumours (GCTs) and cryptorchidism has been known for many years, although the stated increased risk associated with this abnormality varies considerably in different publications, from a fourfold increase in patients with this condition in some reports, to a forty-fold increase in others. The existence of a proposed testicular dysgenesis syndrome has been proposed, which includes a constellation of pathological conditions – cryptorchidism, low sperm count, and hypospadias – although this syndrome remains hypothetical and is contested by some. There is also a small familial incidence of testicular tumours. The vast majority of testicular tumours show a specific genetic abnormality, namely multiple copies of the long arm of chromosome 12.
Sperm Banking
Published in Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh, Male Infertility in Reproductive Medicine, 2019
Rakesh Sharma, Alyssa M. Giroski, Ashok Agarwal
Testicular cancers have local and systemic influences on spermatogenesis because of their relationship to local paracrine factors such as β-human chorionic gonadotropin (β-hCG) [10] and cytokines [11]. Malignancy may disrupt the blood-testis barrier resulting in antisperm antibodies [12]. Reports suggest that testicular cancer and male infertility is a result of testicular insults culminating into testicular dysgenesis syndrome [13]. This theory is supported by a high incidence of carcinoma in situ (CIS) that is common in testicular biopsies from infertile men. CIS can transform into invasive cancer in 50% of cases [14,15]. Some of the systemic effects of cancer include fever, malignancy-related malnutrition, abnormal immune response, altered hormonal milieu, and a generalized stress and inflammatory response. This results in increased production of cytokines such as interleukins (ILs) and tumor necrosis factor (TNF), all of which can have devastating consequences on testicular and sperm function [16,17]. This may also result in chromosomal aneuploidy in the germ cells and sperm damage even prior to cancer treatment [18]. There is no relationship between the severity of male infertility and the stage of the malignancy. Therefore, it is important that oncologists address each cancer patient’s risk of fertility irrespective of the clinical diagnosis or the stage of the disease [19,20].
The future of sperm: a biovariability framework for understanding global sperm count trends
Published in Human Fertility, 2022
Marion Boulicault, Meg Perret, Jonathan Galka, Alex Borsa, Annika Gompers, Meredith Reiches, Sarah Richardson
Levine et al. (2017) are not the first or most recent researchers to suggest that contemporary social and physical environments harm sperm production in men. Debates over whether sperm counts are declining and what such decline might mean have been taking place for decades (Carlsen et al., 1992; Daniels, 2006; Nelson & Bunge, 1974; Sengupta, Dutta et al., 2017; Sengupta, Nwagha et al., 2017; Sengupta, Borges et al., 2018; Sengupta, Dutta et al., 2018, Swan & Colino, 2021). Recent research on sperm count decline is associated with a broader research programme postulating a rise in andrological pathologies, resulting from a hypothesised Testicular Dysgenesis Syndrome, or TDS (Akre & Richiardi, 2009; Skakkebaek et al., 2001). Here we focus our analysis on Levine and colleagues’ meta-analysis for three reasons.
Thyroid hypofunction in aging testicular cancer survivors
Published in Acta Oncologica, 2021
Ragnhild V. Nome, Milada Cvancarova Småstuen, Sophie D. Fosså, Cecilie E. Kiserud, Bjørn Olav Åsvold, Trine Bjøro
As neither RT nor CBCT is an established cause of thyroid hypofunction in TCSs, we speculate whether the TCSs as a group could be vulnerable to thyroid hypofunction irrespective of the testis cancer treatment. Hormonal disturbances related to the underlying pathology of testicular dysgenesis syndrome could theoretically also affect the risk of thyroid hypofunction. Environmental endocrine-disrupting chemical exposure in utero is suspected of affecting thyroid hormones [29–32] in addition to being an etiological factor of the testicular dysgenesis syndrome. This inherent risk is possibly enhanced by orchiectomy in TCSs. As such, these conditions could be a common cause for the thyroid hypofunction observed in the TCSs in addition to the effects from cancer treatment. Environmental disrupting chemicals are also debated as possible causes of both thyroid and testicular cancer [33]. The increased risk of thyroid cancer reported in TCSs [34,35] could support this possibility.
Relationship between maternal age and anogenital distance in patients with primary hypospadias: A case-control study
Published in Arab Journal of Urology, 2021
Khaled M. Abdelhalim, Ahmed I. El-Sakka
Fetal testis maldevelopment at an early gestational age can lead to testicular dysgenesis syndrome (TDS), which includes hypospadias, UDT, testicular germ cell tumour, and oligospermia. The ‘male programming window’ (MPW) is likely to be at 8–14 weeks of gestation during which time genital development is programmed and has been identified a critical period in both animals and humans [13].