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The urinary tract and male reproductive system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Luis Beltran, Daniel M. Berney
Cryptorchidism, or maldescent, is the most common congenital abnormality. The testis may reside at any point along its path of descent. Spermatogenesis will proceed satisfactorily only in the lower temperature of the scrotum, and cryptorchidism is therefore a significant cause of male infertility. Maldescent is also an important predisposing factor for testicular germ cell tumours, both within the undescended testis and in the contralateral organ, even if it is normally located in the scrotum. It is therefore important to investigate the position of the testis in male infants and, if possible, to bring any undescended testis down into the scrotum (orchidopexy). Better imaging and laparoscopy now enable the urologist to locate the intra-abdominal testis in a non-invasive manner and to remove it if it cannot be brought down into the scrotum surgically. This will also reveal rare cases of anorchia (congenital absence of the testis) and those of the vanishing testis, where only epididymal remnants are identified at the site of the testis with no remaining testicular tubules present.
Developmental abnormalities of the genitalia: intersex, hypospadias, and cryptorchidism
Published in J Kellogg Parsons, E James Wright, The Brady Urology Manual, 2019
Müllerian-inhibiting substance (MIS), inhibin B, and FSH levels: Increased FSH in a prepubescent boy suggests anorchia.
Microsurgery Techniques in Andrology *
Published in Waldemar L. Olszewski, CRC Handbook of Microsurgery, 2019
The absence of testis in the scrotum may be a result of the following conditions: agenesis of the testis and maldescended testicle (ectopic and cryptorchic). A patient with no elevation in testosterone after an adequate trial of chorionic gonadotropin is certainly anorchic and surgical exploration is not indicated. If, however, the gonadotropin test is positive, surgical intervention is necessary to bring the testicle down into the scrotum when the peritoneal sac does not extend further than the testicle. Generally, if a cryptorchic testis is palpable either at the external ring or in the inguinal canal, one should expect to be able to bring it to the scrotum without any complicated microvascular procedures. The spermatic artery anastomoses to the epigastric artery should be done by means of microsurgical technique. This opens up new possibilities in those cryptorchids with spermatic vessels that are too short.33–36
Usefulness of routine assessment of free testosterone for the diagnosis of functional male hypogonadism
Published in The Aging Male, 2022
Paolo Facondo, Elena Di Lodovico, Letizia Chiara Pezzaioli, Carlo Cappelli, Alberto Ferlin, Andrea Delbarba
Male hypogonadism is a clinical syndrome resulting from a failure of the testis to produce physiological concentrations of testosterone (T) and/or a normal number of spermatozoa, due to a testicular impairment (primary hypogonadism) or an alteration at the hypothalamus-pituitary axis (secondary hypogonadism)[1–3]. The main causes of primary hypogonadism are Klinefelter syndrome, cryptorchidism, testicular trauma, anorchia or iatrogenic testicular damage, while some causes of secondary hypogonadism are obesity, use of opioids and pituitary diseases [1]. Moreover, hypogonadism can be classified as organic or functional [2,4]: the organic form is generally an irreversible condition due to pathological perturbations of the hypothalamic-pituitary-testis (HPT) axis, whereas functional hypogonadism is a syndrome occurring in the absence of structural impairment of HPT axis [2]. The latter is frequent in middle-aged or older men (often referred in this case to as late-onset or adult-onset hypogonadism) with co-morbidities [such as obesity [5], metabolic syndrome [6], diabetes mellitus type 2 [7], cardiopathies [2], hepatopathy [2], multi-therapy [2], Human Immunodeficiency Virus (HIV) [8,9]] and it may be potentially reversible if the underlying causes are treated or removed [2].
Safety of testosterone therapy in men with prostate cancer
Published in Expert Opinion on Drug Safety, 2019
Abraham Morgentaler, Monica Caliber
By the 1980s it was axiomatic that high T levels contributed to the development of PCa and its aggressive nature, and that low levels of T were protective [50]. These two ‘arms’ of the androgen hypothesis prevented any use of TTh except in the most severe cases of T deficiency in young men, such as the presence of pituitary tumors, or following pituitary resection, or anorchia, as it was clear that these young men required testosterone for male development and function. The first direct evidence that the androgen hypothesis was flawed was the observation that men with symptomatic low T levels, normal PSA and normal DRE had a surprisingly high rate (14%) of PCa on sextant biopsy [51]. Since then, a growing number of studies have demonstrated that low levels of total [52,53], free [53–55] or bioavailable [55] serum testosterone at PCa diagnosis are associated with more aggressive PCa, biochemical recurrence, and predict poor PCa survival. A meta-analysis of endogenous T levels and PCa prognosis found that in patients with advanced PCa higher testosterone levels before ADT were associated with a 42% reduced risk of death (HR = 0.58; 95% CI, 0.45–0.74; P < .0001) [56].
Systematic review of hormone replacement therapy in the infertile man
Published in Arab Journal of Urology, 2018
Amr El Meliegy, Ahmad Motawi, Mohamed Ahmed Abd El Salam
The term primary hypergonadotrophic hypogonadism refers to testicular disorders and is characterised by low serum testosterone despite high levels of FSH and LH. Low testosterone production results in impaired spermatogenesis (primary testicular failure) as seen in congenital anorchia, undescended testis, Sertoli cell only syndrome (germ cell aplasia), or after testicular injury from trauma, infection, surgery, exposure to chemo/radiotherapy or drug induced (e.g. ketoconazole, flutamide, spironolactone, etc.). In addition, genetic causes for primary testicular failure are described such as numerical chromosome aberrations including: Klinefelter syndrome, XX-male syndrome, XYY syndrome and Y chromosome microdeletions [16].