Hormonal Aspects of the Pathogenesis and Treatment of Cryptorchidism

Abstract

A normal functioning hypothalamic-pituitary-testicular axis is required for normal testicular descent. The percentage of cases that result from a disturbance in this axis remains controversial. Much has yet to be learnt about cryptorchidism, but is seems that the existence of A dark spermatogonia (Ad spermatogonia) is essential for later fertility. Bilateral cryptorchid patients have a high risk of later infertility, even though they undergo early surgery for cryptorchidism. It is possible today to distinguish-to a certain extent-between three different groups of cryptorchid patients based on testicular histology, gonadotropins, and inhibin B at the time of early surgery: Group 1, patients suspected of prepubertal transient hypothalamic-pituitary-testicular hypofunction and a high risk of later infertility; Group 2, patients with hypergonadotropic hypogonadism and a primary testicular dysfunction; and Group 3, patients with normal histology and normal serum levels of inhibin B and gonadotropins at the time of early surgery and a low risk of later infertility. Given the potential adverse effects of hormonal treatment, attention should be directed toward small doses of adjuvant gonadotropin-releasing hormone (GnRH) treatment for those who might benefit the most, that is, bilateral cryptorchid boys at early surgery without evidence of normal maturation of gonocytes into Ad spermatogonia. Optimally, gonadotropin levels in such patients should be measured to ensure that levels are not compensatory elevated, thereby supporting the suspicion of hypothalamic-pituitary-testicular hypofunction. Studies of GnRH-supplementary treatment should include testicular biopsy at surgery and at follow-up in childhood as well as examinations of fertility potential in adulthood.

Postnatal Testicular Activity in Healthy Boys and Boys With Cryptorchidism

“…Accordingly, a causal role for hormonal activity during minipuberty has been suggested (84). However, the role of gonadotropins and testicular hormones in this process has yet to be clarified and existing data on the role of androgens are controversial (85). The maturation of spermatogonia continues after minipuberty and some primary spermatocytes can be observed around 3–4 years of age (86).…”

Caveolin 1 Regulates the Tight Junctions between Sertoli Cells and Promotes the Integrity of Blood–Testis Barrier in Yak via the FAK/ERK Signaling Pathway

“…Cryptorchidism is constantly associated with decreased sperm motility, decreased sperm count, decreased sperm mass, and abnormal sperm morphology [8]. It is now recognized that cryptorchidism is caused by the failure of testicular descent to the scrotum, which is located in the abdominal cavity and subcutaneous fat layer, resulting in hyperthermia, ischemia, hypoxia and the thickening of the capillary endothelium [9]. These changes in the internal environment hinder the exchange of testosterone and nutrients between cells, and disrupt the tight junctions between Sertoli cells (SCs) and spermatogenic cells and between SCs and Sertoli cells.…”