Abstract

Verkauskasa et al. are to be commended on the depth of their investigation on hormonal parameters and histological changes in boys with cryptorchidism [1]. The overall finding of the study, which is that Ad spermatogonia counts decrease with age of cryptorchid testis biopsy, is consistent with other studies and highlights the need for prompt treatment of cryptorchid patients after 6 months of age [2]. In the subgroup that had a high risk of infertility because of absence of Ad spermatogonia stem cells, the LH levels were lower than expected, consistent with this subgroup having a hypogonadotropic hypogonadism. However, this group is small, less than 20% of the total sample. While the Ad numbers were low in the patients studied, it appears that the count was zero in only 21/51 pts (i.e. the majority of testes showed some germ cell maturation). The authors claim that transformation of gonocytes into Ad spermatogonia is testosterone dependent; however, there are also contrary animal and human studies which show that, even in complete androgen insensitivity, Ad spermatogonia appear normal initially. This would suggest that gonocyte transformation into Ad spermatogonia may be androgen-independent. Furthermore, several recent studies in animals and humans show that the pathogenesis and etiology of isolated cryptorchidism is likely multifactorial and in most cases unknown [3]. The bottom line is this: while men with a history of unilateral cryptorchidism tend to have lower sperm counts than the normal

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