[Cryptorchidism]

Abstract

Cryptorchidism is the most frequent anomaly of an endocrine gland; it entails risks of infertility and testicular cancer. Its pathogenesis is thought to be multifactorial including anatomical and mechanical together with endocrine causes. In the last decades most Authors favoured the hypothesis that some degree of androgen insufficiency during fetal life may play a role in determining testicular maldescent. Morphological alterations have been demonstrated in cryptorchidism testes since birth; both tubular and interstitial damage already can be found in the first months of life. A critical phase in germinal development occurs during the third month when gonadotropin and testosterone postnatal surge induces the first maturational step in germ cells development. In cryptorchid infants, gonadotropin insufficiency at this time reduces germ cells differentiation, leading to progressive germinal decline, which becomes manifest after 12 months of life. In the opinion of some Authors, germinal alteration can be partially reversed by early scrotal reposition of the cryptorchid testes. Hormonal therapy with human chorionic gonadotropin (HCG) and luteinizing hormone releasing hormone (LHRH) has been used in the past decades with variable results. A combination of the two hormones has had a greater effect in inducing testicular descent compared to single hormone treatment. Although some surgeons already treat cryptorchid patients during childhood, an increasing number of pediatric surgeons believe that early treatment, performed during infancy is preferable, when considering the early and progressive histological damage seen in cryptorchid gonads. In our opinion, also hormonal treatment performed during the first year of life seems preferable since it can at the same time induce scrotal descent of cryptorchid testes and substitute postnatal gonadotropin insufficiency.