Hypogonadism and Cryptorchidism.

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Abstract

Congenital cryptorchidism (undescended testis) is one of the most common congenital urogenital malformations in boys. Prevalence of cryptorchidism at birth among boys born with normal birth weight ranges from 1.8 to 8.4%. Cryptorchidism is associated with a risk of low semen quality and an increased risk of testicular germ cell tumors. Testicular hormones, androgens and insulin-like peptide 3 (INSL3), have an essential role in the process of testicular descent from intra-abdominal position into the scrotum in fetal life. This explains the increased prevalence of cryptorchidism among boys with diseases or syndromes associated with congenitally decreased secretion or action of androgens, such as patients with congenital hypogonadism and partial androgen insensitivity syndrome. There is evidence to support that cryptorchidism is associated with decreased testicular hormone production later in life. It has been shown that cryptorchidism impairs long-term Sertoli cell function, but may also affect Leydig cells. Germ cell loss taking place in the cryptorchid testis is proportional to the duration of the condition, and therefore early orchiopexy to bring the testis into the scrotum is the standard treatment. However, the evidence for benefits of early orchiopexy for testicular endocrine function is controversial. The hormonal treatments using human chorionic gonadotropin (hCG) or gonadotropin-releasing hormone (GnRH) to induce testicular descent have low success rates, and therefore they are not recommended by the current guidelines for management of cryptorchidism. However, more research is needed to assess the effects of hormonal treatments during infancy on future male reproductive health.

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Identification in rats of a programming window for reproductive tract masculinization, disruption of which leads to hypospadias and cryptorchidism.

Michael Hutchison, M Fisken, Richard Sharpe … (2008)

Becoming a phenotypic male is ultimately determined by androgen-induced masculinization. Disorders of fetal masculinization, resulting in hypospadias or cryptorchidism, are common, but their cause remains unclear. Together with the adult-onset disorders low sperm count and testicular cancer, they can constitute a testicular dysgenesis syndrome (TDS). Although masculinization is well studied, no unifying concept explains normal male reproductive development and its abnormalities, including TDS. We exposed rat fetuses to either anti-androgens or androgens and showed that masculinization of all reproductive tract tissues was programmed by androgen action during a common fetal programming window. This preceded morphological differentiation, when androgen action was, surprisingly, unnecessary. Only within the programming window did blocking androgen action induce hypospadias and cryptorchidism and altered penile length in male rats, all of which correlated with anogenital distance (AGD). Androgen-driven masculinization of females was also confined to the same programming window. This work has identified in rats a common programming window in which androgen action is essential for normal reproductive tract masculinization and has highlighted that measuring AGD in neonatal humans could provide a noninvasive method to predict neonatal and adult reproductive disorders. Based on the timings in rats, we believe the programming window in humans is likely to be 8-14 weeks of gestation.

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Klinefelter's syndrome.

Fabio Lanfranco, Axel Kamischke, Michael Zitzmann … (2015)

Klinefelter's syndrome is the most common genetic cause of human male infertility, but many cases remain undiagnosed because of substantial variation in clinical presentation and insufficient professional awareness of the syndrome itself. Early recognition and hormonal treatment of the disorder can substantially improve quality of life and prevent serious consequences. Testosterone replacement corrects symptoms of androgen deficiency but has no positive effect on infertility. However, nowadays patients with Klinefelter's syndrome, including the non-mosaic type, need no longer be considered irrevocably infertile, because intracytoplasmic sperm injection offers an opportunity for procreation even when there are no spermatozoa in the ejaculate. In a substantial number of azoospermic patients, spermatozoa can be extracted from testicular biopsy samples, and pregnancies and livebirths have been achieved. The frequency of sex chromosomal hyperploidy and autosomal aneuploidies is higher in spermatozoa from patients with Klinefelter's syndrome than in those from normal men. Thus, chromosomal errors might in some cases be transmitted to the offspring of men with this syndrome. The genetic implications of the fertilisation procedures, including pretransfer or prenatal genetic assessment, must be explained to patients and their partners.

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Consensus statement on management of intersex disorders.

I.A. Hughes, C. Houk, S.F. Ahmed … (2006)

The birth of an intersex child prompts a long-term management strategy that involves a myriad of professionals working with the family. There has been progress in diagnosis, surgical techniques, understanding psychosocial issues and in recognizing and accepting the place of patient advocacy. The Lawson Wilkins Paediatric Endocrine Society (LWPES) and the European Society for Paediatric Endocrinology (ESPE) considered it timely to review the management of intersex disorders from a broad perspective, to review data on longer term outcome and to formulate proposals for future studies. The methodology comprised establishing a number of working groups whose membership was drawn from 50 international experts in the field. The groups prepared prior written responses to a defined set of questions resulting from an evidence based review of the literature. At a subsequent gathering of participants, a framework for a consensus document was agreed. This paper constitutes its final form.