Cryptorchidism: Testicular Dysgenesis Syndrome
One of the commonest disorders in newborn male infants is Cryptorchidism. During the last two decades, the prevalence of cryptorchidism among boys has varied from 2.1 to 8.4% in different countries. Testicular dysgenesis syndrome (TDS) is the consequence of disruption of embroyonal programming and gonadal development during fetal life and associated with symptoms like poor semen quality, testis cancer, undescended testis and hypospadias. Cryptorchidism being part of testicular dysgenesis syndrome involve genetic or extrinsic disturbance in steroid hormone metabolism, possibly through a perturbed hypothalamic, pituitary, genital axis. Cryptorchidism is related with impaired spermatogenesis and endocrine function and raises the risk of testicular
cancer. Several causative risk factors such as preterm birth and low birth weight, as well as environmental factor play a role in in the etiology of cryptorchidism. Testicular descent occurs in two phases. During the first phase, before mid gestation, testis remains anchored to the inguinal area by insulin like hormone 3 (INSL3)-driven development of the gubernaculum. The second inguinoscrotal phase is dependent on testicular androgens and it is usually completed by the time of birth. Recently, leydig insulin like hormones (INSL3) proposed as putative trophic hormone who absence in male mice result in bilateral cryptorchidism and mutation involving this gene. INSL3 expression in fetal testis is inhibited by maternal exposure to estrogens. But in man, the only sequence variant was an amino acid substitution in a C-peptide of molecule which is also observed in normal fertile man suggesting that involvement of human INSL3 gene is not the main cause of cryptorchidism in man.
cancer. Several causative risk factors such as preterm birth and low birth weight, as well as environmental factor play a role in in the etiology of cryptorchidism. Testicular descent occurs in two phases. During the first phase, before mid gestation, testis remains anchored to the inguinal area by insulin like hormone 3 (INSL3)-driven development of the gubernaculum. The second inguinoscrotal phase is dependent on testicular androgens and it is usually completed by the time of birth. Recently, leydig insulin like hormones (INSL3) proposed as putative trophic hormone who absence in male mice result in bilateral cryptorchidism and mutation involving this gene. INSL3 expression in fetal testis is inhibited by maternal exposure to estrogens. But in man, the only sequence variant was an amino acid substitution in a C-peptide of molecule which is also observed in normal fertile man suggesting that involvement of human INSL3 gene is not the main cause of cryptorchidism in man.