Abstract

Cryptorchidism is common in infants born preterm, yet the mechanism for its occurrence is still debated. In a study of 21 premature babies with cryptorchidism at 18 months post-term and 21 case matched controls, cryptorchid preterm infants failed to show the normal rise in plasma testosterone in the first postnatal week. This rise is thought to relate to residual maternal human chorionic gonadotrophin in the neonatal circulation. Infants with cryptorchidism also failed to show the later testosterone surge in the second month which has been related to endogenous gonadotrophin release. We speculate that inadequate stimulation of testosterone release by human chorionic gonadotrophin in the fetus might contribute to the pathogenesis of cryptorchidism in preterm infants. Our findings have implications for the medical treatment or possible prophylaxis of undescended testes in premature babies.