TY - JOUR
T1 - Testicular dysgenesis syndrome: foetal origin of adult reproductive problems
AU - Wohlfahrt-Veje, Christine
AU - Main, Katharina M
AU - Skakkebaek, Niels Erik
N1 - Keywords: Adult; Animals; Cryptorchidism; Disease Models, Animal; Endocrine Disruptors; Female; Follicle Stimulating Hormone; Gonadal Dysgenesis; Humans; Hypospadias; Infertility, Male; Luteinizing Hormone; Male; Pregnancy; Rats; Syndrome; Testicular Neoplasms; Testis
PY - 2009
Y1 - 2009
N2 - The evidence for the existence of testicular dysgenesis syndrome (TDS) is presented in this review. Several epidemiological studies have shown that conditions like cryptorchidism, impaired spermatogenesis, hypospadias and testicular cancer can be associated as risk factors for each other. Thus, the risk of testis cancer is significantly increased in men with cryptorchidism and/or infertility. Several recent studies point towards early dysgenesis of the foetal testis as the biological link between these disorders. Dysgenesis has been demonstrated in biopsies of the contralateral testis of men with testis cancer and in infertile men. The histological evidence includes immature seminiferous tubules with undifferentiated Sertoli cells, microliths and Sertoli-cell only tubules. Dysgenetic testes often have an irregular ultrasound pattern, where microliths may also be visible. Our current hypothesis is that maternal exposure to endocrine disrupting chemicals may contribute to the pathogenesis of TDS. Animal experiments have shown that all TDS symptoms, except testicular cancer, can be induced by foetal exposure to anti-androgenic chemicals. However, the cause of TDS in humans remains to be determined.
AB - The evidence for the existence of testicular dysgenesis syndrome (TDS) is presented in this review. Several epidemiological studies have shown that conditions like cryptorchidism, impaired spermatogenesis, hypospadias and testicular cancer can be associated as risk factors for each other. Thus, the risk of testis cancer is significantly increased in men with cryptorchidism and/or infertility. Several recent studies point towards early dysgenesis of the foetal testis as the biological link between these disorders. Dysgenesis has been demonstrated in biopsies of the contralateral testis of men with testis cancer and in infertile men. The histological evidence includes immature seminiferous tubules with undifferentiated Sertoli cells, microliths and Sertoli-cell only tubules. Dysgenetic testes often have an irregular ultrasound pattern, where microliths may also be visible. Our current hypothesis is that maternal exposure to endocrine disrupting chemicals may contribute to the pathogenesis of TDS. Animal experiments have shown that all TDS symptoms, except testicular cancer, can be induced by foetal exposure to anti-androgenic chemicals. However, the cause of TDS in humans remains to be determined.
U2 - 10.1111/j.1365-2265.2009.03545.x
DO - 10.1111/j.1365-2265.2009.03545.x
M3 - Journal article
C2 - 19222487
SN - 0300-0664
VL - 71
SP - 459
EP - 465
JO - Clinical Endocrinology
JF - Clinical Endocrinology
IS - 4
ER -
