Testicular dysgenesis syndrome: foetal origin of adult reproductive problems

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Testicular dysgenesis syndrome: foetal origin of adult reproductive problems. / Wohlfahrt-Veje, Christine; Main, Katharina M; Skakkebaek, Niels Erik.

In: Clinical Endocrinology, Vol. 71, No. 4, 2009, p. 459-65.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Wohlfahrt-Veje, C, Main, KM & Skakkebaek, NE 2009, 'Testicular dysgenesis syndrome: foetal origin of adult reproductive problems', Clinical Endocrinology, vol. 71, no. 4, pp. 459-65. https://doi.org/10.1111/j.1365-2265.2009.03545.x

APA

Wohlfahrt-Veje, C., Main, K. M., & Skakkebaek, N. E. (2009). Testicular dysgenesis syndrome: foetal origin of adult reproductive problems. Clinical Endocrinology, 71(4), 459-65. https://doi.org/10.1111/j.1365-2265.2009.03545.x

Vancouver

Wohlfahrt-Veje C, Main KM, Skakkebaek NE. Testicular dysgenesis syndrome: foetal origin of adult reproductive problems. Clinical Endocrinology. 2009;71(4):459-65. https://doi.org/10.1111/j.1365-2265.2009.03545.x

Author

Wohlfahrt-Veje, Christine ; Main, Katharina M ; Skakkebaek, Niels Erik. / Testicular dysgenesis syndrome: foetal origin of adult reproductive problems. In: Clinical Endocrinology. 2009 ; Vol. 71, No. 4. pp. 459-65.

Bibtex

@article{7a757ed068a411df928f000ea68e967b,
title = "Testicular dysgenesis syndrome: foetal origin of adult reproductive problems",
abstract = "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.",
author = "Christine Wohlfahrt-Veje and Main, {Katharina M} and Skakkebaek, {Niels Erik}",
note = "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",
year = "2009",
doi = "10.1111/j.1365-2265.2009.03545.x",
language = "English",
volume = "71",
pages = "459--65",
journal = "Clinical Endocrinology",
issn = "0300-0664",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

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

VL - 71

SP - 459

EP - 465

JO - Clinical Endocrinology

JF - Clinical Endocrinology

SN - 0300-0664

IS - 4

ER -

ID: 19977596