title: Testicular dysgenesis syndrome: possible role of endocrine disrupters.
abstract: The testicular dysgenesis syndrome (TDS) hypothesis proposes that the four conditions cryptorchidism, hypospadias, impaired spermatogenesis and testis cancer may all be manifestations of disturbed prenatal testicular development. The TDS hypothesis is based on epidemiological, clinical and molecular studies, all suggestive of an interrelation between the different symptoms. The aetiology of TDS is suspected to be related to genetic and/or environmental factors, including endocrine disrupters. Few human studies have found associations/correlations between endocrine disrupters, including phthalates, and the different TDS components. However, for ethical reasons, evidence of a causal relationship between prenatal exposure and TDS is inherently difficult to establish in human studies, rendering the recently developed animal TDS model an important tool for investigating the pathogenesis of TDS. Clinically, the most common manifestation of TDS is probably a reduced sperm concentration, whereas the more severe form may include a high risk of testis cancer. Clinicians should be aware of the interconnection between the different features of TDS, and inclusion of a programme for early detection of testis cancer in the management of infertile men with poor semen quality is recommended.
authors.affiliation: University Department of Growth and Reproduction, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark. katrine.bay@rh.hosp.dk
authors.forename: Katrine
authors.initials: K
authors.lastname: Bay
authors.forename: Camilla
authors.initials: C
authors.lastname: Asklund
authors.forename: Niels E
authors.initials: NE
authors.lastname: Skakkebaek
authors.forename: Anna-Maria
authors.initials: AM
authors.lastname: Andersson
mesh_terms: D003456:Cryptorchidism / Q000139:chemically induced; D052244:Endocrine Disruptors / Q000633:toxicity*; D005060:Europe / Q000453:epidemiology; D005260:Female; D006059:Gonadal Dysgenesis / Q000139:chemically induced*; D006801:Humans; D007021:Hypospadias / Q000139:chemically induced; D007248:Infertility, Male / Q000139:chemically induced; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D012661:Semen / Q000166:cytology; D013577:Syndrome; D013733:Testicular Diseases / Q000139:chemically induced*; D013736:Testicular Neoplasms / Q000139:chemically induced / Q000453:epidemiology; D013737:Testis / Q000196:embryology
chemical_list: D052244:Endocrine Disruptors