cyproterone and Hypospadias

1. Malformations and functional disturbances of the male genitalia may be caused by teratogens. 2. A short review of the prenatal development points out the possible sites of action. 3. In animals some distinct teratogens produce typical malformation syndromo spermatogenetic cells. Cyproteronacetat, an antiandrogen, suppresses the development of the accessoric genital organs and produces an external feminisation. 4. In man, cryptorchidism, agenesis of the spermatic tracts, anorchia and hypospady are known as non-hereditary malformations. 5. The teratogenic etiology of some disturbances of the spermatogenesis is discussed.. In males, malformations of the exterior genitalia, and perhaps sperm absence or malfunction, can be traced to teratogenic disturbances. In rats, Busulfan administered in pregnancy can cause destruction of gonocytes and lack of spermatogenesis in adult male rats. Cyproterone acetate taken in pregnancy interferes with development of the Wolff passages, so that adult male rats lack the accessory genitals and suffer from exterior feminism. Other toxics possibly responsible for damage to the prenatal male genital system include antiandrogens, estrogens, testosterone, cytostatics, antimetabolites, antibiotics, and tranquilizers. In man cryptorchidism or testicle dystopis is accessible to therapy if treated early by administration of 250-500 E/Woche human chorionic gonodotropin 10 times a week, or later by operation to relocate the testicles. Spermatogenic disturbances occur in 1% of the male population and are extremely difficult to treat. Testicle aplasia may be treated with androgen substitution and epispadia and hypospadia may be improved by operative procedures. The rare cases of anochia, aphallia, and agenisis of spermatic tracts do not respond to treatment.

Topics: Abnormalities, Drug-Induced; Adult; Busulfan; Cryptorchidism; Cyproterone; Female; Genitalia, Male; Humans; Hypospadias; Infant, Newborn; Infertility, Male; Male; Pregnancy; Spermatogenesis