[Endocrinological and histomorphological studies of testicular atrophy in myotonic dystrophy (author's transl)].
Testicular atrophy in myotonic dystrophy is caused by a primary and progressive atrophy of the seminiferous tubules. Endocrinological studies with synthetic LH(ICSH)-RH in two patients demonstrated the complete absence of FSH feed back mechanism. Glycogen content was markedly diminished or completely absent, as demonstrated histochemically, both in the morphologically intact and in damaged tubules. The endocrinological and morphological results both demonstrate that insufficiency of the Sertoli cells is the primary damage in the pathogenesis of testicular atrophy in myotonic dystrophy.
D000324:Adrenocorticotropic Hormone; D000328:Adult; D000367:Age Factors; D001284:Atrophy / Q000378:metabolism; D003907:Dexamethasone; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D006801:Humans; D007986:Luteinizing Hormone / Q000378:metabolism; D008297:Male; D008797:Metyrapone; D009223:Myotonic Dystrophy / Q000150:complications* / Q000175:diagnosis / Q000378:metabolism; D013733:Testicular Diseases / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D013739:Testosterone / Q000378:metabolism
D013739:Testosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D008797:Metyrapone
Endokrinologische und histomorphologische Untersuchungen zur Hodenatrophie bei Dystrophia myotonica