(第32回泌尿器科中部連合総会特別講演)精巣生検よりみた特発性男子不妊症

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We have been studying the cause of idiopathic male infertility by means of testicular biopsy, and already have made several reports. This is a summary of these reports and a presentation of our concept for hypothetic pathogenesis of idiopathic infertile testes. Testicular biopsies were performed by Charny's accepted technique and tissues examined by light microscopic, histochemical, and transmission and scanning electron microscopic procedures. Also the circulatory sexual hormones; follicle stimulating hormone, luteinizing hormone, and testosterone of all patients were measured. The primary pathogenetic changes occur in the seminiferous tubular walls which are thickened by increase in immature collagen fibers and lamellation of seminiferous basement membrane, and they are followed by increase of follicle stimulating hormone. These seminiferous tubular changes occur discontinuously, so the idiopathic infertile seminiferous tubules resemble a rope strangulated in various places, or a tail-like rope gradually becoming thinner. Also, activated mast cells increase around the strangulated places. Thus, spermatogenesis in strangulated tubular parts decreases because of the nutritional disturbance caused by thickened tubular walls, and the strangulation of tubules interferes with the travel of sperms in the seminiferous tubules by interrupted seminiferous tubular peristalsis. Sloughing or disorganization in the infertile seminiferous tubules can be observed. In the infertile testes, Leydig cells generally increase with the elevation in the level of luteinizing hormone, but serum testosterone does not increase. And this normal value of serum testosterone is statistically found to be caused by the degradation in the quality of Leydig cells in idiopathic infertile testes. Also, galactose deficiency in glycoproteins of idiopathic infertile testicular tissue is reported.
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(第32回泌尿器科中部連合総会特別講演)精巣生検よりみた特発性男子不妊症

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