男子不妊症の内分泌動態

Abstract

精子形成の内分泌学的コントロールを検討する目的で77例の無精子症および乏精子症(精子数50×106/ml以下)について, testosterone (T), luteinizing hormone (LH), follicle-stimulating hormone (FSH)を測定し, 精巣生検による組織像を検索した.軽度の乏精子症(10～50×106/ml)と比べ無精子症では血清T濃度が有意に低かった.無精子症や高度の乏精子症(10×106/ml以下)では軽度の乏精子症と比べ血清LHやFSHが有意に高かった.血中ゴナドトロピン高値の症例の精巣組織所見は, 胚細胞欠乏もしくはLeydig細胞過形成を伴っていた.今回の成績から, 精子形成とゴナドトロピン分泌との間に何らかのfeed-back機構が存在する, もしくは精細管の高度の機能障害がLeydig細胞機能を抑制することが示唆された

To study the endocrine control of spermatogenesis, we measured the concentrations of testosterone (T), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in 77 patients with azoospermia or oligozoospermia (less than 50×10[6]/ml), as well as the histological index of testicular biopsy specimens investigated. Serum T concentration in patients with azoospermia was significantly lower than that in patients with mild oligozoospermia (10-50×10[6]/ml). Both serum LH and FSH were significantly higher in the patients with azoospermia or severe oligozoospermia (less than 10×10[6]/ml

ml) than in those with mild oligozoospermia. The histologic appearance of the testis of the patients who had elevated gonadotropins was accompanied by germ cell depletion and Leydig cell hyperplasia. These results suggest that there may be some feed-back mechanism between spermatogenesis and gonadotropin secretion and that severe functional disorder of the seminiferous tubules may inhibit Leydig cell function.