{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:01:20Z","timestamp":1761058880351},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"4","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1981,4]]},"abstract":"<jats:title>Abstract.<\/jats:title>\n<jats:p>The basal plasma 17\u03b1-hydroxyprogesterone (17-OHP) and testosterone (T) levels were proportionally decreased in 10 hypergonadotropic patients with Klinefelter's syndrome. The ratio 17-OHP to T was however about twice as high as in 10 eugonadal male controls, suggesting the presence of a block in the conversion of 17-hydroxylated steroids to androgens in the Klinefelter patients under basal circumstances. Administration of human chorionic gonadotrophin (hCG, 1500 IU im daily for 3 days) to the Klinefelter patients disclosed a response pattern quite different from that observed in controls. In the control subjects 17-OHP and the ratio 17-OHP\/T sharply rose to maximum values at 24 h after the first injection. Thereafter both progressively fell to lowest values at 72 h, when T levels reached their maximum. In the Klinefelter patients the T response to hCG administration was greatly diminished but the 17-OHP response was similar to that in the controls. Maximum 17-OHP and 17-OHP\/T values however were not achieved until 72 h after the first injection when T levels also reached their maximum. Unlike in the controls in the Klinefelter patients maximum 17-OHP and T increments and the 17-OHP and T levels 48 and 72 h after the injection were positively correlated.<\/jats:p>\n<jats:p>Together the findings of a decreased T synthesis and reserve in the presence of relative 17-OHP accumulation, further increasing after acute hCG administration in a pattern quite different from that in normal men, suggest that in Klinefelter's syndrome the Leydig cells may be chronically desensitized by the persistent endogenous hypergonadotropism.<\/jats:p>","DOI":"10.1530\/acta.0.0960552","type":"journal-article","created":{"date-parts":[[2008,12,15]],"date-time":"2008-12-15T21:36:12Z","timestamp":1229376972000},"page":"552-556","update-policy":"http:\/\/dx.doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":7,"title":["Indirect evidence of chronic Leydig cell desensitization in Klinefelter's syndrome"],"prefix":"10.1093","volume":"96","author":[{"given":"Anthony G.","family":"Smals","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerlach F.","family":"Pieters","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter W.","family":"Kloppenborg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","container-title":["Acta Endocrinologica"],"original-title":[],"link":[{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/96\/4\/acta_96_4_019.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/96\/4\/acta_96_4_019.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,2,14]],"date-time":"2023-02-14T16:10:49Z","timestamp":1676391049000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ejendo\/article\/96\/4\/552\/6803738"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1981,4]]},"references-count":0,"journal-issue":{"issue":"4"},"URL":"https:\/\/doi.org\/10.1530\/acta.0.0960552","relation":{},"ISSN":["0804-4643","1479-683X"],"issn-type":[{"value":"0804-4643","type":"print"},{"value":"1479-683X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1981,4]]}}}