{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T07:05:55Z","timestamp":1784099155611,"version":"3.55.0"},"reference-count":39,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,6,15]],"date-time":"2005-06-15T00:00:00Z","timestamp":1118793600000},"content-version":"vor","delay-in-days":7258,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[1985,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>This ultrastructural and quantitative study of Leydig cells in Klinefelter's syndrome has been performed using the entire testes obtained from four autopsies plus testicular biopsies from 20 patients. The total Leydig cell volume per testis in Klinefelter's syndrome was similar to that of control testes. However, the total number of Leydig cells per testis was significantly lower in the patients with Klinefelter's syndrome than in the controls. This may be attributed to the Leydig cell hypertrophy that these patients underwent. In patients with Klinefelter's syndrome the average volume of each Leydig cell was significantly higher than that of the controls. Electron microscopic findings revealed that besides ultrastructurally normal Leydig cells there were three other morphologically abnormal Leydig cell types: abnormally differentiated cells; multivacuolated cells; and immature Leydig cells. The ultrastructurally normal Leydig cells were probably the cells principally responsible for testosterone biosynthesis in these patients, whereas the other Leydig cell types were probably barely or not at all functional. The hypertrophy showed by the ultrastructurally normal Leydig cells may be interpreted as an attempt to increase testosterone production.<\/jats:p>","DOI":"10.1002\/path.1711460405","type":"journal-article","created":{"date-parts":[[2005,6,22]],"date-time":"2005-06-22T10:33:19Z","timestamp":1119436399000},"page":"323-331","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Quantitative and ultrastructural study of Leydig cells in klinefelter's syndrome"],"prefix":"10.1002","volume":"146","author":[{"given":"M.","family":"Nistal","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Santamaria","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Paniagua","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,6,15]]},"reference":[{"key":"e_1_2_1_2_2","first-page":"671","article-title":"Etude en microscope e\u00e9lectronique de la cellule de Leydig dans la maladie de Klinefelter en p\u00e9riodes pre, per et postpubertaires","volume":"32","author":"Rubin P","year":"1971","journal-title":"Ann Endocrinol"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1439-0272.1979.tb02185.x"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-33-4-683"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0046-8177(82)80132-9"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-25-10-1325"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5347(17)55685-2"},{"key":"e_1_2_1_8_2","first-page":"552","article-title":"Indirect evidence of chronic Leydig cells desensitization in Klinefelter's syndrome","volume":"96","author":"Smals AG","year":"1981","journal-title":"Acta Endocrinol"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02889055"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0046-8177(84)80059-3"},{"key":"e_1_2_1_11_2","first-page":"851","article-title":"Syndrome de Klinefelter. 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