Preorchiectomy Leydig Cell Dysfunction in Patients With Testicular Cancer

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• 作者：Mikkel Bandak¹ ; ^{mikkel.bandak@regionh.dk} ; Niels Jø ; rgensen² ; ³ ; Anders Juul² ; ³ ; Jakob Lauritsen¹ ; Maria Gry Gundgaard Kier¹ ; ⁴ ; Mette Saksø ; Mortensen¹ ; Gedske Daugaard¹
• 关键词：Estradiol ; Luteinizing hormone ; Reproductive hormones ; Testicular germ cell cancer ; Testosterone
• 刊名：Clinical Genitourinary Cancer
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：15
• 期：1
• 页码：e37-e43
• 全文大小：503 K
• 卷排序：15

文摘

Little is known about preorchiectomy Leydig cell function in patients with testicular germ cell cancer (TGCC). The aim was to estimate the prevalence of preorchiectomy Leydig cell dysfunction and evaluate factors associated with this condition in a cohort of patients with TGCC.Patients and MethodsWe evaluated luteinizing hormone (LH), total testosterone (TT), calculated free T (cFT), estradiol, and sex hormone–binding globulin (SHBG) preorchiectomy in 561 patients with TGCC and compared with 561 healthy controls. We calculated TT/LH and cFT/LH ratios and constructed bivariate charts of TT/LH and cFT/LH from the controls. Logistic regression analysis with an abnormal cFT/LH ratio as outcome and clinical stage, tumor size, age, histology, presence of contralateral germ cell neoplasia in situ (GCNIS), and bilateral tumors as covariates was performed.ResultsIn patients who were negative for human chorionic gonadotropin (hCG) (n = 374), TT (P = .004), cFT (P < .001), TT/LH ratio (P = .003), and cFT/LH ratio (P = .002) were lower than in controls. A total of 95 (25%) and 91 (24%) of hCG-negative patients had abnormal values when using combined evaluation of TT/LH and cFT/LH, respectively. Increasing tumor size, contralateral GCNIS, and increasing age were associated with Leydig cell dysfunction. In patients positive for hCG (n = 187), all reproductive hormones except SHBG were different from controls (P < .001).ConclusionPatients with TGCC are at increased risk of Leydig cell dysfunction before orchiectomy. Contralateral GCNIS, increasing age, and increasing tumor size are associated with Leydig cell dysfunction. We hypothesize that patients with preexisting Leydig cell dysfunction are at increased risk of testosterone deficiency following treatment.