Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors. (October 2017)

• Record Type: Journal Article
• Authors: Bandak, M.; Jørgensen, N.; Juul, A.; Lauritsen, J.; Oturai, P.S.; Mortensen, J.; Hojman, P.; Helge, J.W.; Daugaard, G.
• Is Part Of: European journal of cancer. Volume 84(2017)
• Page Start: 9
• Page End: 17
• Publication Date: 2017-10
• Subjects: Testicular cancer -- Leydig cell dysfunction -- Metabolic syndrome; Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Cancer; Tumors; Electronic journals; Periodicals; Electronic journals; 616.994
• DOI: 10.1016/j.ejca.2017.07.006
• Languages: English
• ISSNs: 0959-8049

Abstract

Abstract: Background: Twenty to thirty percent of testicular cancer (TC) survivors have elevated serum levels of luteinising hormone (LH) with or without corresponding low testosterone levels (Leydig cell dysfunction) during clinical follow-up for TC. However, it remains to be clarified if this subgroup of TC survivors has an increased long-term risk of systemic inflammation and metabolic syndrome (MetS) when compared with TC survivors with normal Leydig cell function during follow-up. Patients and methods: TC survivors with Leydig cell dysfunction and a control group of TC survivors with normal Leydig cell function during follow-up were eligible for participation in the study. Markers of systemic inflammation and prevalence of MetS were compared between TC survivors with Leydig cell dysfunction and the control group. Results: Of 158 included TC survivors, 28 (18%) had uncompensated Leydig cell dysfunction, 59 (37%) had compensated Leydig cell dysfunction and 71 (45%) had normal Leydig cell function during follow-up. MetS and markers of systemic inflammation were evaluated at a median follow-up of 9.7 years (interquartile range 4.1–17.1) after TC treatment. The prevalence of MetS was significantly lower among patients with compensated Leydig cell dysfunction during follow-up (12% versus 27%, p = 0.04), whereas there was no difference between TC survivors with uncompensated Leydig cell dysfunction and controls (33% versus 27%, p = 0.5). Apart from high-sensitivity C-reactive protein which was higher in TC survivors with uncompensated Leydig cell dysfunction during follow-up, there was no evidence of increased systemic inflammation in patients with Leydig cell dysfunction during clinical follow-up. Total testosterone at follow-up was significantly associated with MetS, whereas there was no association between LH and MetS. Conclusion: We did not find evidence that TC survivors with Leydig cell dysfunction during clinical follow-up had increased long-term risk of MetS. Total testosterone at follow-up was significantly associated with MetS. The study is registered atwww.clinicaltrials.gov NCT02240966 . Highlights: Low serum levels of total testosterone were associated with metabolic syndrome. Elevated serum levels of luteinising hormone were not associated with metabolic syndrome. Low total testosterone and elevated luteinising hormone on >1 occasion is suggestive of testosterone deficiency. Testosterone treatment may reduce the risk of metabolic syndrome in testicular cancer survivors with testosterone deficiency.