Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors

TY - JOUR

T1 - Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors

AU - Bandak, M

AU - Jørgensen, N

AU - Juul, A

AU - Lauritsen, J

AU - Oturai, P S

AU - Mortensen, J

AU - Hojman, P

AU - Helge, J W

AU - Daugaard, G

N1 - Copyright © 2017 Elsevier Ltd. All rights reserved.

PY - 2017/10

Y1 - 2017/10

N2 - 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 at www.clinicaltrials.govNCT02240966.

AB - 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 at www.clinicaltrials.govNCT02240966.

KW - Adult

KW - Biomarkers

KW - Case-Control Studies

KW - Denmark

KW - Hormone Replacement Therapy

KW - Humans

KW - Inflammation

KW - Leydig Cells

KW - Luteinizing Hormone

KW - Male

KW - Metabolic Syndrome X

KW - Middle Aged

KW - Prevalence

KW - Protective Factors

KW - Risk Factors

KW - Survivors

KW - Testicular Neoplasms

KW - Testosterone

KW - Time Factors

KW - Treatment Outcome

KW - Journal Article

U2 - 10.1016/j.ejca.2017.07.006

DO - 10.1016/j.ejca.2017.07.006

M3 - Journal article

C2 - 28772110

SN - 0959-8049

VL - 84

SP - 9

EP - 17

JO - European Journal of Cancer

JF - European Journal of Cancer

ER -