Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors
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Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors. / Bandak, M; Jørgensen, N; Juul, A; Lauritsen, J; Oturai, P S; Mortensen, J; Hojman, P; Helge, J W; Daugaard, G.
I: European Journal of Cancer, Bind 84, 10.2017, s. 9-17.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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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
VL - 84
SP - 9
EP - 17
JO - European Journal of Cancer, Supplement
JF - European Journal of Cancer, Supplement
SN - 0959-8049
ER -
ID: 184740188