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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

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 tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Bandak, M, Jørgensen, N, Juul, A, Lauritsen, J, Oturai, PS, Mortensen, J, Hojman, P, Helge, JW & Daugaard, G 2017, 'Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors', European Journal of Cancer, bind 84, s. 9-17. https://doi.org/10.1016/j.ejca.2017.07.006

APA

Bandak, M., Jørgensen, N., Juul, A., Lauritsen, J., Oturai, P. S., Mortensen, J., ... Daugaard, G. (2017). Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors. European Journal of Cancer, 84, 9-17. https://doi.org/10.1016/j.ejca.2017.07.006

Vancouver

Bandak M, Jørgensen N, Juul A, Lauritsen J, Oturai PS, Mortensen J o.a. Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors. European Journal of Cancer. 2017 okt;84:9-17. https://doi.org/10.1016/j.ejca.2017.07.006

Author

Bandak, M ; Jørgensen, N ; Juul, A ; Lauritsen, J ; Oturai, P S ; Mortensen, J ; Hojman, P ; Helge, J W ; Daugaard, G. / Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors. I: European Journal of Cancer. 2017 ; Bind 84. s. 9-17.

Bibtex

@article{4cdf5d6d6ace4a4298aa1ff8ca1892d8,
title = "Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors",
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 at www.clinicaltrials.govNCT02240966.",
keywords = "Adult, Biomarkers, Case-Control Studies, Denmark, Hormone Replacement Therapy, Humans, Inflammation, Leydig Cells, Luteinizing Hormone, Male, Metabolic Syndrome X, Middle Aged, Prevalence, Protective Factors, Risk Factors, Survivors, Testicular Neoplasms, Testosterone, Time Factors, Treatment Outcome, Journal Article",
author = "M Bandak and N J{\o}rgensen and A Juul and J Lauritsen and Oturai, {P S} and J Mortensen and P Hojman and Helge, {J W} and G Daugaard",
note = "Copyright {\circledC} 2017 Elsevier Ltd. All rights reserved.",
year = "2017",
month = "10",
doi = "10.1016/j.ejca.2017.07.006",
language = "English",
volume = "84",
pages = "9--17",
journal = "European Journal of Cancer",
issn = "0959-8049",
publisher = "Pergamon",

}

RIS

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

JF - European Journal of Cancer

SN - 0959-8049

ER -

ID: 184740188