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High risk of hypogonadism in young male cancer survivors

Isaksson, S. LU ; Bogefors, K. LU ; Ståhl, O. LU ; Eberhard, J. LU ; Giwercman, Y. L. LU ; Leijonhufvud, I. LU ; Link, K. ; Øra, I. LU ; Romerius, P. LU and Bobjer, J. LU , et al. (2018) In Clinical Endocrinology 88(3). p.432-441
Abstract

Objective: Cancer and its treatment in childhood and young adulthood can cause hypogonadism, leading to increased risk of long-term morbidity and mortality. The aim of this study was to evaluate the risk of presenting with biochemical signs of hypogonadism in testicular cancer survivors (TCS) and male childhood cancer survivors (CCS) in relation to the type of treatment given. Design: Case-control study. Patients: Ninety-two TCS, 125 CCS (mean age 40 and median age 34 years, respectively; mean follow-up time 9.2 and 24 years, respectively) and a corresponding number of age-matched controls. Measurements: Fasting morning blood samples were analysed for total testosterone (TT), follicle-stimulating hormone (FSH) and luteinizing hormone... (More)

Objective: Cancer and its treatment in childhood and young adulthood can cause hypogonadism, leading to increased risk of long-term morbidity and mortality. The aim of this study was to evaluate the risk of presenting with biochemical signs of hypogonadism in testicular cancer survivors (TCS) and male childhood cancer survivors (CCS) in relation to the type of treatment given. Design: Case-control study. Patients: Ninety-two TCS, 125 CCS (mean age 40 and median age 34 years, respectively; mean follow-up time 9.2 and 24 years, respectively) and a corresponding number of age-matched controls. Measurements: Fasting morning blood samples were analysed for total testosterone (TT), follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The odds ratios (OR) for hypogonadism, defined as primary, secondary, compensated or ongoing androgen replacement, were calculated for TCS and CCS and for subgroups defined by diagnosis and treatment. Results: Hypogonadism was found in 26% of CCS and 36% of TCS, respectively (OR: 2.1, P = .025 and OR = 2.3, P = .021). Among CCS, the OR was further increased in those given testicular irradiation (OR = 28, P = .004). Radiotherapy other than cranial or testicular irradiation plus chemotherapy, or cranial irradiation without chemotherapy, associated also with increased ORs (OR = 3.7, P = .013, and OR = 4.4, P = .038, respectively). Among TCS, those receiving >4 cycles of cisplatin-based chemotherapy had OR = 17, P = .015. Conclusions: Biochemical signs of testosterone deficiency are recognized as markers of decreased life expectancy. Thus, the risk of hypogonadism in TCS and CCS should be recognized and emphasizes the need of long-term follow-up for these men.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Childhood cancer, Cytotoxic drugs, Hypogonadism, Radiotherapy, Testicular neoplasms
in
Clinical Endocrinology
volume
88
issue
3
pages
432 - 441
publisher
Wiley-Blackwell
external identifiers
  • pmid:29245176
  • scopus:85040180618
ISSN
0300-0664
DOI
10.1111/cen.13534
language
English
LU publication?
yes
id
20142aef-ca51-47e8-a6f1-ac2a7ab813b4
date added to LUP
2018-01-23 15:18:50
date last changed
2024-03-18 04:08:50
@article{20142aef-ca51-47e8-a6f1-ac2a7ab813b4,
  abstract     = {{<p>Objective: Cancer and its treatment in childhood and young adulthood can cause hypogonadism, leading to increased risk of long-term morbidity and mortality. The aim of this study was to evaluate the risk of presenting with biochemical signs of hypogonadism in testicular cancer survivors (TCS) and male childhood cancer survivors (CCS) in relation to the type of treatment given. Design: Case-control study. Patients: Ninety-two TCS, 125 CCS (mean age 40 and median age 34 years, respectively; mean follow-up time 9.2 and 24 years, respectively) and a corresponding number of age-matched controls. Measurements: Fasting morning blood samples were analysed for total testosterone (TT), follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The odds ratios (OR) for hypogonadism, defined as primary, secondary, compensated or ongoing androgen replacement, were calculated for TCS and CCS and for subgroups defined by diagnosis and treatment. Results: Hypogonadism was found in 26% of CCS and 36% of TCS, respectively (OR: 2.1, P = .025 and OR = 2.3, P = .021). Among CCS, the OR was further increased in those given testicular irradiation (OR = 28, P = .004). Radiotherapy other than cranial or testicular irradiation plus chemotherapy, or cranial irradiation without chemotherapy, associated also with increased ORs (OR = 3.7, P = .013, and OR = 4.4, P = .038, respectively). Among TCS, those receiving &gt;4 cycles of cisplatin-based chemotherapy had OR = 17, P = .015. Conclusions: Biochemical signs of testosterone deficiency are recognized as markers of decreased life expectancy. Thus, the risk of hypogonadism in TCS and CCS should be recognized and emphasizes the need of long-term follow-up for these men.</p>}},
  author       = {{Isaksson, S. and Bogefors, K. and Ståhl, O. and Eberhard, J. and Giwercman, Y. L. and Leijonhufvud, I. and Link, K. and Øra, I. and Romerius, P. and Bobjer, J. and Giwercman, A.}},
  issn         = {{0300-0664}},
  keywords     = {{Childhood cancer; Cytotoxic drugs; Hypogonadism; Radiotherapy; Testicular neoplasms}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{432--441}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Clinical Endocrinology}},
  title        = {{High risk of hypogonadism in young male cancer survivors}},
  url          = {{http://dx.doi.org/10.1111/cen.13534}},
  doi          = {{10.1111/cen.13534}},
  volume       = {{88}},
  year         = {{2018}},
}