Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers. / Bandak, M.; Jorgensen, N.; Juul, A.; Lauritsen, J.; Kier, M. G. G.; Mortensen, M. S.; Oturai, P. S.; Mortensen, J.; Hojman, P.; Helge, J. W.; Daugaard, G.

I: Andrology, Bind 5, Nr. 4, 07.2017, s. 718-724.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Bandak, M, Jorgensen, N, Juul, A, Lauritsen, J, Kier, MGG, Mortensen, MS, Oturai, PS, Mortensen, J, Hojman, P, Helge, JW & Daugaard, G 2017, 'Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers', Andrology, bind 5, nr. 4, s. 718-724. https://doi.org/10.1111/andr.12355

APA

Bandak, M., Jorgensen, N., Juul, A., Lauritsen, J., Kier, M. G. G., Mortensen, M. S., Oturai, P. S., Mortensen, J., Hojman, P., Helge, J. W., & Daugaard, G. (2017). Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers. Andrology, 5(4), 718-724. https://doi.org/10.1111/andr.12355

Vancouver

Bandak M, Jorgensen N, Juul A, Lauritsen J, Kier MGG, Mortensen MS o.a. Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers. Andrology. 2017 jul.;5(4):718-724. https://doi.org/10.1111/andr.12355

Author

Bandak, M. ; Jorgensen, N. ; Juul, A. ; Lauritsen, J. ; Kier, M. G. G. ; Mortensen, M. S. ; Oturai, P. S. ; Mortensen, J. ; Hojman, P. ; Helge, J. W. ; Daugaard, G. / Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers. I: Andrology. 2017 ; Bind 5, Nr. 4. s. 718-724.

Bibtex

@article{86e97803ff8b4987986482fb1d1bcc41,
title = "Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers",
abstract = "Testicular cancer survivors have impaired gonadal function and increased risk of metabolic syndrome when compared to healthy controls. However, because of the fetal etiology of testicular cancer, familial unrelated healthy men might not be an optimal control group. The objective of this study was to clarify if testicular cancer survivors have impaired gonadal function and increased risk of metabolic syndrome when compared to their biological brothers. A cross-sectional study of testicular cancer survivors (ClinicalTrials.gov number, NCT02240966) was conducted between 2014 and 2016. Of 158 testicular cancer survivors included, 24 had a biological brother who accepted to participate in the study. Serum levels of reproductive hormones and prevalence of metabolic syndrome according to International Diabetes Federation Criteria and National Cholesterol Education Program (Adult Treatment Panel III) criteria comprised the main outcome measures of the study. Median age was similar in testicular cancer survivors and their biological brothers [44 years (IQR 39–50) vs. 46 (40–53) years respectively (p = 0.1)]. In testicular cancer survivors, follow-up since treatment was 12 years (7–19). Serum levels of luteinizing hormone and follicle-stimulating hormone were elevated (p ≤ 0.001), while total testosterone, free testosterone, inhibin B and anti-M{\"u}llerian hormone were lower (p ≤ 0.001) in testicular cancer survivors than in their biological brothers. The prevalence of metabolic syndrome was similar and apart from HDL-cholesterol, which was lower in testicular cancer survivors (p = 0.01); there were no differences in the individual components of the metabolic syndrome between testicular cancer survivors and their brothers. In conclusion, gonadal function was impaired in testicular cancer survivors, while we did not detect any difference in the prevalence of metabolic syndrome between testicular cancer survivors and their biological brothers.",
keywords = "androgens, genitourinary cancer, metabolic syndrome",
author = "M. Bandak and N. Jorgensen and A. Juul and J. Lauritsen and Kier, {M. G. G.} and Mortensen, {M. S.} and Oturai, {P. S.} and J. Mortensen and P. Hojman and Helge, {J. W.} and G. Daugaard",
year = "2017",
month = jul,
doi = "10.1111/andr.12355",
language = "English",
volume = "5",
pages = "718--724",
journal = "Journal of Andrology",
issn = "2047-2919",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - Reproductive hormones and metabolic syndrome in 24 testicular cancer survivors and their biological brothers

AU - Bandak, M.

AU - Jorgensen, N.

AU - Juul, A.

AU - Lauritsen, J.

AU - Kier, M. G. G.

AU - Mortensen, M. S.

AU - Oturai, P. S.

AU - Mortensen, J.

AU - Hojman, P.

AU - Helge, J. W.

AU - Daugaard, G.

PY - 2017/7

Y1 - 2017/7

N2 - Testicular cancer survivors have impaired gonadal function and increased risk of metabolic syndrome when compared to healthy controls. However, because of the fetal etiology of testicular cancer, familial unrelated healthy men might not be an optimal control group. The objective of this study was to clarify if testicular cancer survivors have impaired gonadal function and increased risk of metabolic syndrome when compared to their biological brothers. A cross-sectional study of testicular cancer survivors (ClinicalTrials.gov number, NCT02240966) was conducted between 2014 and 2016. Of 158 testicular cancer survivors included, 24 had a biological brother who accepted to participate in the study. Serum levels of reproductive hormones and prevalence of metabolic syndrome according to International Diabetes Federation Criteria and National Cholesterol Education Program (Adult Treatment Panel III) criteria comprised the main outcome measures of the study. Median age was similar in testicular cancer survivors and their biological brothers [44 years (IQR 39–50) vs. 46 (40–53) years respectively (p = 0.1)]. In testicular cancer survivors, follow-up since treatment was 12 years (7–19). Serum levels of luteinizing hormone and follicle-stimulating hormone were elevated (p ≤ 0.001), while total testosterone, free testosterone, inhibin B and anti-Müllerian hormone were lower (p ≤ 0.001) in testicular cancer survivors than in their biological brothers. The prevalence of metabolic syndrome was similar and apart from HDL-cholesterol, which was lower in testicular cancer survivors (p = 0.01); there were no differences in the individual components of the metabolic syndrome between testicular cancer survivors and their brothers. In conclusion, gonadal function was impaired in testicular cancer survivors, while we did not detect any difference in the prevalence of metabolic syndrome between testicular cancer survivors and their biological brothers.

AB - Testicular cancer survivors have impaired gonadal function and increased risk of metabolic syndrome when compared to healthy controls. However, because of the fetal etiology of testicular cancer, familial unrelated healthy men might not be an optimal control group. The objective of this study was to clarify if testicular cancer survivors have impaired gonadal function and increased risk of metabolic syndrome when compared to their biological brothers. A cross-sectional study of testicular cancer survivors (ClinicalTrials.gov number, NCT02240966) was conducted between 2014 and 2016. Of 158 testicular cancer survivors included, 24 had a biological brother who accepted to participate in the study. Serum levels of reproductive hormones and prevalence of metabolic syndrome according to International Diabetes Federation Criteria and National Cholesterol Education Program (Adult Treatment Panel III) criteria comprised the main outcome measures of the study. Median age was similar in testicular cancer survivors and their biological brothers [44 years (IQR 39–50) vs. 46 (40–53) years respectively (p = 0.1)]. In testicular cancer survivors, follow-up since treatment was 12 years (7–19). Serum levels of luteinizing hormone and follicle-stimulating hormone were elevated (p ≤ 0.001), while total testosterone, free testosterone, inhibin B and anti-Müllerian hormone were lower (p ≤ 0.001) in testicular cancer survivors than in their biological brothers. The prevalence of metabolic syndrome was similar and apart from HDL-cholesterol, which was lower in testicular cancer survivors (p = 0.01); there were no differences in the individual components of the metabolic syndrome between testicular cancer survivors and their brothers. In conclusion, gonadal function was impaired in testicular cancer survivors, while we did not detect any difference in the prevalence of metabolic syndrome between testicular cancer survivors and their biological brothers.

KW - androgens

KW - genitourinary cancer

KW - metabolic syndrome

U2 - 10.1111/andr.12355

DO - 10.1111/andr.12355

M3 - Journal article

C2 - 28598554

VL - 5

SP - 718

EP - 724

JO - Journal of Andrology

JF - Journal of Andrology

SN - 2047-2919

IS - 4

ER -

ID: 183825135