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Insulin‐like factor 3, luteinizing hormone and testosterone in testicular cancer patients: effects of β‐ hCG and cancer treatment
Author(s) -
Steggink L. C.,
Beek A. P.,
Boer H.,
Meijer C.,
Lubberts S.,
Oosting S. F.,
Jong I. J.,
Ginkel R. J.,
Lefrandt J. D.,
Gietema J. A.,
Nuver J.
Publication year - 2019
Publication title -
andrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.947
H-Index - 43
eISSN - 2047-2927
pISSN - 2047-2919
DOI - 10.1111/andr.12581
Subject(s) - testosterone (patch) , chemotherapy , medicine , luteinizing hormone , endocrinology , cohort , testicular cancer , leydig cell , cancer , follicle stimulating hormone , urology , hormone , oncology
Summary Background Primary hypogonadism (low testosterone and high luteinizing hormone, LH ) is present in approximately 20% of testicular cancer ( TC ) survivors after orchidectomy with or without chemotherapy. Objectives We investigated insulin‐like factor 3 ( INSL 3), a novel marker of Leydig cell function, in TC patients. Materials and Methods We analyzed: (I) a cross‐sectional cohort of TC patients after orchidectomy with or without chemotherapy (1988–1999) at long‐term follow‐up (median 36 and 35 years of age at follow‐up, respectively) and healthy men of similar age; ( II ) a longitudinal cohort of chemotherapy‐treated TC patients (2000–2008), analyzed before and 1 year after chemotherapy (median 29 years of age at chemotherapy). INSL 3, testosterone, and LH were compared between groups and over time and related to pre‐chemotherapy β‐ hCG levels. Results In the cross‐sectional cohort, TC patients at median 7 years after orchidectomy and chemotherapy ( n = 79) had higher LH ( p < 0.001), lower testosterone ( p = 0.001), but similar INSL 3 as controls ( n = 40). After orchidectomy only ( n = 25), higher LH ( p = 0.02), but no differences in testosterone or INSL 3 were observed compared to controls. In the longitudinal cohort, patients with normal pre‐chemotherapy β‐ hCG (≤5 mU /L, n = 35) had increased LH 1 year after chemotherapy compared to pre‐chemotherapy ( p = 0.001), and no change in testosterone or INSL 3. In contrast, patients with high β‐ hCG pre‐chemotherapy ( n = 42) had suppressed LH , markedly elevated testosterone, and low INSL 3 at start of chemotherapy, with increased LH , decreased testosterone, and increased INSL 3 1 year later (all p < 0.001). Discussion Changes in LH show that gonadal endocrine function is disturbed before chemotherapy, 1 year later, and at long‐term follow‐up in chemotherapy‐treated TC patients. Conclusion Pre‐chemotherapy, β‐ hCG ‐producing tumors affect the gonadal endocrine axis, demonstrated by increased testosterone and decreased LH . INSL 3 did not uniformly follow the pattern of testosterone.