Endocrine Abstracts (2009) 19 P286

Inhibin B and AMH are NOT predictors of serum testosterone in young men after cancer

DM Greenfield1, SJ Walters1, RJM Ross1, RE Coleman1, BW Hancock1, JA Snowden2 & WL Ledger1


1University of Sheffield, Sheffield, UK; 2Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK.


Background: In men inhibin B is correlated with sperm count, concentration and testicular volume. Anti-müllerian hormone (AMH) is significantly positively correlated with inhibin B and significantly negatively correlated with FSH. Raised FSH is a traditional marker of infertility. Young male cancer patients treated with gonadotoxic agents are at high risk of hypogonadism (HG). The relationship between inhibin B and AMH with serum total testosterone is unclear.

Objectives: To establish if serum total testosterone can be predicted from FSH, inhibin B and AMH in young men with cancer-treatment induced HG.

Patients and methods: We studied 176 male cancer survivors (mean age 37.3 years SD 5.8) who previously received gonadotoxic therapy of whom 13.6% have HG (≤10 nmol/l). Total testosterone (tT) and FSH were measured from serum using ECLIA immunoassay (Roche). Inhibin B and AMH were measured by ELISA (Beckman-Coulter).

Analysis: Student’s t-tests were used for comparisons of markers between cancer survivors with and without HG. Logistic regression was used to predict low tT. Receiver operating characteristics (ROC) analyses estimated the sensitivity and specificity (area under the curve (AUC)) of the fertility markers solely and as a composite value.

Results: The mean values of inhibin B for cancer survivors with and without HG were 54 and 113 pg/ml respectively (P<0.001, 95% CI 32 to 86). The differences in means for both FSH and AMH were not statistically significant by HG status. ROC analysis demonstrated that the composite value of fertility markers did not have better sensitivity and specificity than inhibin B alone but the AUC for the latter was only slightly better than chance at 0.679.

Conclusions: Production of testosterone by the Leydig cell is largely autonomous from pituitary FSH and also from gonadal AMH and inhibin B. These fertility markers do not correlate with hypogonadism in male cancer survivors.

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