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Risk factors for post-treatment hypogonadism in testicular cancer patients.

¹ Department of Oncology, Lund University Hospital, Lund University, SE 221 85 Lund, Sweden² Reproductive Medicine Centre, Malmö University Hospital, Lund University, SE 205 02 Malmö, Sweden³ Department of Clinical Sciences, Lund University, SE 205 20 Malmö, Sweden⁴ Department of Radiology, Centre for Imaging and Physiology, Lund University Hospital, Lund University, SE 221 85 Lund, Sweden

(Correspondence should be addressed to J Eberhard; Email: jakob.eberhard{at}med.lu.se)

Objectives: Testicular germ-cell cancer (TGCC) patients are at risk of developing hypogonadism but no risk factors have yet been defined.

Methods: Blood was collected from 143 TGCC patients (after orchidectomy, prior to further therapy (T0) and 6, 12, 24, 36 and 60 months (T6, T12, T24, T36 and T60) after therapy). Biological hypogonadism (BH) was defined as: serum testosterone below 10 nmol/l and/or LH >10 IU/l; odds ratios (ORs) for BH with BH at T0, age, stage of disease, testicular characteristics, and androgen receptor polymorphism as predictors were calculated as well as the OR for developing BH post-treatment (one to two cycles of adjuvant chemotherapy (ACT) versus three to four cycles of higher dose chemotherapy (HCT) versus adjuvant radiotherapy (RT)).

Results: HCT increased the OR for BH at T6 (OR 22, 95% confidence interval (CI) 4.4–118) and T12 (OR 5.8, 95% CI 1.5–22). RT increased the OR at T6 (OR 10, 95% CI 2.1–47) and at T12 (OR 3.9, 95% CI 1.1–14). Microlithiasis predicted BH at T0 (OR 11, 95% CI 1.2–112), T12 (OR 3.9, 95% CI 1.1–13), T24 (OR 3.0, 95% CI 1.0–8.8), T36 (OR 5.4, 95% CI 1.7–17) and T60 (OR 4.4, 95% CI 1.2–16). BH at T0 was a risk for BH at T6 (OR 53, 95% CI 19–145), T12 (OR 125, 95% CI 37–430), T24 (OR 88, 95% CI 26–300) and T36 (OR 121, 95% CI 32–460).

Conclusions: It is clinically relevant that BH at T0 and testicular microlithiasis were predictive factors for post-treatment BH. HCT and RT gave temporary BH.

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