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Childhood, testicular cancers increase risk for hypogonadism
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Men who are survivors of childhood cancer or testicular cancer are at markedly increased risk for developing hypogonadism vs. men in the overall population, with the risk rising for men who underwent testicular or cranial irradiation or combination chemotherapy plus radiotherapy, according to a study.
“Although the survival rates for malignant diseases in childhood and in young adulthood (eg, testicular cancer) are very high, it is well known that these patients have increased risk of developing diabetes and cardiovascular disease as well as osteoporosis,” Sigrid Isaksson, MD, of the department of translational medicine at Lund University in Malmö, Sweden, told Endocrine Today. “Some of these long-term health problems may be related to testosterone deficiency. By simple measurements of testosterone levels in a blood samples, men being of increased risk of these serious diseases can be identified and offered preventive measures.”
Isaksson and colleagues analyzed data from two patient cohorts participating in studies of reproductive function: 125 male childhood cancer survivors identified through the Swedish Cancer Registry (mean age, 34 years; mean follow-up time, 24 years) and 92 testicular cancer survivors aged 26 to 58 years treated at Lund University Hospital between March 1996 and October 2006 (mean age, 40 years; mean follow-up time, 9.2 years). Each patient was matched by birth date with controls through the Swedish Population Register. Participants provided fasting blood samples between December 2009 and August 2013; researchers assessed levels of total testosterone, luteinizing hormone, follicle stimulating hormone and sex hormone-binding globulin. Researchers calculated ORs for hypogonadism, defined as primary, secondary, compensated or ongoing androgen replacement for both childhood cancer survivors and testicular cancer survivors.
Within the cohort of childhood cancer survivors, 26% were classified as hypogonadal vs. 14% of controls. Among childhood cancer survivors, 5.8% had primary hypogonadism, 7.4% had secondary hypogonadism, 1.7% had compensated hypogonadism and 10.7% had ongoing testosterone replacement therapy. In analyzing diagnostic subgroups of the childhood cancer survivors, researchers found the risk for hypogonadism further elevated among those with testicular cancer (OR = 6.9; 95% CI, 1.2-3.8) or leukemia (OR = 3.9; 95% CI, 1.4-11). The risk for hypogonadism also increased further for patients with leukemia receiving radiotherapy (OR = 5.7; 95% CI, 1.8-18) vs. those with leukemia not receiving radiotherapy (OR = 1.9; 95% CI, 0.36-10).
Within the cohort of testicular cancer survivors, 36% were classified as hypogonadal vs. 19% of controls (OR = 2.3; 95% CI, 1.1-4.7). Within this group, 13.5% had primary hypogonadism, 5.6% had secondary hypogonadism, 6.7% had compensated hypogonadism and 10.1% had ongoing testosterone replacement therapy. Researchers found that, among testicular cancer survivors who received at least four cycles of cisplatin-based chemotherapy, 80% were hypogonadal (OR = 17; 95% CI, 1.7-168).
“Longitudinal studies are needed with male cancer survivors to investigate at what time point, and how long time cancer treatment, testosterone deficiency develops,” Isaksson said. “There is also a need of developing optimal measures for prevention of diseases associated with this hormonal deficiency.” – by Regina Schaffer
For more information:
Sigrid Isaksson, MD, can be reached at the Lund University, Department of Translational Medicine, J Waldenströms gata 35, 205 02, Malmö, Sweden; email: sigrid.isaksson@med.lu.se.
Disclosures: The authors report no relevant financial disclosures.
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