Gonadal function is influenced by obesity in very long-term male survivors of childhood cancer

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 524-553-Male Reproductive Endocrinology
Bench to Bedside
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-544
Karin Blijdorp*1, Wendy van Dorp2, Joop S E Laven3, Rob Pieters4, Frank H. de Jong5, Saskia Pluijm6, Aart Jan Van der Lely7, Marry van den Heuvel8 and Sebastian JCMM Neggers9
1Erasmus University Medical Centre, Rotterdam, Netherlands, 2Erasmus MC University Medical Center, Rotterdam, Netherlands, 3Erasmus Medical Center, Rotterdam, Netherlands, 4Erasmus MC University Medical Center - Sophia's Children's Hospital Rotterdam, 5Erasmus MC, Rotterdam, Netherlands, 6Erasmus MC-Sophia Children’s Hospital, Netherlands, 7Erasmus University Medical Center, Rotterdam, Netherlands, 8Erasmus MC-Sophia Children’s Hospital, 9Erasmus MC, Netherlands
Objective Obesity and gonadal dysfunction are well-described major side effects of treatment in adult childhood cancer survivors. In the general population, obesity has a negative influence on spermatogenesis and reproductive hormone levels. We aimed to evaluate whether obesity is associated with decreased gonadal reserve markers in male childhood cancer survivors.

Patients Data of 351 male survivors of childhood cancer were analyzed retrospectively. Median age diagnosis was 5.9 years (0-17.8) and median age at follow-up was 25.6 years (18.0-45.8). Outcome measures were total and free testosterone, sex hormone binding globulin (SHBG), inhibin B, follicle stimulating hormone (FSH) and luteinizing hormone (LH). Potential risk factors were body mass index (BMI), waist circumference, waist-hip ratio and body composition measures, determined by dual energy X-ray absorptiometry (total fat percentage, lean body mass and visceral fat percentage).

Results Survivors with high fat percentage (≥25%) had significantly lower inhibin B and inhibin B / FSH ratios than survivors with normal total fat percentage in univariate and multivariate analysis after adjustment for age at follow-up, age at diagnosis, smoking, total body and abdominal irradiation and alkylating agent dose score (inhibin B: ß -25, P=0.047; inhibin B / FSH ratio: ß -34%, P=0.041). Total testosterone and SHBG were significantly decreased in survivors with obesity (BMI ≥30 kg/m2) (ß –3.6, P=0.002 and ß –7.5, P=0.003), high fat percentage (ß –2.9, P<0.001 and ß –6.7, P<0.001), and high waist circumference (>102 cm) (ß -4.1, P=0.005 and ß -7.5, P=0.015).

Conclusion Obesity is an independent risk factor for decreased gonadal reserve markers in a large cohort of adult male survivors of childhood cancer.

Disclosure: JSEL: Researcher, Ferring Pharmaceuticals, Researcher, Merck BV, Founder, Genovum. Nothing to Disclose: KB, WV, RP, FHD, SP, AJV, MV, SJN

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm