Effect of childhood cancer treatment on fertility markers in adult male long‐term survivors

Pediatric Blood and Cancer - Tập 52 Số 1 - Trang 108-112 - 2009
Niels J. van Casteren1, G Linden2, F.G.A.J. Hakvoort-Cammel2, Karel Hählen2, Gert R. Dohle1, Marry M. van den Heuvel‐Eibrink2
1Section of Andrology, Department of Urology, Erasmus MC–University Medical Center, Rotterdam, The Netherlands
2Department of Pediatric Oncology/Hematology, Erasmus MC-Sophia Children's Hospital, Rotterdam, The Netherlands

Tóm tắt

AbstractBackgroundAlthough it is accepted that pediatric cancer treatment harbors a risk of gonadal damage, large cohort studies using up‐to‐date fertility markers are lacking.ProcedureThe aim of our study was to evaluate the gonadal toxicity of childhood cancer treatment using fertility markers. We included 248 adult male long‐term survivors of childhood cancer. Median age at diagnosis: 5 years, median age at follow‐up: 24 years, median follow‐up time 18 years. We evaluated patient characteristics, treatment modalities, testicular size, and endocrinological parameters including Inhibin B, luteinizing hormone (LH), follicle‐stimulating hormone (FSH), and testosterone.ResultsThe median value of Inhibin B in the cancer survivor group was 126 ng/L versus 177 ng/L in the control group (P < 0.001). In the survivors, 67% had Inhibin B levels below the normal reference value of 150 ng/L compared with 26% in the control group (P < 0.05). Inhibin B was the most sensitive discriminator between survivors and controls. Significantly decreased Inhibin B levels and increased FSH levels were found in men treated for Hodgkin and non‐Hodgkin lymphoma, acute‐myeloid leukemia, neuroblastoma, and sarcoma as compared to other malignancies. Cumulative dosages of procarbazine and cyclophosphamide were the only independent chemotherapy‐related predictors for decrease of Inhibin B levels and increase of FSH. Age at time of treatment did not influence post‐treatment Inhibin B or FSH levels.ConclusionsSevere gonadal impairment is a risk in a considerable subgroup of childhood cancer survivors based on current fertility markers like Inhibin B. Males receiving gonadotoxic treatment before puberty are not protected from post treatment gonadal dysfunction. Pediatr Blood Cancer 2009;52:108–112. © 2008 Wiley‐Liss, Inc.

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Tài liệu tham khảo

10.1200/JCO.2005.00.554

10.3322/canjclin.40.6.355

10.1200/JCO.2006.07.3114

Brougham MF, 2003, Male fertility following childhood cancer: Current concepts and future therapies, Asian J Androl, 5, 325

10.1007/s004310050021

10.1002/(SICI)1096-911X(199608)27:2<74::AID-MPO2>3.0.CO;2-Q

10.1111/j.1365-2605.1991.tb01098.x

10.1002/mpo.2950170510

10.1046/j.1365-2605.2001.00260.x

Pierik FH, 1998, Serum inhibin B as a marker of spermatogenesis, J Clin Endocrinol Metab, 83, 3110, 10.1210/jcem.83.9.5121

10.1016/j.fertnstert.2006.01.022

10.1093/humrep/12.11.2376

10.1210/jc.82.12.4059

10.1080/07853890310004084

10.1093/humrep/dem313

10.1530/eje.0.1450561

10.3233/CBM-2005-1109

WHO, 1999, WHO laboratory manual for the examination of human semen and sperm‐cervical mucus interaction

van Casteren NJ, 2007, Semen cryopreservation in pubertal boys before gonadotoxic treatment and the role of endocrinologic evaluation in predicting sperm yield, Fertil Steril

10.1002/1096-911X(200007)35:1<52::AID-MPO9>3.0.CO;2-Y

10.1046/j.1365-2265.2003.01712.x

10.1016/S0140-6736(02)09606-X

10.1111/j.1365-2141.2005.05740.x

10.1136/bmj.291.6507.1457

10.1159/000067835

10.1016/j.eururo.2007.03.085

10.1002/pbc.10422

10.1259/0007-1285-53-628-271

10.1002/mpo.2950180304

10.1016/S0022-3476(96)70119-1

10.1210/jc.76.5.1325

10.1001/jama.1988.03720140043031

10.1046/j.1365-2605.2002.00365.x

10.1093/humrep/17.5.1367

10.1097/00043426-199809000-00004

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Pediatric Blood and Cancer

Tập 52 Số 1

108-112

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