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Use of Testosterone To Prevent Cyclophosphamide-Induced Azoospermia

Antonio Masala, MD; Rossana Faedda, MD; Sergio Alagna, MD; Andrea Satta, MD; Giorgio Chiarelli, MD; Pier Paolo Rovasio, MD; Riccardo Ivaldi, MD; Marianna Simona Taras, MD; Elisabetta Lai, MD; and Ettore Bartoli, MD
[+] Article and Author Information

From University of Sassari, Sassari, Italy; and the University of Udine, Udine, Italy. Grant Support: Full support was provided by grants from Ministero della Universita e della Ricerca Scientifica e Tecnologica and Consiglio Nazionale delle Ricerche, Rome, Italy. Requests for Reprints: Ettore Bartoli, MD, Medicina Interna, Policlinico Universitario, Piazzale S.M. Misericordia 1, 33100 Udine, Italy. Current Author Addresses: Drs. Masala, Faedda, Alagna, Satta, Chiarelli, Rovasio, Ivaldi, Taras, and Lai: Istituto di Patologia Medica, Viale San Pietro 8, 07100 Sassari, Italy.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1997;126(4):292-295. doi:10.7326/0003-4819-126-4-199702150-00005
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Background: Prepubertal patients receiving chemotherapy are relatively resistant to cyclophosphamide-induced germinal cell alterations.

Objective: To study the possible protective effect of testosterone used to inhibit germinal cell activity in men who are receiving cyclophosphamide.

Design: Randomized, clinical trial.

Setting: University medical center.

Patients: 15 patients with the nephrotic syndrome who were treated with cyclophosphamide for 6 to 8 months.

Intervention: Five patients received daily oral cyclophosphamide, five received cyclophosphamide in monthly bolus injections, and five received monthly intravenous boluses of cyclophosphamide plus testosterone (100 mg intramuscularly every 15 days).

Measurements: Sperm counts, serum follicle-stimulating hormone levels, and serum luteinizing hormone levels were measured before, during, and after treatment with cyclophosphamide alone or cyclophosphamide plus testosterone.

Results: The 10 patients who did not receive testosterone became azoospermic during cyclophosphamide therapy. In only 1 of the 10 patients did the sperm count return to normal 6 months after discontinuation of therapy. Follicle-stimulating hormone levels were elevated in these patients (mean ± SE, 19.20 ± 1.28 IU/L in patients receiving oral cyclophosphamide and 16.04 ± 2.22 IU/L in patients receiving intravenous cyclophosphamide alone). All 5 patients who received testosterone became azoospermic or severely oligospermic during treatment but had a normal sperm count 6 months after the discontinuation of therapy. In these patients, the mean sperm count was 45.78 ± 3.89 × 106/mL and follicle-stimulating hormone levels were normal (5.08 ± 0.56 IU/L).

Conclusion: Testosterone given to men before and during an 8-month cycle of cyclophosphamide therapy for the nephrotic syndrome may preserve fertility.

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