Volume 44, Issue s1 pp. 219-225
ORIGINAL ARTICLE

Low inhibin B levels alone are not a reliable marker of dysfunctional spermatogenesis in childhood cancer survivors

R. Rendtorff

R. Rendtorff

Department of Paediatric Oncology/Haematology, Charité-Universitätsmedizin Berlin, Berlin, Germany

The authors contributed equally to this manuscript.

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M. Beyer

M. Beyer

Department of Dermatology, Venereology and Allergology, Charité-Universitätsmedizin Berlin, Berlin, Germany

The authors contributed equally to this manuscript.

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A. Müller

A. Müller

Department of Reproductive Health, Erlangen University Hospital, Erlangen, Germany

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R. Dittrich

R. Dittrich

Department of Reproductive Health, Erlangen University Hospital, Erlangen, Germany

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C. Hohmann

C. Hohmann

Institute of Social Medicine, Epidemiology and Health Economics, Charité-Universitätsmedizin Berlin, Berlin, Germany

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T. Keil

T. Keil

Institute of Social Medicine, Epidemiology and Health Economics, Charité-Universitätsmedizin Berlin, Berlin, Germany

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G. Henze

G. Henze

Department of Paediatric Oncology/Haematology, Charité-Universitätsmedizin Berlin, Berlin, Germany

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A. Borgmann

A. Borgmann

Department of Paediatric Oncology/Haematology, Charité-Universitätsmedizin Berlin, Berlin, Germany

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First published: 05 July 2011
Citations: 17
Anja Borgmann, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, Otto-Heubner-Centrum für Kinder-und Jugendmedizin, Klinik für Pädiatrie mit Schwerpunkt Onkologie/Hämatologie, Augustenburger Platz 1/Mittelallee 6a, 13353 Berlin, Germany.
Tel.: +49 30 450 666 204;
E-mail: [email protected]

Summary

Hormone and semen analyses were carried out to examine the diagnostic value of hormones and hormone combinations as markers of spermatogenesis in male patients who had received oncological treatment in childhood. Hormone analyses from 73 participants and spermiograms from 42 participants were evaluated. Spearman’s correlation coefficients and measures of diagnostic accuracy were calculated for the hormone and semen analysis values. Inhibin B levels of <80 ml/ml, follicle-stimulating hormone (FSH) levels of >10 IU l−1 and a combination of the two parameters showed positive predictive values for azoospermia of 0.423, 0.6154 and 0.6667 respectively. While 32% of the 73 participants showed a combination of abnormal inhibin B and FSH values, which strongly indicates impaired spermatogenesis, 31% of the 42 spermiogram results revealed azoospermia. The hormone and semen analyses showed that approximately one-third of the participants had fertility impairment. Inhibin B alone thus does not reflect spermatogenesis as well as inhibin B in combination with FSH in patients who have undergone cancer treatment in childhood. Both parameters should therefore be evaluated in paediatric cancer follow-up programmes to allow better identification of treatment regimens that cause persistent azoospermia in male childhood cancer survivors.

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