Clinical correlates of the biological variation of sperm DNA fragmentation in infertile men attending an andrology outpatient clinic

• Published in: International journal of andrology 2007-02, Vol.30 (1), p.48-55
• Main Authors: Smit, M., Dohle, G. R., Hop, W. C. J., Wildhagen, M. F., Weber, R. F. A., Romijn, J. C.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; biological variation; Birth control; Chromatin - metabolism; DNA Fragmentation; follicle-stimulating hormone; Fundamental and applied biological sciences. Psychology; Gynecology. Andrology. Obstetrics; Humans; Infertility, Male - diagnosis; Inhibin-B; Male; Male genital diseases; male infertility; Mammalian male genital system; Medical sciences; Non tumoral diseases; Outpatient Clinics, Hospital; Semen - cytology; Sensitivity and Specificity; sperm chromatin structure assay; Sperm Count; sperm DNA; Sperm Motility; Spermatozoa - metabolism; Spermatozoa - ultrastructure; Sterility. Assisted procreation; varicocele; Vertebrates: reproduction
• ISSN: 0105-6263; 1365-2605
• DOI: 10.1111/j.1365-2605.2006.00710.x

Summary Determination of sperm DNA fragmentation, as assessed by the sperm chromatin structure assay (SCSA), has become an important tool for the evaluation of semen quality. The aim of the present study was to describe the biological variation of sperm DNA fragmentation in men attending an andrology clinic and to identify clinical correlates of the biological variation of sperm DNA fragmentation. For this study, two consecutive semen samples from 100 patients attending our andrology outpatient clinic were subjected to semen analysis, performed in parallel according to WHO guidelines and by SCSA. A good agreement between pairs of samples was found for SCSA‐derived variables, as indicated by a significantly lower median coefficient of variation (CV) of the DNA Fragmentation Index (DFI) and the high DNA stainability (HDS) compared with WHO semen parameters. In half of the men attending our andrology clinic, however, the individual biological variation of DFI and HDS, expressed as CV of two samples, exceeded 10%. Dysregulation of spermatogenesis, as seen as testicular insufficiency or varicocele, was not associated with increased variability of DFI or HDS. A backward multiple linear regression analysis, however, indicated that the biological variation of DFI may be more profound in men with characteristics of normal spermatogenesis. In conclusion, we confirm previous reports that sperm DNA fragmentation has a lower biological variability than classical semen parameters. We hypothesize that the sperm chromatin structure may be more influenced in patients with normal spermatogenesis, whereas in men with disturbed spermatogenesis, the chromatin structure may be already so impaired that the effect of unidentified factors leading to variability of sperm DNA fragmentation in time may not be as profound.