LETTER TO THE EDITOR
Ahead of print publication  

Re: Commentary on "The association between sexual function and prostate cancer risk in US veterans"


Department of Surgery, Cedars-Sinai Medical Center, Samuel Oschin Cancer Institute, Los Angeles, CA 90048, USA

Date of Submission07-Dec-2016
Date of Acceptance14-Dec-2016
Date of Web Publication07-Mar-2017

Correspondence Address:
Adriana C Vidal,
Department of Surgery, Cedars Sinai Medical Center, Samuel Oschin Cancer Institute, Los Angeles, CA 90048, USA

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Source of Support: None, Conflict of Interest: None


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How to cite this URL:
Vidal AC, Freedland SJ. Re: Commentary on "The association between sexual function and prostate cancer risk in US veterans". Asian J Androl [Epub ahead of print] [cited 2017 Mar 27]. Available from: http://www.ajandrology.com/preprintarticle.asp?id=196854

Dear Editor,

Kai Wang and Linda B Cottler recently commented on our article entitled, "The association between sexual function and prostate cancer risk in US veterans", published in Asian Journal of Andrology.[1] They made the good point that sexual function could be a clinical symptom of low serum testosterone, and that men with low testosterone may be using testosterone replacement therapy (TRT) which could be confounding the associations between sexual function and prostate cancer risk.

To clarify their concerns, we reran our analysis excluding 12 men of 448 men in the original study, who received testosterone within 1 year before the biopsy. This new analysis did not change our results. Excluding those men, higher sexual function remained associated with lower risk of overall prostate cancer (OR = 0.91, 95%CI: 0.85-0.97, P = 0.004), and high-grade prostate cancer (OR = 0.88, 95%CI: 0.79-0.94, P = 0.001), after accounting for PSA, body mass index, race, age, year of consent, pack-years smoking, heart disease, and diabetes type 2. Thus, although Wang and Cotler's idea is interesting and plausible, it does not explain our findings.

A second concern that was raised is the cross-sectional nature of the data on sexual function collected from the study participants. We agree that the results are cross-sectional and no longitudinal data are available. Thus, we are unable to assess whether the cancer induced the sexual dysfunction or vice versa (reverse causation). As most cancers were low-grade small tumors, it is unlikely they would induce sexual dysfunction, though we cannot exclude this possibility. As such, we cannot state that sexual dysfunction causes prostate cancer. Indeed, we do not believe that this is the likely explanation but rather that sexual dysfunction and prostate cancer are both related to some other conditions such as metabolic disorders or hypogonadism. However, if confirmed in future studies, sexual dysfunction can be used at the time of biopsy to predict prostate cancer risk and thus may have an important role in risk stratification of whom to biopsy. Nonetheless, as we said in our original manuscript, confirmatory studies are needed to validate our results.


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Both authors declared no competing interests.

 
  References Top

1.
Wang K, Cottler LB. Commentary on "The association between sexual function and prostate cancer risk in US veterans". Asian J Androl 2017; doi: 10.4103/1008-682X.196853. [Epub ahead of print].  Back to cited text no. 1
    




 

 
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