Can one blood draw replace transrectal ultrasonography‐estimated prostate volume to predict prostate cancer risk?. (28th February 2013)

• Record Type: Journal Article
• Authors: Carlsson, Sigrid V.; Peltola, Mari T.; Sjoberg, Daniel; Schröder, Fritz H.; Hugosson, Jonas; Pettersson, Kim; Scardino, Peter T.; Vickers, Andrew J.; Lilja, Hans; Roobol, Monique J.
• Is Part Of: BJU international. Volume 112:Number 5(2013:Sep.)
• Page Start: 602
• Page End: 609
• Publication Date: 2013-02-28
• Subjects: prostate cancer -- transrectal ultrasonography -- kallikreins -- prostate‐specific antigen; Genitourinary organs -- Diseases -- Periodicals; Genitourinary organs -- Surgery -- Periodicals; Urology -- Periodicals; 616.6
• DOI: 10.1111/j.1464-410X.2012.11690.x
• Languages: English
• ISSNs: 1464-4096

Abstract

Abstract : What's known on the subject? and What does the study add?: Previous studies have shown that a statistical model based on a panel of kallikrein markers in blood (total, free and intact PSA and kallikrein‐related peptidase 2) can predict prostate cancer on biopsy. The current study explores the relationship between the above‐mentioned panel and prostate volume, and whether this panel could be an alternative for clinical measures such as DRE and TRUS in predicting prostate cancer on biopsy. Objective: To explore whether a panel of kallikrein markers in blood: total, free and intact prostate‐specific antigen (PSA) and kallikrein‐related peptidase 2, could be used as a non‐invasive alternative for predicting prostate cancer on biopsy in a screening setting. Subjects and Methods: The study cohort comprised previously unscreened men who underwent sextant biopsy owing to elevated PSA (≥3 ng/mL) in two different centres of the European Randomized Study of Screening for Prostate Cancer, Rotterdam ( n = 2914) and Göteborg ( n = 740). A statistical model, based on kallikrein markers, was compared with one based on established clinical factors for the prediction of biopsy outcome. Results: The clinical tests were found to be no better than blood markers, with an area under the curve in favour of the blood measurements of 0.766 vs. 0.763 in Rotterdam and 0.809 vs. 0.774 in Göteborg. Adding digital rectal examination (DRE) or DRE plus transrectal ultrasonography (TRUS) volume to the markers improved discrimination, although the increases were small. Results were similar for predicting high‐grade cancer. There was a strong correlation between the blood measurements and TRUS‐estimated prostate volume (Spearman's correlation 0.60 in Rotterdam and 0.57 in Göteborg). Conclusions: In previously unscreened men, each with indication for biopsy, a statistical model based on kallikrein levels was similar to a clinical model in predicting prostate cancer in a screening setting, outside the day‐to‐day clinical practice. Whether a clinical approach can be replaced by laboratory analyses or used in combination with decision models (nomograms) is a clinical judgment that may vary from clinician to clinician depending on how they weigh the different advantages and disadvantages (harms, costs, time, invasiveness) of both approaches.