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European Urology
Volume 55, issue 5, pages 1003-1250, May 2009Letters to the Editor published online
Reply to Rune Kvåle, Eivor Hernes and Freddie Bray's Letter to the Editor re: E. David Crawford, Per-Anders Abrahamsson. PSA-based Screening for Prostate Cancer: How Does It Compare with Other Cancer Screening Tests? Eur Urol 2008;54:262–73
E. David Crawford a 
, Per-Anders Abrahamsson b.
Accepted 21 November 2008, Published online 1 December 2008, pages e90 - e91
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Refers to article:
PSA-based Screening for Prostate Cancer: How Does It Compare with Other Cancer Screening Tests?
Accepted 18 May 2008
August 2008 (Vol. 54, Issue 2, pages 262 - 273)
Refers to article:
Re: E. David Crawford, Per-Anders Abrahamsson. PSA-based Screening for Prostate Cancer: How Does It Compare with Other Cancer Screening Tests? Eur Urol 2008;54:26273
Accepted 21 November 2008
May 2009 (Vol. 55, Issue 5, pages e88 - e89)
Article Outline
The primary basis of our article was to remind our colleagues that, with regard to cancer screening, we live in an imperfect world [1]. Although prostate-specific antigen (PSA), in common with other screening tests, has a less-than-perfect sensitivity and specificity profile, it has been depicted by some in negative terms that belie the findings from studies such as the European Randomised Study of Screening for Prostate Cancer (ERSPC) [2], and [3] and the Prostate Cancer Prevention Trial (PCPT) [4]. Although the ERSPC study remains incomplete, analyses from the Rotterdam section demonstrate statistically significant shifts to more favourable clinical stages and histological grades, as well as a reduction in distant metastases, and lower rates for biochemical progression after surgery, radiotherapy, and endocrine therapy for screened versus unscreened men [2], and [3]. One of the most important findings of the PCPT, which does not suffer from the ascertainment biases seen in screening studies, was that PSA is indeed more effective at detecting high-grade disease than low-grade disease [4]. While we await the mortality outcomes of the ERSPC and the Prostate, Lung, Colorectal, and Ovary (PLCO) studies with great interest, we believe the current evidence base is compelling, if incomplete.
The evidence to date does not suggest that the psychological burden of watchful waiting for early disease, more frequently detected through screening, is a substantive issue. In the Scandinavian Prostatic Cancer Group Study Number 4, which randomised men with localised disease to radical prostatectomy or watchful waiting, the prevalence of anxiety and depression, overall well-being, and quality of life were similar in the two groups [5]. We do not believe, and have no evidence to suggest, that this concern should interfere with a basic premise: that the morbidity, both physical and psychological, associated with delayed diagnosis is considerable and that earlier detection is therefore desirable. The use of PSA is now widespread in our society. The health inequality created by providing the test on demand to men who ask for it but denying it to those who do not is a real concern.
We concur that PSA-based screening needs to be tailored to the individual patient. One of the features of PSA is that, beyond its predictive value for a positive biopsy at the time of screening, it has value as a marker of longitudinal risk [6], [7], [8], and [9]. An initial PSA value for a middle-aged man can be used to determine future screening frequency, a concept enshrined in the current US National Comprehensive Cancer Network guidelines [10]. In an analysis from the Rotterdam section of the ERSPC, just 0.9% of men with a PSA of ≤1.0 ng/ml in first-round screening went on to have a PSA ≥3.0 ng/ml at the second round 4 yr later, while around 50% of those with a PSA of 2.0–2.9 ng/ml progressed over this threshold. Almost one in three men with an initial PSA of 2.0–2.9 ng/ml who traversed this threshold 4 yr later and were biopsied had prostate cancer, with 70% having an intermediate or high 2-yr risk of PSA recurrence [11]. These data demonstrate the importance of more frequent screening for some men versus others, based on an initial PSA assessment.
Conflicts of interest: E. David Crawford and Per-Anders Abrahamsson are on the GlaxoSmithKline advisory board. E. David Crawford has been a speaker for GlaxoSmithKline, BPH.
References
- [1] E.D. Crawford, P.-A. Abrahamsson. PSA-based screening for prostate cancer: how does it compare with other cancer screening tests?. Eur Urol 54 (2008) (262 - 273) Abstract, Full-text, PDF, Crossref.
- [2] I.W. van der Cruijsen-Koeter, A.N. Vis, M.J. Roobol, et al.. Comparison of screen detected and clinically diagnosed prostate cancer in the European Randomized Study of Screening for Prostate Cancer, Section Rotterdam. J Urol 174 (2005) (121 - 125) Crossref.
- [3] S. Roemeling, M.J. Roobol, C. Gosselaar, F.H. Schroder. Biochemical progression rates in the screen arm compared to the control arm of the Rotterdam Section of the European Randomized Study of Screening for Prostate Cancer (ERSPC). Prostate 66 (2006) (1076 - 1081) Crossref.
- [4] I.M. Thompson, D.P. Ankerst, C. Chi, et al.. Operating characteristics of prostate-specific antigen in men with an initial PSA level of 3.0 ng/ml or lower. JAMA 294 (2005) (66 - 70) Crossref.
- [5] G. Steineck, F. Helgesen, J. Adolfsson, et al.. Quality of life after radical prostatectomy or watchful waiting. N Engl J Med 347 (2002) (790 - 796) Crossref.
- [6] J. Fang, E.J. Metter, P. Landis, et al.. Low levels of prostate-specific antigen predict long-term risk of prostate cancer: results from the Baltimore Longitudinal Study of Aging. Urology 58 (2001) (411 - 416) Crossref.
- [7] J.A. Antenor, M. Han, K.A. Roehl, R.B. Nadler, W.J. Catalona. Relationship between initial prostate specific antigen level and subsequent prostate cancer detection in a longitudinal screening study. J Urol 172 (2004) (90 - 93) Crossref.
- [8] G. Aus, J.E. Damber, A. Khatami, et al.. Individualized screening interval for prostate cancer based on prostate-specific antigen level: results of a prospective, randomized, population-based study. Arch Intern Med 165 (2005) (1857 - 1861) Crossref.
- [9] H. Lilja, D. Ulmert, T. Bjork, et al.. Long-term prediction of prostate cancer up to 25 years before diagnosis of prostate cancer using prostate kallikreins measured at age 44 to 50 years. J Clin Oncol 25 (2007) (431 - 436) Crossref.
- [10] M.H. Kawachi, R.R. Bahnson, M. Barry, et al.. National Comprehensive Cancer Network. Prostate cancer early detection. Clinical practice guidelines in oncology. J Natl Compr Canc Netw 5 (2007) (714 - 736)
- [11] F.H. Schroder, R. Raaijmakers, R. Postma, T.H. van der Kwast, M.J. Roobol. 4-year prostate specific antigen progression and diagnosis of prostate cancer in the European Randomized Study of Screening for Prostate Cancer, Section Rotterdam. J Urol 174 (2005) (489 - 494) discussion 493–4 Crossref.
Footnotes
a Department of Urologic Oncology, University of Colorado Health Sciences Center, Denver, Colorado, USA
b Department of Urology, Malmö University Hospital, Malmö, Sweden
Corresponding author. University of Colorado Health Science Center, Section of Urologic Oncology – Radiation Oncology Department, 1665 N, Ursula Street, Suite 1004, Aurora, CO 80010, United States. Tel. +1 303 315 59 36, +1 303 668 8393 (Mobile); Fax: +1 303 315 76 11.
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