Abstract
Objective: To determine whether higher intensity of prostate-specific antigen (PSA) surveillance was associated with earlier detection of biochemical recurrence (BCR) or survival. Patients and Methods: We identified a population-based cohort of 832 men diagnosed with nonmetastatic prostate cancer between January 1, 1995, and July 31, 2006. These men were treated with radical prostatectomy (RP), brachytherapy or external beam radiation therapy (RT), or primary androgen deprivation therapy or chose watchful waiting. To test the associations of intensity in PSA surveillance with study outcomes, we used a 2-year landmark analysis to assess whether the number of PSA tests during the first 2 years after treatment was associated with earlier detection of BCR, prostate cancer-related mortality, and all-cause mortality. We used landmark analysis to assess the association of PSA intensity, adjusting for clinicopathologic covariate, with outcome. Results: Median follow-up time for the entire cohort was 6.7 years. Higher Gleason score was the only clinicopathologic variable associated with higher PSA frequency in multivariable analysis for both the RP and RT groups (P value of .001 and .05, respectively). After adjustment for other covariates, the frequency of PSA tests during the first 2 years after RP did not increase the ability to detect BCR (hazard ratio, 1.00; 95% confidence interval, 0.84-1.19) or all-cause mortality (hazard ratio, 0.95; 95% confidence interval, 0.70-1.30) in the landmark analysis. Conclusion: Higher intensity of PSA surveillance during the 2 years after RP or RT did not improve earlier detection of BCR or survival. Evidence-based guidelines for PSA surveillance after primary treatment are needed.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 540-547 |
| Number of pages | 8 |
| Journal | Mayo Clinic Proceedings |
| Volume | 87 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 2012 |
Bibliographical note
Funding Information:Grant Support: The work was supported by grant 5 P50 CA 91956-07CD2 from the National Cancer Institute ; grant 1 KL2 RR024151 from the National Center for Research Resources ; and the Healthcare Delivery Research Scholars Program, Mayo Clinic.
Funding Information:
This publication was made possible by grants 5 P50 CA 91956-07CD2 from the National Cancer Institute and 1 KL2 RR024151 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and the NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. Information on NCRR is available at http://www.ncrr.nih.gov/ . Information on Reengineering the Clinical Research Enterprise can be obtained from http://nihroadmap.nih.gov .
