The age at which to discontinue prostate-specific antigen (PSA) screening for prostate cancer is debated. The US Preventive Services Task Force (USPSTF) recommends against PSA screening in men aged 70 yr and older because the benefits do not outweigh the harms, particularly an “increased risk of false-positive results, diagnostic harms from biopsies, and harms from treatment ” [1]. However, this disregards the utility of PSA in diagnosing prostate cancer at an early stage, the horrendous deaths that men suffer from advanced prostate cancer, and the excessive cost to the health care system [2]. Since recommendations for PSA screening have become more restricted, we have seen an increase in patients presenting with widespread metastases [3].
We understand why public health policy decision-makers recommend stopping population-based PSA-screening programs at age 70 yr. European screening trials demonstrated a reduction in prostate cancer mortality from screening men aged 50–69 yr but no benefit for men aged 70 yr and older [4,5]. Prostate cancer is prevalent but not often lethal; one-third of men aged 70–79 yr have prostate cancer on autopsy [6]. Stopping screening at age 70 yr can nearly halve overdiagnosis [7]. In a Scandinavian trial comparing radical prostatectomy to watchful waiting for localized prostate cancer, surgery reduced prostate cancer mortality in men younger than 65 yr but not those 65 yr and older [8]. Older men with limited life expectancy have high competing mortality and may be unfit for aggressive treatment; the risk of prostate cancer mortality after treatment depends strongly on comorbidity status [9].
However, the age of 70 yr might be too early to discontinue screening for an individual man. At 10 yr after termination of a biennial PSA screening program for men aged between 50 and 70 yr, the incidence of lethal cancers among screened men equals that among nonscreened men [10]. Men aged 70 yr and older have a high likelihood of harboring high-grade cancer with aggressive molecular features [11–13]. Complications after prostate biopsy increase with age yet are often self-limiting [14]. In contrast to surgery, radiotherapy is beneficial in men aged 70 yr and older with locally advanced prostate cancer [15] and there is evidence of undertreatment of high-risk nonmetastatic prostate cancer in men in their 70s [16]. The mean life expectancy for a 70-yr-old man in the USA is 14.4 yr, and some men will live considerably longer. Therefore, the recommendation to stop at 70 yr is imprecise considering the variety of projected survival [17].
We argue that the current paradigm of denying men aged >70 yr access to PSA testing—based solely on chronologic age—is ageist; the USPSTF recommends biennial screening mammography for women up to 74 yr [18]. Rather, PSA testing can continue as long as the man has sufficient life expectancy to benefit from treatment, which is not based on chronologic age but physiologic assessment of life expectancy. We believe that measuring PSA and comparing the value to the man’s prior values, his age, and his general health is a sensible component of follow-up for men with increased risk, worry, or clinical suspicion or symptoms of prostate cancer. PSA is also a good surrogate for prostate size and benign prostatic hyperplasia [19]. The National Comprehensive Cancer Network (NCCN) guidelines recommend local treatment of high-risk clinically localized prostate cancer for men with a life expectancy >5 yr [20]. Because increasing age is associated with increasing risk of high-grade cancer, an argument can be made to continue screening until life expectancy is <5 yr. We call for a new terminology to describe this strategy, which could be named “PSA surveillance in the septuagenarian”. We need to stop PSA from being considered a “dirty word” for men aged >70 yr. Just because physicians follow PSA in men aged >70 yr does not mean they must act on it with immediate biopsy for an elevated value or aggressive treatment if a cancer is found. Rather, it allows an opportunity to identify prostate cancer in men who could benefit from considering treatment.
Acknowledgments:
Work by Sigrid V. Carlsson and James A. Eastham on this manuscript was supported in part by the Sidney Kimmel Center for Prostate and Urologic Cancers, a Specialized Program of Research Excellence grant (P50 CA92629) from the National Institutes of Health/National Cancer Institute to Dr. Howard Scher, and a National Institutes of Health/National Cancer Institute Cancer Center Support Grant (P30 CA008748) to Memorial Sloan Kettering Cancer Center. Sigrid V. Carlsson’s work was further supported by a grant from the National Cancer Institute as part of the Cancer Intervention and Surveillance Modelling Network (U01-CA199338-02) and a National Institutes of Health/National Cancer Institute Transition Career Development Award (K22 CA234400-01A1).
Footnotes
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Conflicts of interest: The authors have nothing to disclose.
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