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Sudden PSA rise to ≥20 ng/ml and prostate cancer diagnosis in the United States: A population‐based study
Author(s) -
Vilson Fernandino L.,
Li Shufeng,
Brooks James D.,
Eisenberg Michael L.
Publication year - 2020
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.24075
Subject(s) - medicine , prostate cancer , incidence (geometry) , prostate specific antigen , population , prostate cancer screening , gynecology , prostate , confidence interval , cancer , demography , urology , physics , environmental health , sociology , optics
Purpose While prostate‐specific antigen (PSA) screening protocols vary, many clinicians have anecdotes of screened men with low PSA levels that rise significantly and are associated with high‐risk prostate cancer (PC). We sought to better understand the frequency of high‐risk cases that appear suddenly in a screened population. Methods We utilized data from a Commercial and Medicare advantage claims database to identify all US men ages 50 and above undergoing PSA screening who then had a sudden interval rise in PSA (e.g., PSA ≥ 20) and diagnosis of PC. We determined associations with age, race, screening intensity, and baseline PSA levels. Results In all, 526,120 men met entry criteria with an average age of 60.7 and follow‐up of 5.6 years. As the baseline PSA increased, the rate of high‐risk PC increased from 2/10,000 persons among men with the lowest baseline PSA (<1 ng/ml) to 14/10,000 person‐years among men with a baseline PSA < 5 ng/ml. Moreover, as a man's age at baseline PSA increased, the rate of high‐risk PC also increased. In contrast, the incidence of high‐risk PC did not vary significantly by race/ethnicity. More screening PSAs and shorter intervals between PSA screenings were associated with a lower incidence of high‐risk PC. Conclusions The incidence of high‐risk PC in a screened population is low (<0.1%). Our findings suggest that systematic screening cannot eliminate all PC deaths and provide an estimate for the risk of the rapid development of high‐risk cancers that is comparable to that observed in active surveillance populations.