Abstract
During the past 12 years, routine use of serum prostate-specific antigen (PSA) has resulted in a major rise in the proportion of patients initially diagnosed with clinically localized disease and the average age at diagnosis has declined. 1,2 These important demographic changes, coupled with major improvements in surgical technique, resulted in a sharp increase in the number of advocates for radical prostatectomy (RP) as definitive treatment for prostate cancer. 3,4 After curative RP, the serum PSA level should become undetectable, and the detection of elevated levels at any time after about 4 weeks postoperatively reflects evidence of disease recurrence. 5 The incidence of disease recurrence while PSA is undetectable is extremely low, although it might be observed in very poorly differentiated tumors or neoplasms of distinct histologic subtypes. 6,7 The first evidence of disease recurrence after RP is manifested by a consistent elevation of serial serum PSA tests, usually without any associated objective findings. 5 The probability of biochemical relapse at 5 and 10 years, reported in several large series, has ranged between 20% and 31% and 27% and 53%, respectively. 7‐10 Various factors, including differences in patient populations, duration of followup, and the definition of PSA recurrence (0.2 to 0.6 ng/mL), might account for the variance in the reported rates. On the basis of the number of RPs performed and the cumulative figures of biochemical relapse rates, it can be estimated that thousands of patients present annually to clinicians throughout the world with an elevated PSA level as the only evidence of disease. At present, the natural history of the patient with biochemical relapse after RP remains poorly defined, and no criteria are uniformly accepted for implementation of treatment for these patients. The management philosophy has been influenced primarily by physicians’ and patients’ biases, and it is becoming obvious that despite the lack of consensus, early interventions are more commonly applied than observation only. Our objective was to review the published reports dealing with the evaluation, natural history, and treatment of patients with a rising PSA after RP for clinically localized prostate cancer and to provide the necessary groundwork for the development of clinical research on this challenging problem.
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