sion, but rather classified men a priori as high risk basedon a PSA doubling time of approximately 3 years.

H. Ballentine CarterDepartment of Urology

Johns Hopkins School of MedicineBaltimore, Maryland

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The major limitation of our study is that it is not a truenatural history cohort. Rather it is a report of our experienceusing a defined strategy which incorporates PSA DT withselect patients for intervention. The limitation of PSA kinet-ics as a trigger for intervention is the large biological vari-ability in serum PSA levels. The major objective of ourreport was to model PSA measurements over time and tofacilitate the use of PSA DT as a trigger. We observed that inmost cases the optimal time to determine the allocationbetween ongoing surveillance and definitive therapy is after2.3 years of followup and 9 serial PSA determinations.

The empirical identification of PSA DT of 3 years or lessas a threshold was based on several inferences. This thresh-old represented the 20th percentile of PSA DT, which ap-proximated the proportion of patients we estimated shouldbe reclassified as high risk. For patients with a PSA in theintermediate range of 4 to 8, this value roughly correspondsto a PSA velocity of greater than 2.0 ng/ml per year, whichwas described by D’Amico et al as a high risk factor forprogression and prostate cancer mortality (references 18and 19 in article).

Of the surveillance patients 44% were eventuallytreated radically because of a PSA DT of less than 3 years,grade progression on rebiopsy and personal choice bythose who did not meet the criteria for reclassification ashigh risk. Approximately 20% of the cohort was treatedradically based on a short PSA doubling time alone. Thecohort has a 99% prostate cancer survival rate with amedian followup of 7 years. Notwithstanding that longerfollowup is required, this compelling statistic providessupport for active surveillance.

MODELING PROSTATE SPECIFIC ANTIGEN KINETICS DURING SURVEILLANCE1398