title: Death in patients with recurrent prostate cancer after radical prostatectomy: prostate-specific antigen doubling time subgroups and their associated contributions to all-cause mortality.
abstract: OBJECTIVE
  Among patients with biochemical recurrence after radical prostatectomy, we found previously that postoperative prostate-specific antigen doubling time (PSADT) was associated with risk of prostate cancer death. However, given the small number of patients in the highest risk PSADT subgroup, it is unclear which PSADT subgroups contribute the greatest to prostate cancer-specific death and how this influences all-cause mortality.
  
  
  METHODS
  This study was a retrospective analysis of 379 patients treated with radical prostatectomy between 1982 and 2000 who had a biochemical recurrence and PSADT data available. Mean and median follow-up after surgery was 11.4 (standard deviation, 5.4) and 11.0 years, respectively (range, 1.6 to 23.0 years).
  
  
  RESULTS
  Shorter PSADT was significantly associated with prostate cancer-specific and all-cause mortality (P < .001). Although patients with a PSADT less than 3 months were at the greatest risk of death, because of the limited number of patients in this group, they accounted for only 13% of prostate cancer deaths at 15 years after biochemical recurrence, whereas patients with an intermediate PSADT (3.0 to 8.9 months) accounted for 58% of all prostate cancer deaths. Among patients with a PSADT less than 15 months, prostate cancer accounted for 90% of all deaths. Only patients in the slowest PSADT subgroup (> or = 15 months) had a greater risk of competing-causes mortality compared with that from prostate cancer.
  
  
  CONCLUSIONS
  Among a select cohort of young, healthy patients with PSA recurrence after radical prostatectomy and a PSADT less than 15 months, prostate cancer accounted for an estimated 90% of all deaths by 15 years after recurrence. The majority of prostate cancer deaths occurred among patients with an intermediate PSADT (3.0 to 8.9 months).
authors.affiliation: Department of Urology, The James Buchanan Brady Urological Institute, Johns Hopkins Medicine, Baltimore, MD, USA. steve.freedland@duke.edu
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Freedland
authors.forename: Elizabeth B
authors.initials: EB
authors.lastname: Humphreys
authors.forename: Leslie A
authors.initials: LA
authors.lastname: Mangold
authors.forename: Mario
authors.initials: M
authors.lastname: Eisenberger
authors.forename: Frederick J
authors.initials: FJ
authors.lastname: Dorey
authors.forename: Patrick C
authors.initials: PC
authors.lastname: Walsh
authors.forename: Alan W
authors.initials: AW
authors.lastname: Partin
mesh_terms: D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use; D002423:Cause of Death; D003131:Combined Modality Therapy; D006801:Humans; D008297:Male; D011379:Prognosis; D016016:Proportional Hazards Models; D017430:Prostate-Specific Antigen / Q000097:blood*; D011468:Prostatectomy / Q000379:methods*; D011471:Prostatic Neoplasms / Q000188:drug therapy / Q000401:mortality* / Q000473:pathology / Q000601:surgery; D012008:Recurrence; D012189:Retrospective Studies; D016019:Survival Analysis
chemical_list: D018931:Antineoplastic Agents, Hormonal; D017430:Prostate-Specific Antigen