title: Clinical outcomes of androgen deprivation as the sole therapy for localized and locally advanced prostate cancer.
abstract: OBJECTIVE
  To characterize the clinical outcomes of androgen deprivation therapy (ADT) as the sole therapy for localized prostate cancer, and to determine independent predictors of disease progression, as recent studies indicate an increasing use of ADT.
  
  
  METHODS
  The records of all patients with cT1-4NXM0 adenocarcinoma of the prostate treated with ADT as the primary initial therapy at the Portland Veterans Affairs Medical Center between 1993 and 2000 were reviewed. Age, race, Charlson Health Index, family history, prostate-specific antigen (PSA) level, PSA density, digital rectal examination (DRE) findings, Gleason score, and percentage of positive biopsy cores at diagnosis were recorded for 81 patients. Patients had a median (SD, range) age of 73 (5.6, 58-84) years, a PSA level of 14.3 (34.6, 1.4-252) ng/mL and tumours were classified as Gleason score < or = 5 in 9% of patients, 6 in 31%, 7 in 31% and 8-10 in 30%. Outcomes extracted were PSA progression, PSA nadir, bone fractures, local progression, distant progression and overall survival.
  
  
  RESULTS
  With a median (range) follow-up of 54 (6-115) months, the incidence of local progression, distant progression, bone fractures, PSA progression, and death were 10%, 7%, 25%, 21% and 41% respectively. The percentage of positive biopsy cores > or = 83%, age < 70 years, Gleason score > or = 7, abnormal DRE, and PSA nadir > or = 0.2 ng/mL were significantly associated with PSA progression by univariate analysis. The multivariate analysis identified age < 70 years (hazard ratio 6.52, 95% confidence interval 2.29-18.55) and Gleason score > or = 6 (4.0, 2.0-12.0) as independent risk factors for PSA progression.
  
  
  CONCLUSIONS
  ADT resulted in modest control of localized prostate cancer, but younger patients and those with Gleason > or = 6 cancers were at higher risk of treatment failure. Toxicity, principally in the form of bone fractures, was high.
authors.affiliation: Division of Urology, Oregon Health & Science University and Portland VA Medical Center, Oregon 97239, USA.
authors.forename: Daniel M
authors.initials: DM
authors.lastname: Janoff
authors.forename: Chad
authors.initials: C
authors.lastname: Peterson
authors.forename: Solange
authors.initials: S
authors.lastname: Mongoue-Tchokote
authors.forename: Laura
authors.initials: L
authors.lastname: Peters
authors.forename: Tomasz M
authors.initials: TM
authors.lastname: Beer
authors.forename: Emily M
authors.initials: EM
authors.lastname: Wersinger
authors.forename: Motomi
authors.initials: M
authors.lastname: Mori
authors.forename: Mark
authors.initials: M
authors.lastname: Garzotto
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy* / Q000401:mortality; D000367:Age Factors; D000368:Aged; D000726:Androgen Antagonists / Q000009:adverse effects / Q000627:therapeutic use*; D000813:Anilides / Q000009:adverse effects / Q000627:therapeutic use*; D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000097:blood; D018450:Disease Progression; D018572:Disease-Free Survival; D005500:Follow-Up Studies; D050723:Fractures, Bone / Q000209:etiology; D007987:Gonadotropin-Releasing Hormone / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009570:Nitriles; D016016:Proportional Hazards Models; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000401:mortality; D015996:Survival Rate; D014105:Tosyl Compounds; D017211:Treatment Failure
chemical_list: D000726:Androgen Antagonists; D000813:Anilides; D018931:Antineoplastic Agents, Hormonal; D014408:Biomarkers, Tumor; D009570:Nitriles; D014105:Tosyl Compounds; D007987:Gonadotropin-Releasing Hormone; C053541:bicalutamide; D017430:Prostate-Specific Antigen