PSA doubling time as a predictor of clinical progression after biochemical failure following radical prostatectomy for prostate cancer.
PSA doubling time as a predictor of clinical progression after biochemical failure following radical prostatectomy for prostate cancer.
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DOI：
10.4065/76.6.576
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发表时间：
2001-06
影响因子：
8.9
通讯作者：
S. G. Roberts;M. Blute;E. Bergstralh;J. Slezak;H. Zincke
中科院分区：
文献类型：
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作者：
S. G. Roberts;M. Blute;E. Bergstralh;J. Slezak;H. Zincke
目的研究临床局限性前列腺癌患者行前列腺癌切除术后发生生化衰竭(前列腺特异性抗原(PSA)水平升高)的临床进展特点，并找出临床疾病进展的预测指标，包括PSA倍增时间(PSADT)的可能影响。研究对象与方法1987~1993年，对2809例临床定位(OR=0.4 ng/mL)的耻骨后前列腺癌根治术患者进行分析。对生化失败后15个月内的所有PSA值(不包括激素治疗后测定的值)进行对数线性回归，以估算PSADT。从手术开始到随访期间，所有患者都定期进行PSA测量。全身进展(SP)被定义为骨扫描上有转移性疾病的证据。根据直肠指诊、经直肠超声和活检确定局部复发(LR)。用Kaplan-Meier方法估计生化衰竭后的无SP生存期和无LR/SP生存期(既无LR又无SP)。生化失败后接受前列腺癌治疗的患者在治疗时的随访被从这项研究中删除。结果879例(31%)术后发生生化衰竭。生化失败后平均随访4.7年(0.5~11年)。生化失败的平均时间为2.9年(中位数为2.4年)。生化失败后5年和10年的总体无SP生存率分别为94%和91%。5年和10年的平均无LR/SP生存率分别为%和53%。对587例有PSADT资料的患者进行单因素分析，发现有意义的危险因素是PSADT(P<；.001)和病理Gleason评分(P=.005)，对于LR/SP，有意义的危险因素包括PSADT(P<；.001)和病理Gleason评分(P<；.001)。在多变量COX模型分析中，只有PSADT仍然是SP和LR/SP的显著危险因素(P<；.001)。PSADT>10年、1.0~9.9年、0.5~0.9年、<0.5年的患者平均5年无SP生存率分别为99%、95%、93%和%，LR/SP无瘤生存率分别为87%、62%、46%和38%。首次临床事件类型为SP的PSADT患者少于0.5年的患者比例(48%)显著高于LR患者(18%)(P<；.001)。结论对于接受根治性前列腺癌切除术的患者，PSA水平升高提示有前列腺癌残留或复发的证据。许多男性在临床局限性前列腺癌的根治性前列腺癌切除术后生化失败后，在很长一段时间内没有临床疾病。PSADT似乎是预测SP和任何临床进展(局部或全身)的重要指标。这些数据在为男性提供有关辅助治疗时机的咨询时可能很有用。
OBJECTIVES To characterize the clinical progression of disease in men who have undergone prostatectomy for clinically localized prostate cancer and have postoperative biochemical failure (elevated prostate-specific antigen [PSA] level) and to identify predictors of clinical disease progression, including the possible effect of PSA doubling time (PSADT). PATIENTS AND METHODS Between 1987 and 1993, 2809 patients underwent radical retropubic prostatectomy for clinically localized ( or =0.4 ng/mL) were identified. The PSADT was estimated using log linear regression on all PSA values (excluding those values determined after administration of hormonal therapy) within 15 months after biochemical failure. All patients had regular PSA measurements from the time of surgery through the follow-up period. Systemic progression (SP) was defined as evidence of metastatic disease on a bone scan. Local recurrence (LR) was defined on the basis of digital rectal examination, transrectal ultrasonography, and biopsy. The SP-free survival and LR/SP-free survival (survival free of both LR and SP) after biochemical failure was estimated with use of the Kaplan-Meier method. Patients with prostate cancer treatment after biochemical failure had their follow-up censored from this study at the time of treatment. RESULTS Postoperative biochemical failure occurred in 879 men (31%). The mean follow-up from time of biochemical failure was 4.7 years (range, 0.5-11 years). The mean time to biochemical failure was 2.9 years (median, 2.4 years). The overall mean SP-free survival from time of biochemical failure was 94% and 91% at 5 and 10 years, respectively. The mean LR/SP-free survival was 64% and 53% at 5 and 10 years, respectively. By using univariate analysis on the 587 patients with PSADT data, significant risk factors for SP were PSADT (P<.001) and pathologic Gleason score (P=.005); for LR/SP, significant risk factors included PSADT (P<.001) and pathologic Gleason score (P<.001). In multivariate Cox models analysis, only PSADT remained a significant risk factor for both SP and LR/SP (P<.001). Mean 5-year SP-free survival was 99%, 95%, 93%, and 64% for patients with PSADT of 10 years or longer, 1.0 to 9.9 years, 0.5 to 0.9 year, and less than 0.5 year, respectively; the respective mean LR/SP-free survivals were 87%, 62%, 46%, and 38%. The percentage of patients with PSADT of less than 0.5 year was considerably higher if the type of first clinical event was SP (48%) compared with LR (18%) (P<.001). CONCLUSIONS For patients who have undergone radical prostatectomy, a rising PSA level suggests evidence of residual or recurrent prostate cancer. Many men remain free of clinical disease for an extended time after biochemical failure following radical prostatectomy for clinically localized prostate cancer. The PSADT appears to be an important predictor of SP and also of any clinical progression (local or systemic). These data may be useful when counseling men regarding the timing of adjuvant therapies.