Mitchell Darren M, Swindell Ric, Elliott Tony, Wylie James P, Taylor Cathy M, Logue John P
Department of Clinical Oncology, Christie NHS Trust, Manchester, UK.
Radiother Oncol. 2008 Jul;88(1):102-7. doi: 10.1016/j.radonc.2008.04.004. Epub 2008 Apr 29.
To report on the incidence of benign prostate-specific antigen bounce following permanent I(125) prostate brachytherapy, to describe the associations in our population and review the relationship of bounce to subsequent biochemical failure.
From February 2000 to May 2005, 374 patients with localised prostate cancer were treated with I(125) permanent prostate brachytherapy at a single institution. A prospectively collected database was used to identify cases of prostate-specific antigen (PSA) bounce, defined as a rise of 0.2 ng/ml above an initial PSA nadir with subsequent decline to or below that nadir without treatment. The patients who received neo-adjuvant or adjuvant hormone manipulation were excluded. Biochemical failure was determined using the both the ASTRO consensus definition and Phoenix (nadir +2 ng/mL) definition.
Two hundred and five patients were identified with a median follow-up of 45 months (24-85). PSA bounce was noted in 79 (37%) men, occurring at a median of 14.8 months (1.7-40.6) following implant. The median peak PSA was 1.8 ng/ml (0.4-7.4) with a bounce magnitude of 0.91 ng/ml (0.2-5.8). When pre- and post-implant factors were assessed for association to bounce, only younger age was statistically significant (p=0.002). The threshold for biochemical failure as defined by the ASTRO consensus definition (1997) was met in 4 (5%) patients after experiencing bounce as opposed to 19 (15%) non-bounce patients (p=0.01). The threshold for Phoenix (nadir +2 ng/mL) was met in 6 (7.5%) patients following bounce versus 22 (17%) of non-bounce patients (p=0.003). Both definitions are prone to false positive calls during bounce. Median PSA velocity during the bounce was 0.08 ng/mL/month (0.02-0.98) and was statistically significantly lower than the median velocity prior to the Phoenix biochemical failure at 0.28 ng/mL/month (0.07-2.04) (p=0.0005).
PSA bounce is a common finding in our population and is associated with a lower rate of subsequent biochemical failure. The noted differences in PSA velocity will require verification in a future analysis to reduce the influence of median follow-up on this finding. Patients should be advised of the potential of bounce in PSA follow-up after permanent I(125) prostate brachytherapy and physicians involved in follow-up of prostate brachytherapy patients should be aware of this phenomenon, allowing them to commit to appropriate PSA surveillance, avoiding the premature and inappropriate initiation of salvage therapy during PSA bounce.
报告永久性碘-125前列腺近距离放射治疗后良性前列腺特异性抗原反弹的发生率，描述我们研究人群中的相关因素，并回顾反弹与随后生化失败的关系。
2000年2月至2005年5月，一家机构对374例局限性前列腺癌患者进行了碘-125永久性前列腺近距离放射治疗。使用前瞻性收集的数据库来识别前列腺特异性抗原（PSA）反弹病例，定义为在初始PSA最低点基础上上升0.2 ng/ml以上，随后未经治疗下降至或低于该最低点。排除接受新辅助或辅助激素治疗的患者。使用ASTRO共识定义和Phoenix（最低点+2 ng/mL）定义确定生化失败。
确定了205例患者，中位随访时间为45个月（24 - 85个月）。79例（37%）男性出现PSA反弹，植入后中位时间为14.8个月（1.7 - 40.6个月）。PSA峰值中位数为1.8 ng/ml（0.4 - 7.4），反弹幅度为0.91 ng/ml（0.2 - 5.8）。在评估植入前和植入后因素与反弹的关联时，只有年龄较小具有统计学意义（p = 0.002）。经历反弹后，4例（5%）患者达到ASTRO共识定义（1997年）的生化失败阈值，而未反弹患者为19例（15%）（p = 0.01）。Phoenix（最低点+2 ng/mL）阈值在反弹后6例（7.5%）患者中达到，未反弹患者为22例（17%）（p = 0.003）。两种定义在反弹期间都容易出现假阳性判断。反弹期间PSA速度中位数为0.08 ng/mL/月（0.02 - 0.98），在Phoenix生化失败前的速度中位数为0.28 ng/mL/月（0.07 - 2.04），显著低于该值（p = 0.0005）。
PSA反弹在我们的研究人群中是常见现象，且与随后较低的生化失败率相关。PSA速度的显著差异需要在未来分析中进行验证，以减少中位随访对这一发现的影响。应告知患者永久性碘-125前列腺近距离放射治疗后PSA随访中存在反弹的可能性，参与前列腺近距离放射治疗患者随访的医生应了解这一现象，以便他们进行适当的PSA监测，避免在PSA反弹期间过早和不恰当地开始挽救治疗。
