Division of Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Int J Radiat Oncol Biol Phys. 2010 Mar 1;76(3):816-23. doi: 10.1016/j.ijrobp.2009.02.059. Epub 2009 Jun 12.
The primary aim of this study was to assess pulmonary radiation toxicity quantitatively in patients who received thoracic radiotherapy combined with induction and/or concurrent chemotherapy with or without taxanes for esophageal cancer.
The study subjects were 139 patients treated at the University of Texas M.D. Anderson Cancer Center for esophageal cancer and who had undergone [(18)F]-fluorodeoxyglucose positron emission tomography/computed tomography between November 1, 2003 and December 15, 2007 for disease restaging after chemoradiotherapy. The patients were grouped into those who had not received taxanes (Group 1), those who had received induction or concurrent taxanes (Group 2), and those who had received both induction and concurrent taxanes (Group 3). Clinical pulmonary toxicity was scored using the National Cancer Institute Common Terminology Criteria for Adverse Events, version 3. Linear regression was applied to the fluorodeoxyglucose uptake vs. radiation dose to determine the pulmonary metabolic radiation response (PMRR) for each case. The clinical toxicity scores and PMRR among the groups were evaluated for significance differences.
The crude rate of pneumonitis symptoms was 46%, 62%, and 74% for Group 1, 2, and 3, respectively. The analysis of variance test of log(PMRR) by treatment was significant (p = .0046). Group 3 had a 61% greater PMRR compared with Group 1 (p = .002). Group 2 had a 38% greater PMRR compared with Group 1 (p = .015). Finally, Group 3 had a 17% greater PMRR compared with Group 2 (p = .31). A PMRR enhancement ratio of 1.60 (95% confidence interval, 1.19-2.14) was observed for Group 3 vs. Group 1.
Patients given induction and concurrent taxane chemotherapy had a significantly greater PMRR and clinical pneumonitis symptoms compared with the patients whose chemotherapy regimen did not include taxanes.
本研究的主要目的是评估接受胸部放疗联合诱导和/或同步化疗（含或不含紫杉烷类药物）治疗食管癌的患者的肺部放射性毒性。
本研究纳入了 139 名在德克萨斯大学 MD 安德森癌症中心接受治疗的食管癌患者，这些患者在接受放化疗后于 2003 年 11 月 1 日至 2007 年 12 月 15 日期间进行了 [(18)F]-氟脱氧葡萄糖正电子发射断层扫描/计算机断层扫描（用于疾病放化疗后再分期）。患者被分为未接受紫杉烷类药物组（第 1 组）、接受诱导或同步紫杉烷类药物组（第 2 组）和接受诱导和同步紫杉烷类药物组（第 3 组）。使用美国国立癌症研究所不良事件常用术语标准（第 3 版）对临床肺部毒性进行评分。采用线性回归分析确定每个病例的氟脱氧葡萄糖摄取与辐射剂量之间的肺部代谢辐射反应（PMRR）。评估了各组之间的临床毒性评分和 PMRR 的差异。
第 1、2 和 3 组的肺炎症状发生率分别为 46%、62%和 74%。治疗组之间的对数 PMRR 方差分析检验具有统计学意义（p=0.0046）。第 3 组的 PMRR 比第 1 组高 61%（p=0.002），第 2 组的 PMRR 比第 1 组高 38%（p=0.015），第 3 组的 PMRR 比第 2 组高 17%（p=0.31）。第 3 组与第 1 组相比，PMRR 增强率为 1.60（95%置信区间，1.19-2.14）。
与化疗方案中未包含紫杉烷类药物的患者相比，接受诱导和同步紫杉烷类药物化疗的患者的 PMRR 和临床肺炎症状明显更高。
