Kuo Angera H, Ancukiewicz Marek, Kozak Kevin R, Yock Torunn I, Padera Timothy P
Department of Radiation Oncology, MGH Cancer Center, Massachusetts General Hospital and Harvard Medical School, Cox-737, 100 Blossom Street, Boston, MA, 02114, USA.
Current Affiliation: Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Radiat Oncol. 2015 Jan 9;10:5. doi: 10.1186/s13014-014-0324-1.
Thoracic and cardiac irradiation increases the risk of pulmonary and cardiovascular disease. In addition, radiation, often in combination with chemotherapy, can cause treatment-related pneumonitis. Previously, we showed that the common marker for cardiac damage, troponin T, was not elevated by chemoradiation [Lung Cancer 62:351-355, 2008]. In this study, we explore whether dose-volume metrics and biomarkers for cardiac damage, inflammation or angiogenesis could identify patients receiving thoracic radiation who would later have cardiac or pulmonary complications.
To this end, we quantified cardiac biomarkers including c-reactive protein (cRP) as well as a panel of angiogenic and inflammatory molecules in thirty patients who received radiation therapy to the thorax with or without concurrent chemotherapy between May 2006 and May 2007. Serum was collected at baseline, 2 weeks into radiation treatment and at the completion of radiation therapy. Heart and lung dosimetric parameters and clinical risk factors were also examined, along with the monitoring of adverse pulmonary and cardiac events during follow-up. Contrary to our hypothesis, there was no correlation between serum biomarker levels and cardiac radiation dose. Similarly there was little association between lung dose-volume metrics and inflammatory or angiogenic biomarkers. Furthermore, there was no correlation with serum biomarkers and adverse pulmonary or cardiovascular events.
Based on these data, acute elevations in serum biomarkers of cardiac damage, inflammation or angiogenesis should not be attributed to thoracic (chemo)radiation and elevations in such biomarkers of tissue damage should be further evaluated.
胸部和心脏放疗会增加肺部和心血管疾病的风险。此外,放疗通常与化疗联合使用,可导致与治疗相关的肺炎。此前,我们发现心脏损伤的常见标志物肌钙蛋白T在放化疗后并未升高[《肺癌》62:351 - 355,2008年]。在本研究中,我们探讨心脏损伤、炎症或血管生成的剂量 - 体积指标和生物标志物是否能够识别接受胸部放疗后可能出现心脏或肺部并发症的患者。
为此,我们对2006年5月至2007年5月期间接受胸部放疗(有或无同步化疗)的30例患者的心脏生物标志物进行了定量分析,包括C反应蛋白(cRP)以及一组血管生成和炎症分子。在基线、放疗2周时以及放疗结束时采集血清。同时还检查了心脏和肺部的剂量学参数及临床危险因素,并在随访期间监测不良肺部和心脏事件。与我们的假设相反,血清生物标志物水平与心脏辐射剂量之间没有相关性。同样,肺剂量 - 体积指标与炎症或血管生成生物标志物之间也几乎没有关联。此外,血清生物标志物与不良肺部或心血管事件之间也没有相关性。
基于这些数据,心脏损伤、炎症或血管生成的血清生物标志物急性升高不应归因于胸部(化疗)放疗,此类组织损伤生物标志物的升高应进一步评估。