McDonald Jennifer S, McDonald Robert J, Ekins Jacob B, Tin Anthony S, Costes Sylvain, Hudson Tamara M, Schroeder Dana J, Kallmes Kevin, Kaufmann Scott H, Young Philip M, Lu Aiming, Kadirvel Ramanathan, Kallmes David F
Department of Radiology, College of Medicine, Mayo Clinic, Rochester, MN, United States of America.
Exogen Biotechnology Inc., Berkeley, CA, United States of America.
PLoS One. 2018 Jan 8;13(1):e0190890. doi: 10.1371/journal.pone.0190890. eCollection 2018.
Magnetic resonance imaging is considered low risk, yet recent studies have raised a concern of potential damage to DNA in peripheral blood leukocytes. This prospective Institutional Review Board-approved study examined potential double-strand DNA damage by analyzing changes in the DNA damage and repair markers γH2AX and 53BP1 in patients who underwent a 1.5 T gadolinium-enhanced cardiac magnetic resonance (MR) exam. Sixty patients were enrolled (median age 55 years, 39 males). Patients with history of malignancy or who were receiving chemotherapy, radiation therapy, or steroids were excluded. MR sequence data were recorded and blood samples obtained immediately before and after MR exposure. An automated immunofluorescence assay quantified γH2AX or 53BP1 foci number in isolated peripheral blood mononuclear cells. Changes in foci number were analyzed using the Wilcoxon signed-rank test. Clinical and MR procedural characteristics were compared between patients who had a >10% increase in γH2AX or 53BP1 foci numbers and patients who did not. The number of γH2AX foci did not significantly change following cardiac MR (median foci per cell pre-MR = 0.11, post-MR = 0.11, p = .90), but the number of 53BP1 foci significantly increased following MR (median foci per cell pre-MR = 0.46, post-MR = 0.54, p = .0140). Clinical and MR characteristics did not differ significantly between patients who had at least a 10% increase in foci per cell and those who did not. We conclude that MR exposure leads to a small (median 25%) increase in 53BP1 foci, however the clinical relevance of this increase is unknown and may be attributable to normal variation instead of MR exposure.
磁共振成像被认为风险较低,但最近的研究引发了对其可能损害外周血白细胞中DNA的担忧。这项经机构审查委员会批准的前瞻性研究,通过分析接受1.5T钆增强心脏磁共振(MR)检查患者的DNA损伤和修复标志物γH2AX和53BP1的变化,来检测潜在的双链DNA损伤。招募了60名患者(中位年龄55岁,39名男性)。排除有恶性肿瘤病史或正在接受化疗、放疗或类固醇治疗的患者。记录MR序列数据,并在MR暴露前后立即采集血样。采用自动免疫荧光测定法对外周血单个核细胞中γH2AX或53BP1病灶数进行定量。使用Wilcoxon符号秩检验分析病灶数的变化。比较γH2AX或53BP1病灶数增加>10%的患者与未增加的患者的临床和MR程序特征。心脏MR检查后,γH2AX病灶数无显著变化(MR前每细胞中位病灶数=0.11,MR后=0.11,p=0.90),但53BP1病灶数在MR后显著增加(MR前每细胞中位病灶数=0.46,MR后=0.54,p=0.0140)。每细胞病灶数至少增加10%的患者与未增加的患者在临床和MR特征上无显著差异。我们得出结论,MR暴露导致53BP1病灶数小幅增加(中位增加25%),然而这种增加的临床相关性尚不清楚,可能归因于正常变异而非MR暴露。