Fitzgerald Ryan T, Wright Steven M, Samant Rohan S, Kumar Manoj, Ramakrishnaiah Raghu H, Van Hemert Rudy, Brown Aliza T, Angtuaco Edgardo J
Department of Radiology, University of Arkansas for Medical Sciences, 4301 W. Markham Street, #556, Little Rock, AR 72205-7199, USA.
Department of Radiology, University of Arkansas for Medical Sciences, 4301 W. Markham Street, #556, Little Rock, AR 72205-7199, USA.
J Clin Neurosci. 2014 Sep;21(9):1575-8. doi: 10.1016/j.jocn.2014.03.004. Epub 2014 Apr 26.
The pathophysiology of posterior reversible encephalopathy syndrome (PRES) is incompletely understood; however, an underlying state of immune dysregulation and endothelial dysfunction has been proposed. We examined alterations of serum lactate dehydrogenase (LDH), a marker of endothelial dysfunction, relative to the development of PRES in patients receiving chemotherapy. A retrospective Institutional Review Board approved database of 88 PRES patients was examined. PRES diagnosis was confirmed by congruent clinical diagnosis and MRI. Clinical features at presentation were recorded. Serum LDH values were collected at three time points: prior to, at the time of, and following PRES diagnosis. Student's t-test was employed. LDH values were available during the course of treatment in 12 patients (nine women; mean age 57.8 years [range 33-75 years]). Chemotherapy-associated PRES patients were more likely to be normotensive (25%) versus the non-chemotherapy group (9%). LDH levels at the time of PRES diagnosis were higher than those before and after (p=0.0263), with a mean difference of 114.8 international units/L. Mean time intervals between LDH measurement prior to and following PRES diagnosis were 44.8 days and 51.4 days, respectively. Mean elapsed time between last chemotherapy administration and PRES onset was 11.1days. In conclusion, serum LDH, a marker of endothelial dysfunction, shows statistically significant elevation at the onset of PRES toxicity in cancer patients receiving chemotherapy. Our findings support a systemic process characterized by endothelial injury/dysfunction as a factor, if not the prime event, in the pathophysiology of PRES.
后部可逆性脑病综合征（PRES）的病理生理学尚未完全明确；然而，有人提出其潜在机制是免疫调节异常和内皮功能障碍。我们研究了接受化疗患者中，作为内皮功能障碍标志物的血清乳酸脱氢酶（LDH）的变化与PRES发生发展的关系。我们检查了经机构审查委员会批准的88例PRES患者的回顾性数据库。PRES诊断通过临床诊断和MRI结果一致得以证实。记录了患者就诊时的临床特征。在三个时间点收集血清LDH值：PRES诊断前、诊断时和诊断后。采用学生t检验。12例患者（9名女性；平均年龄57.8岁[范围33 - 75岁]）在治疗过程中可获得LDH值。与非化疗组（9%）相比，化疗相关PRES患者血压正常的可能性更高（25%）。PRES诊断时的LDH水平高于诊断前和诊断后（p = 0.0263），平均差异为114.8国际单位/升。PRES诊断前和诊断后LDH测量的平均时间间隔分别为44.8天和51.4天。最后一次化疗给药至PRES发作的平均间隔时间为11.1天。总之，作为内皮功能障碍标志物的血清LDH在接受化疗的癌症患者发生PRES毒性时出现统计学上的显著升高。我们的研究结果支持一种全身性过程，其特征为内皮损伤/功能障碍是PRES病理生理学中的一个因素，即便不是主要事件。
