Inflammatory response after influenza vaccination in men with and without carotid artery disease
Inflammatory response after influenza vaccination in men with and without carotid artery disease
复制标题
DOI：
10.1161/01.atv.0000248534.30057.b5
复制
发表时间：
2006-12-01
影响因子：
8.7
通讯作者：
Jarvik, Gail P.
中科院分区：
文献类型：
--
作者：
Carty, Cara L.;Heagerty, Patrick;Jarvik, Gail P.
目的：炎症标志物与血管疾病相关；然而，急性期反应（APR）的变化尚未得到评估。我们评估了严重颈动脉疾病（CAAD）男性（狭窄度< 80%）的APR大小是否与没有狭窄（狭窄度< 15%）的男性不同。方法和结果：招募患有（n = 43）和未患有（n = 61）严重CAAD且接受临床流感疫苗接种的白人男性。他们的基线和接种疫苗后24小时的血液样本检测c反应蛋白（CRP）、IL-6和血清淀粉样蛋白-a （SAA）。疫苗接种的体内APR是可测量的，并且在受试者之间存在差异。经年龄、吸烟、口服降糖药、阿司匹林和染色剂等因素调整后，CAAD患者1n（CRP）、1n（IL-6）和1n（SAA）水平的相对24小时变化高于非CAAD患者，但只有SAA反应显著（P = 0.02）；CAAD患者的相对SAA反应是无CAAD患者的1.6倍（95%可信区间，1.1 - 2.5）。所有指标的APR似乎与基线水平无关。结论：流感疫苗接种可导致有或无CAAD的男性出现轻微但可测量的APR。SAA APR变异性可能是独立于基础SAA水平的严重血管疾病的预测因子。
Objective - Inflammatory markers are associated with vascular disease; however, variation in the acute phase response (APR) has not been evaluated. We evaluated whether the APR magnitude in men with severe carotid artery disease (CAAD) (> 80% stenosis) differed from that of men without stenosis (< 15% stenosis).Methods and Results - White males with (n = 43) and without (n = 61) severe CAAD receiving clinical influenza vaccinations were recruited. Their baseline and 24-hour after - vaccination blood samples were assayed for C-reactive protein (CRP), IL-6, and serum amyloid-a (SAA). In vivo APR to vaccination was measurable and varied among subjects. Adjusted for age, smoking, oral hypoglycemics, aspirin, and stain use, the relative 24-hour changes in levels of 1n(CRP), 1n( IL-6), and 1n(SAA) were higher in men with CAAD than in men without, but only the SAA response was significant (P = 0.02); the relative SAA response was 1.6 (95% confidence interval, 1.1 to 2.5) times higher in men with than without CAAD. The APR for all markers appeared to be independent of baseline levels.Conclusions - Influenza vaccination results in a mild, but measurable, APR in men with and without CAAD. SAA APR variability may be a predictor of severe vascular disease that is independent of basal SAA level.