缓激肽在遗传性血管性水肿发病机制中的作用  

Role of Bradykinin in the Pathogenesis of Hereditary Angioedema

作　　者：任华丽[1] 张宏誉[2] 

机构地区：[1]首都医科大学宣武医院风湿变态科,北京100053 [2]中国医学科学院北京协和医学院北京协和医院变态反应科,北京100073

出　　处：《中华临床免疫和变态反应杂志》2007年第1期38-42,共5页Chinese Journal of Allergy & Clinical Immunology

摘　　要：目的评价缓激肽在遗传性血管性水肿(HAE)发病过程中的作用。方法应用放射免疫法测定23例HAE 缓解期患者和40名健康志愿者的血浆缓激肽水平。结果正常对照组和 HAE 缓解期患者的血浆缓激肽水平分别为(264.67±124.54)和(308.82±135.96)pg/ml,两组比较无统计学差异(P=0.201)。9例 HAE 患者急性期血浆缓激肽水平为(748.60±249.64)pg/ml,较缓解期的(369.89±212.29)pg/ml 显著增高(P=0.003)。单侧肘部水肿患者的患侧血浆缓激肽水平高于健侧。1例服用血管紧张素转换酶抑制剂引起水肿的患者。水肿发作期血浆缓激肽水平为550.16 pg/ml,缓解期下降至326.16 pg/ml.但仍略高于正常对照。结论缓激肽水平升高可能参与了 HAE的发病过程。本研究建立了可用于临床研究的缓激肽测定方法.可应用于其他缓激肽参与疾病发病机制的研究。Objective To evaluate the role of bradykinin in the pathogenesis of hereditary angioedema （HAE）. Methods We used a commercial available radioimmunoassay kit and a modified sampling method recommended in the kit to determine plasma concentrations of bradykinin in 23 HAE patients and 40 healthy subjects. Results HAE patients in remission phase had bradykinin levels as high as （308.82 ± 135.96） pg/nd, no statistical difference compared with 40 healthy controls [（264.67 ± 124.54） pg/ml, P=0.201] . Nine patients had higher bradykinin levels in acute phase than in remission phase [（748.60± 249.64） vs. （ 369.89 ± 212.29） pg/ml, P = 0.003]. Patients with angioedema in one of their arms had higher plasma bradykinin levels of the affected arms than in the contralateral arms. One patient suspected of angiotensin converting enzyme inhibitor-related angioedema had higher bradykinin level in acute phase than in remission phase （550.16 vs. 326.16 pg/ml）. Conclusions It is proposed that bradykinin is involved in the pathophysiology of HAE. Together with the commercial available kit, this modified sampling method is more feasible and could be routinely applied in the bradykinin measurement of angioedema and many other diseases like inflammation, cardiovascular diseases as well.

关 键 词：遗传性血管性水肿 发病机制 缓激肽 

分 类 号：R596[医药卫生—内科学]