摘要
目的研究N末端B型利钠肽(NT—proBNP)在老年重型脑功能损伤患者急性期变化临床规律、临床意义及可能的影响因素。方法观察严重的颅脑功能损伤患者发病第1、3、5、7天NT-proBNP及心肌肌钙蛋白I(cTn-I)的变化规律,分析颅脑功能损伤致急性神经功能障碍与NT-proBNP、cTn-I,变化的相关性及其对预后的影响。结果死亡组各时点的NT-proBNP在住院第3、5、7天[(759±341)、(1980±839)、(2490±1862)ng/L3明显高于存活组[(594±612)、(733±424)、(315±346)ng/L];两组患者的cTn-I及NT—proBNP升高与进行性加重的颅内水肿相关;死亡组与存活组在早期颅内损伤病灶分布区有明显差别,死亡组基底节、脑干分布区高于存活组;7d后NT—proBNP仍处于较高水平者提示预后不良;NT—proBNP的升高与cTn—I水平无相关性(r-=0.0214,P〉0.05)。结论老年严重颅脑功能损伤患者急性期NT—proBNP进行性升高提示预后不良;老年严重颅脑功能损伤患者急性期其NT—proBNP升高幅度与颅脑损伤功能区有相关性。
Objective To explore the changes and influencing factors of serum NT-proBNP level in aged patients with severe brain dysfunction in acute phase, and the corresponding clinical significance. Methods The serum NT-proBNP and cTmI levels of patients with severe brain dysfunction at day 1, 3, 5 and 7 were measured respectively. The correlation between acute neurological dysfunction caused by brain dysfunction and serum NT-proBNP and cTn I levels were analyzed, and the impact on prognosis was explored. Results The serum NT-proBNP levels were significantly higher in death group at day 3[(759±341)ng/L), 5((1980±839)ng/L] and 7[(2490 ± 1862)ng/L] than in survival group[(594±612)ng/L,(733±424)ng/L,(315±346)ng/L]. Serum NT proBNP and cTn] levels were associated with progressive cerebral edema in both groups. Location of early intracranial lesions was significantly different between two groups. Death group had higher ratio of intracranial lesions in basal ganglia and brainstem than did survival group. High serum NT proBNP level after day 7 suggested poor prognosis. Serum NT-proBNP level was not associated with serum cTn-I level. Conclusions Progressively increased serum NT-proBNP level in aged patients with severe brain dysfunction in acute phase suggests poor prognosis. The increased degree of serum NT-proBNP in aged patients with severe brain dysfunction in acute phase is associated with the location of intracranial lesions.
出处
《中华老年医学杂志》
CAS
CSCD
北大核心
2011年第6期446-448,共3页
Chinese Journal of Geriatrics
关键词
利钠肽
脑
颅脑损伤
Natriuretic peptide, brain
Craniocerebral trauma