尿酸與腦梗死預后相關性的臨床研究
發(fā)布時間:2018-03-10 06:33
本文選題:高尿酸血癥 切入點:腦梗死 出處:《青島大學》2017年碩士論文 論文類型:學位論文
【摘要】:目的:探討血尿酸水平與腦梗死患者急性期治療效果及預后的相關性,干預尿酸后,患者能否獲益。探討血尿酸在腦梗死患者急性期及恢復期中的作用機制。方法:選取2016年1月至2016年12月在淄博市臨淄區(qū)人民醫(yī)院神經(jīng)內(nèi)科一病區(qū)住院治療的急性腦梗死患者207例為研究對象,根據(jù)血尿酸水平分為高尿酸血癥組(n=119)與血尿酸正常組(對照組)(n=88),并將高尿酸血癥的患者隨機分為干預組(主要應用別嘌呤醇等降尿酸藥物)(n=60)及未干預組(n=59),三組腦梗死患者分別在入院的當天、治療1周、治療2周、治療3個月進行神經(jīng)功能缺損評分及尿酸檢查,對結果進行統(tǒng)計學分析。比較患者治療1周、2周時三組患者治療效果、神經(jīng)功能缺損改善程度,即NIHSS評分改善率,比較治療3個月時三組患者的預后、神經(jīng)功能恢復改善程度,即m RS評分改善率,m RS評分≤2判斷為腦梗死預后良好組;m RS量表評分2判斷為腦梗死預后不良組(死亡病例統(tǒng)計到預后不良組)。結果:1.對照組、干預組、未干預組治療1周時NIHSS評分改善率(即NIHSS評分下降率)分別為12.48±4.54%、10.24±4.78%、-1.22±3.51%。對照組、干預組、未干預組治療2周時NIHSS評分改善率分別為28.03±4.44%、25.20±3.81%、-4.38±3.52%。治療1周、2周時,干預組較未干預組患者NIHSS評分改善率顯著升高(p=0.002,p=0.002),對照組較未干預組NIHSS評分改善率顯著升高,有顯著差異性(p=0.001,p=0.001)。2.對照組、干預組、未干預組三組患者治療3個月時m RS評分改善率(即m RS評分下降率)分別為57.83±8.91%、52.26±7.90%、27.52±7.52%。治療3個月時,干預組較未干預組患者的m RS評分改善率顯著提高(p=0.001),對照組較未干預組m RS評分改善率顯著提高(p=0.001),差異有統(tǒng)計學意義(P0.01)。3.干預組預后良好率88.33%,顯著高于未干預組的預后良好率59.32%,有顯著差異性(χ2=21.113,P=0.002)。對照組預后良好率是93.18,顯著高于未干預組預后良好率59.31%,有顯著差異性(χ2=24.929,P=0.002)。而對照組與干預組預后良好率比較差異無統(tǒng)計學意義(χ2=1.047,P0.05)。結論:1.與血尿酸正常的腦梗死患者相比,伴有高尿酸血癥的腦梗死患者其神經(jīng)功能損害程度相對較重,治療效果及預后相對較差。血尿酸水平升高可能與急性腦梗死的發(fā)生發(fā)展、治療效果及臨床預后密切相關。2.伴高尿酸血癥的腦梗死患者降低血尿酸治療后可能會改善臨床預后,降低疾病致殘率。應重視血尿酸水平的變化,高尿酸血癥可促進動脈粥樣硬化發(fā)生,可能進一步加重患者的代謝紊亂,而且在腦梗死急性期參與顱腦組織損傷的級聯(lián)反應,同時引起腦梗死急性期氧自由基的大量釋放,故高尿酸血癥可能與急性腦梗死疾病的進展有著密切關系,高尿酸血癥可能增大患者發(fā)生腦梗死的危險性,增加腦梗死復發(fā)率,增加腦梗死的不良預后?蓪⒋酥笜俗鳛楠毩㈩A測因素加以檢測并干預,指導腦梗死治療及二級預防。
[Abstract]:Objective: to investigate the correlation between serum uric acid level and the therapeutic effect and prognosis of patients with acute cerebral infarction. To explore the mechanism of serum uric acid in acute and convalescent stage of cerebral infarction patients. Methods: from January 2016 to December 2016, the patients were hospitalized in the Department of Neurology, Renmin Hospital, Zibo City. 207 cases of cerebral infarction were studied. According to the level of serum uric acid, the patients were divided into two groups: hyperuricemia group (n = 119) and control group (control group). Patients with hyperuricemia were randomly divided into two groups: intervention group (mainly treated with allopurinol) and non-intervention group (n = 59). The patients with infarction were admitted to hospital on the same day, After 1 week, 2 weeks and 3 months of treatment, the neurological function defect score and uric acid were evaluated, and the results were analyzed statistically, and the results were compared between the three groups after 1 week and 2 weeks of treatment, and the degree of improvement of nerve function defect was compared. That is, the improvement rate of NIHSS score, the prognosis of the three groups after 3 months of treatment, and the degree of improvement of nerve function. That is to say, the improvement rate of MRS score and the mRS score 鈮,
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