中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2009年
8期
685-687
,共3页
组织型纤溶酶原激活物%肽水解酶类%脑梗塞
組織型纖溶酶原激活物%肽水解酶類%腦梗塞
조직형섬용매원격활물%태수해매류%뇌경새
Tissue plasminogen activator%Peptide hydrolases%Brain infarcition
目的 初步评价尤瑞克林在重组组织型纤维蛋白酶原激活剂(rt-PA)静脉溶栓治疗急性缺血性脑梗死中的安全性和有效性.方法 采用随机、对照研究方法 ,入选患者按1:1随机分为对照组和试验组.对照组22例,仅给予rt-PA(0.9 mg/kg);试验组22例,rt-PA(0.9 mg/kg)溶栓后静脉滴注尤瑞克林(0.15 PNAU/d,连续7 d).主要安全性评价指标是溶栓24 h内症状性脑出血发生率,次要评价指标为患者神经功能缺损评分(NIHSS)、日常生活活动能力评分(BI). 结果 溶栓24 h内,试验组与对照组比较,脑出血率差异无统计学意义(4.6%对9.1%,X2=0.00,P>0.05),再梗死率有降低趋势(18.2%对31.8%,X2=1.091,P>0.05).溶栓治疗后1 d、21 d和90 d,试验组NIHSS评分显著低于对照组(t值分别为2.119、2.913、2.187,均P<0.05),试验组90 d BI评分显著高于对照组(t=2.39,P<0.05). 结论 在不增加出血风险的情况下,尤瑞克林提高rt-PA静脉溶栓治疗急性脑梗死的疗效.
目的 初步評價尤瑞剋林在重組組織型纖維蛋白酶原激活劑(rt-PA)靜脈溶栓治療急性缺血性腦梗死中的安全性和有效性.方法 採用隨機、對照研究方法 ,入選患者按1:1隨機分為對照組和試驗組.對照組22例,僅給予rt-PA(0.9 mg/kg);試驗組22例,rt-PA(0.9 mg/kg)溶栓後靜脈滴註尤瑞剋林(0.15 PNAU/d,連續7 d).主要安全性評價指標是溶栓24 h內癥狀性腦齣血髮生率,次要評價指標為患者神經功能缺損評分(NIHSS)、日常生活活動能力評分(BI). 結果 溶栓24 h內,試驗組與對照組比較,腦齣血率差異無統計學意義(4.6%對9.1%,X2=0.00,P>0.05),再梗死率有降低趨勢(18.2%對31.8%,X2=1.091,P>0.05).溶栓治療後1 d、21 d和90 d,試驗組NIHSS評分顯著低于對照組(t值分彆為2.119、2.913、2.187,均P<0.05),試驗組90 d BI評分顯著高于對照組(t=2.39,P<0.05). 結論 在不增加齣血風險的情況下,尤瑞剋林提高rt-PA靜脈溶栓治療急性腦梗死的療效.
목적 초보평개우서극림재중조조직형섬유단백매원격활제(rt-PA)정맥용전치료급성결혈성뇌경사중적안전성화유효성.방법 채용수궤、대조연구방법 ,입선환자안1:1수궤분위대조조화시험조.대조조22례,부급여rt-PA(0.9 mg/kg);시험조22례,rt-PA(0.9 mg/kg)용전후정맥적주우서극림(0.15 PNAU/d,련속7 d).주요안전성평개지표시용전24 h내증상성뇌출혈발생솔,차요평개지표위환자신경공능결손평분(NIHSS)、일상생활활동능력평분(BI). 결과 용전24 h내,시험조여대조조비교,뇌출혈솔차이무통계학의의(4.6%대9.1%,X2=0.00,P>0.05),재경사솔유강저추세(18.2%대31.8%,X2=1.091,P>0.05).용전치료후1 d、21 d화90 d,시험조NIHSS평분현저저우대조조(t치분별위2.119、2.913、2.187,균P<0.05),시험조90 d BI평분현저고우대조조(t=2.39,P<0.05). 결론 재불증가출혈풍험적정황하,우서극림제고rt-PA정맥용전치료급성뇌경사적료효.
Objective To evaluate the safety and efficacy of urinary kallidinogenase for recombinant tissue-type plasminogen activator (rt-PA) intravenous thrombolytic treatment in patients with acute cerebral infartion Methods A randomized control study was applied. All 44 patients with acute cerebral infartion were randomized 1:1 to the experimental group (22 cases) and the control group (22 cases). Patients were administrated rt-PA(0. 9 mg/kg)in control group, and patients were given urinary kallidinogenase by intravenous drip (0.15 PNAU/d, for 7 days) after rt-PA intravenous thrombolytic treatment (0.9 mg/kg)in experimental group. The main evaluation index was the incidence of symptomatic intraeerebral hemorrhage within 24 hours, and the secondary assessing items were NIHSS and BI. Results There was 1 case (4.6%) with symptomatic intracerebral hemorrhage in the experimental group and 2 (9.1%) in the control group (X2 =0.00, P= 1.000),and reinfarction rate showed a decreasing tendency in experimental group (18.2% vs. 31.8%, X2=1.091,P=0.296). Compared with the control group, the NIHSS scores were significantly lower 1,21,90 days after thrombolytic therapy (t=2.119, 2.913, 2.187);P=0.041, 0.0 06, 0.042),and the BI scores were obviously higher at 90 days after thrombolytic therapy in experimental group(t= 2.39,P= 0.012). Conclusions Without increasing the risk of intracerebral hemorrhage, urinary kallidinogenase may improve the curative effect for rt-PA intravenous thrombolytic treatment in patients with acute cerebral infartion