丁苯酞联合阿替普酶对急性脑梗死患者静脉溶栓后神经功能缺损严重程度临床疗效观察
Clinical Efficacy Observation of Butylphthalide Combined with Alteplase on the Severity of Neurological Deficit in Patients with Acute Cerebral Infarction after Intravenous Thrombolysis
DOI: 10.12677/ACM.2023.133716, PDF,   
作者: 胡月圆:锦州医科大学临沂市人民医院研究生培养基地,山东 临沂;车峰远*:山东省临沂市人民医院神经内科,山东 临沂
关键词: 丁苯酞阿替普酶急性脑梗死神经功能缺损预后Butylphthalide Alteplase Acute Cerebral Infarction Neurological Deficit Prognosis
摘要: 目的:探讨丁苯酞联合阿替普酶对急性脑梗死患者静脉溶栓后神经功能缺损严重程度及预后的影响。方法:根据入排标准选取临沂市人民医院神经内科住院治疗的首次急性脑梗死患者200例,实验组给予阿替普酶联合丁苯酞治疗,对照组给予阿替普酶治疗,按照美国国立卫生院卒中量表(NIHSS)评定患者入院时、溶栓后24 h、溶栓后7 d及出院时的NIHSS评分;记录患者入院期间的不良事件(牙龈出血、鼻出血、消化道出血、脑出血、进展性卒中等);90天随访中按照改良的Rankin (mRS)评分量表记录患者预后情况(mRS ≤ 2分预后良,mRS > 2分预后不良)。比较各组间的差异,分析丁苯酞联合阿替普酶对急性脑梗死患者静脉溶栓后神经功能缺损严重程度及预后的影响。结果:两组患者一般临床资料、生化指标、入院时NIHSS评分及溶栓后24 h NIHSS评分相比较,差异均无统计学意义(P > 0.05);实验组患者溶栓后7 d及出院时的NIHSS评分均低于对照组,差异有统计学意义(P < 0.05);随访90天,实验组预后不良发生率低于对照组,差异有统计学意义(P < 0.05);实验组不良事件发生率高于对照组,差异无统计学意义(P > 0.05)。结论:丁苯酞联合阿替普酶能显著改善急性脑梗死患者神经功能缺损程度及预后,且安全性较高。
Abstract: Objective: To investigate the effect of butylphthalide combined with alteplase on the severity and prognosis of neurological deficit in patients with acute cerebral infarction after intravenous throm-bolysis. Methods: A total of 200 patients with first acute cerebral infarction who were hospitalized in the Department of Neurology, Linyi People’s Hospital were selected according to the admission and exclusion criteria. The experimental group was treated with alteplase combined with bu-tylphthalide, and the control group was treated with alteplase. The NIHSS scale (NIHSS) was used to assess the NIHSS score of patients at admission, 24 hours after thrombolysis, 7 days after thrombo-lysis and at discharge; adverse events (gingival bleeding, epistaxis, gastrointestinal bleeding, cere-bral hemorrhage, progressive stroke) were recorded during admission. The prognosis of patients was recorded according to the modified Rankin (mRS) score during the 90-day follow-up (mRS ≤ 2 points, good prognosis, mRS > 2 points, poor prognosis). The differences between the groups were compared, and the effect of butylphthalide combined with alteplase on the severity and prognosis of neurological deficit in patients with acute cerebral infarction after intravenous thrombolysis was analyzed. Results: There was no significant difference in general clinical data, biochemical indexes, NIHSS score at admission and NIHSS score 24 hours after thrombolysis between the two groups (P > 0.05). The NIHSS scores of patients in the experimental group were lower than those in the control group 7 days after thrombolysis and at discharge, compared with the control group, the difference was statistically significant (P < 0.05); after 90 days of follow-up, the incidence of poor prognosis in the treatment group was lower than that in the control group, and the difference was statistically significant (P < 0.05); the incidence of adverse events in the treatment group was higher than that in the control group, the difference was not statistically significant (P > 0.05). Conclusion: Bu-tylphthalide combined with alteplase can significantly improve the degree of neurological deficit and prognosis in patients with acute cerebral infarction, with high safety.
文章引用:胡月圆, 车峰远. 丁苯酞联合阿替普酶对急性脑梗死患者静脉溶栓后神经功能缺损严重程度临床疗效观察[J]. 临床医学进展, 2023, 13(3): 5052-5058. https://doi.org/10.12677/ACM.2023.133716

参考文献

[1] 王陇德, 彭斌, 张鸿祺, 等. 《中国脑卒中防治报告2019》概要[J]. 中国脑血管病杂志, 2020, 17(5): 272-281.
[2] 王陇德, 彭斌, 张鸿祺, 等.《中国脑卒中防治报告2020》概要[J]. 中国脑血管病杂志, 2022, 19(2): 136-144.
[3] Saver, J.L., et al. (2016) Time to Treatment with Endovascular Thrombectomy and Outcomes from Is-chemic Stroke: A Meta-Analysis. JAMA, 316, 1279-1288. [Google Scholar] [CrossRef] [PubMed]
[4] 彭斌, 吴波. 中国急性缺血性脑卒中诊治指南2018 [J]. 中华神经科杂志, 2018, 51(9): 666-682.
[5] 廖晓凌, 王伊龙, 潘岳松, 等. 急性缺血性卒中不同剂量阿替普酶静脉溶栓疗效比较[J]. 中国卒中杂志, 2014, 9(7): 551-556.
[6] Feng, T.L. and Zhao, Y.F. (2013) Effect of Thrombolysis Timing on Thrombolytic Effect of Acute My-ocardial Infarction. Chinese Journal of Integrative Medicine on Cerebrovascular Disease, 11, 235-236.
[7] Peng, Y., Zeng, X., Feng, Y. and Wang, X. (2004) Antiplatelet and Antithrombotic Activity of L-3-n-butylphthalide in Rats. Jour-nal of Cardiovascular Pharmacology, 43, 876-881. [Google Scholar] [CrossRef] [PubMed]
[8] Sun, H., Zhang, J., Wang, J., et al. (2013) Association between Genetic Variants of the Leukotriene Biosynthesis Pathway and the Risk of Stroke: A Case-Control Study in the Chinese Han population. Chinese Medical Journal, 126, 254-259.
[9] Zhao, W., Luo, C., Wang, J., et al. (2014) 3-n-Butylphthalide Improves Neuronal Morphology after Chronic Cerebral Ischemia. Neural Regeneration Research, 9, 719-726. [Google Scholar] [CrossRef] [PubMed]
[10] Wang, Y., Qi, W., Zhang, L., et al. (2017) The Novel Targets of DL-3-n-Butylphthalide Predicted by Similarity Ensemble Approach in Combination with Molecular Docking Study. Quantitative Imaging in Medicine and Surgery, 7, 532-536. [Google Scholar] [CrossRef] [PubMed]
[11] He, W., Zhou, W. and Hu, Z. (2011) Chinese Herbal Extract DL-3n-Butylphthalide: A Commonly Used Drug for the Treat-ment of Ischemic Stroke as a Novel Therapeutic Approach to Treat Neurodegenerative Diseases. Neural Regeneration Research, 6, 2773-2778.
[12] Zhao, H., Yun, W., Zhang, Q., Cai, X., Li, X., Hui, G., et al. (2016) Mobilization of Circulating Endothelial Progenitor Cells by DL-3-n-Butylphthalide in Acute Ischemic Stroke Patients. Journal of Stroke and Cerebrovascular Diseases, 25, 752-760. [Google Scholar] [CrossRef] [PubMed]
[13] Wang, X.-L., Wang, Z.-Y., Ling, J.-J., Zhang, Y.-H. and Yin, J. (2016) Synthesis and Biological Evaluation of Nitric oxide (NO)-Hydrogen Sulfide (H2S) Releasing Derivatives of (S)-3-n-Butylphthalide as Potential Antiplatelet Agents. Chinese Journal of Natural Medicines, 14, 946-953. [Google Scholar] [CrossRef
[14] 郑晶, 左靖. 阿替普酶联合丁苯酞对急性缺血性脑卒中患者静脉溶栓后早期神经功能恶化影响的研究[J]. 中华脑血管病杂志(电子版), 2020, 14(5): 281-285.
[15] Huang, Y., Pan, L. and Wu, T. (2021) Improvement of Cerebral Ischemia-Reperfusion Injury by L-3-n-Butylphthalide through Promoting Angiogenesis. Experimental Brain Research, 239, 341-350. [Google Scholar] [CrossRef] [PubMed]
[16] Wang, Y.-X., Chen, Y., Zhang, C.-H., et al. (2015) Study on the Effect of Urinary Kallidinogenase after Thrombolytic Treatment for Acute Cerebral Infarction. European Review for Medical & Pharmacological Sciences, 19, 1009-1012.
[17] 李其富, 孔双艳, 德吉曲宗. 丁基苯酞对大鼠局灶缺血脑组织VEGF及bFGF表达的影响[J]. 四川大学学报(医学版), 2008(1): 84-88.
[18] Zhang, P., Guo, Z.-F., Xu, Y.-M., Li, Y.-S. and Song, J.-G. (2016) N-Butylphthalide (NBP) Ameliorated Cerebral Ischemia Reperfusion-Induced Brain Injury via HGF-Regulated TLR4/NF-κB Signaling Pathway. Biomedicine & Pharmacotherapy, 83, 658-666. [Google Scholar] [CrossRef] [PubMed]
[19] Ye, J., Zhai, L., Zhang, S., et al. (2015) DL-3-n-Butylphthalide Inhibits Platelet Activation via Inhibition of cPLA2-Mediated TXA2 Synthesis and Phosphodiesterase. Platelets, 26, 736-744. [Google Scholar] [CrossRef] [PubMed]
[20] Yang, C.-S., Guo, A., Li, Y., et al. (2019) DL-3-n-Butylphthalide Reduces Neurovascular Inflammation and Ischemic Brain Injury in Mice. Aging and Disease, 10, 964-976. [Google Scholar] [CrossRef
[21] Zhou, P.-T., Wang, L.-P., Qu, M.-J., et al. (2019) DL-3-n-Butylphthalide Promotes Angiogenesis and Upregulates Sonic Hedgehog Expression after Cerebral Ischemia in Rats. CNS Neuroscience & Therapeutics, 25, 748-758. [Google Scholar] [CrossRef] [PubMed]
[22] Zhao, Q., Zhang, C., Wang, X., Chen, L., Ji, H. and Zhang, Y. (2012) (S)-ZJM-289, a Nitric Oxide-Releasing Derivative of 3-n-Butylphthalide, Protects Against Ischemic Neuronal Injury by Attenuating Mitochondrial Dysfunction and Associated Cell Death. Neurochemistry International, 60, 134-144. [Google Scholar] [CrossRef] [PubMed]
[23] Xiao, H., Deng, M., Yang, B., Hu, Z. and Tang, J. (2018) Pre-treatment with 17β-Estradiol Attenuates Cerebral Ischemia-Induced Blood-Brain Barrier Disruption in Aged Rats: In-volvement of Antioxidant Signaling. Neuroendocrinology, 106, 20-29. [Google Scholar] [CrossRef] [PubMed]
[24] Deng, S., Liu, H., Qiu, K., You, H., Lei, Q. and Lu, W. (2018) Role of the Golgi Apparatus in the Blood-Brain Barrier: Golgi Protection May Be a Targeted Therapy for Neurological Diseases. Molecular Neurobiology, 55, 4788-4801. [Google Scholar] [CrossRef] [PubMed]