帕罗西汀治疗脑卒中后抑郁症的有效性和安全性研究及作用机制

Efficacy and Safety Studies of Paroxetine on Patients with Post Stress Depression and the Related Mechanisms

目的 分析帕罗西汀治疗脑卒中后抑郁症的有效性和安全性及作用机制。方法 选择2012年5月至2014年5月在韩城市人民医院接受住院治疗的脑卒中后抑郁症患者118例作为研究对象,按照随机数字表法分为两组,每组59例。对照组接受常规治疗;观察组接受帕罗西汀20~40 mg/d治疗8周,比较两组患者接受治疗前及治疗后的抑郁及神经功能评分,P物质、神经肽Y、促肾上腺皮质激素释放因子水平及治疗安全性差异。结果 观察组、对照组治疗后4周、8周汉密尔顿抑郁量表评分较治疗前降低[观察组：（14.2±2.1）分,（13.1±1.8）分比（22.2±3.9）分;对照组：（19.4±3.0）分,（18.3±2.8）分比（23.0±3.9）分]（均P〈0.05）,纳维亚卒中量表评分逐渐降低[观察组：（12.1±2.0）分,（8.3±1.8）分比（23.2±4.2）分;对照组：（19.4±3.7）分,（15.2±1.0）分比（22.2±4.1）分]（均P〈0.05）。观察组患者接受治疗后的P物质为（30±6）ng/L、促肾上腺皮质激素释放因子为（45±5）ng/L,均低于对照组的（46±8）ng/L、（58±9）ng/L,观察组神经肽Y水平为（139±23）ng/L,高于对照组患者的（109±14）ng/L（P〈0.05）;两组之间的不良反应发生率比较差异无统计学意义（P〉0.05）。结论 帕罗西汀可有效改善脑卒中后抑郁症患者的抑郁症状及神经功能,优化神经肽水平,同时具有良好的治疗安全性。

Objective To analyze the efficacy and safety of paroxetlne on patients with post stroke depa- ression （PSD）, and the related mechanisms. Methods A total of 118 patients with PSD in Hancheng Peo- ple＇s Hospital from May 2012 to May 2014 Were included. According to random number table method, they were divided into control group which received canventional treatment and observation group which received paroxetine treatment （20-40 mg,/d,8 weeks）, each group with 59 cases. The depression and neurological function score,neurepeptide Y,substanco P （SP） ,and the level of the releasing factor of the adrenal cortex and the safety of the treatment of the two groups before and after treatment were compared. Results 4 weeks and 8 weeks after treatment, Hamilton Anxiety Scale score of both groups were decreased [ observation group： （ 14. 2 ± 2. 1 ） scores, （ 13.1 ± 1. 8 ） scores vs. （ 22.2 ± 3.9 ） scores; control group ： （ 19.4 ± 3.0 ） scores, （ 18.3 ± 2. 8 ） scores vs （23.0 ± 3.9 ） scores ] （ all P 〈 0. 05 ） ; Scandinavia stroke scale gradually decreased [ observation group： （ 12. 1 ± 2. 0） scores, （ 8.3 ± 1.8 ） scores vs （23.2 ± 4. 2） scores; control group： （ 19. 4 ± 3.7 ） scores, （ 15.2 ± 1.0 ） scores vs （22.2 ±4. 1 ） scores ] （ all P 〈 0. 05 ）, The observation group＇ s SP （ 30 ± 6） ng,/L, corticotropin releasing factor （45 ± 5 ） ng/L were lower than control group＇s （46 ± 8 ） ng/L, （58 ±9） ng/L,levels（139 ±23） ng/L was higher than control group＇s （109 ± 14） ng/L （P 〈0. 05） ; the adverse reaction incidence of the two groups had no statistically significant difference （ P 〉 0. 05 ）. Conclu- sion Paroxetine treatment is effective in improving symptoms of PSD and the neurological function, optimize neuropeptide levels,wlth good clinical safety.