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1.
目的探讨血清中超敏C反应蛋白(hs-CRP)、同型半胱氨酸(Hcy)及尿酸(UA)水平与颈动脉粥样硬化的关系。方法采用彩色多普勒超声对脑梗死患者双侧颈动脉进行筛查,根据颈动脉粥样硬化程度将患者分为轻度、中度及重度狭窄组;再根据斑块的不同性质将上述脑梗死患者分为稳定性斑块及不稳定性斑块两组;分别测定86例病例组与25例正常对照组血清hs-CRP、Hcy及UA水平。结果颈动脉斑块组血清hs-CRP、Hcy及UA水平均高于正常对照组。不稳定性斑块组血清hs-CRP与UA水平均高于稳定性斑块组。结论血清hs-CRP、Hcy、UA水平升高与颈动脉粥样硬化形成密切相关;血清中hs-CRP和UA水平异常升高与不稳定斑块形成密切相关。  相似文献   

2.
目的 观察洛伐他汀对脑梗死患者颈动脉粥样硬化斑块、血脂及血清C-反应蛋白(CRP)水平的影响.方法 120例脑梗死合并颈动脉粥样硬化斑块患者随机分为洛伐他汀组和对照组.两组在低脂饮食的基础上,洛伐他汀组口服洛伐他汀20 mg每日1次,共6个月;观察两组治疗8周及 6个月时颈动脉粥样硬化斑块积分、血清CRP及血脂水平的变化.结果 (1)治疗6个月时,洛伐他汀组颈动脉粥样硬化斑块积分(4.20±3.77) 明显低于治疗前(4.77±2.31)及对照组(6.86±1.89)(均P<0.05);(2)治疗8周时,洛伐他汀组血清CRP水平[(6.37±2.16)mg/L]明显低于治疗前 [(16.35±5.18)mg/L] 及对照组[(16.30±4.84)mg/L](均P<0.05);(3)与治疗前及对照组比较,治疗8周及6个月时,洛伐他汀组血总胆固醇、三酰甘油及低密度脂蛋白胆固醇水平明显降低,高密度脂蛋白胆固醇明显升高(均P<0.05).结论 长期服用洛伐他汀可稳定甚至缩小颈动脉粥样硬化斑块,降低CRP及血脂水平,有助于预防脑卒中复发.  相似文献   

3.
目的 探讨长期服用血脂康对脑梗死患者的颈动脉粥样硬化斑块和血清C反应蛋白(CRP)的影响.方法 61例有动脉粥样斑块的脑梗死患者随机分为血脂康组和对照组,利用彩色多普勒超声仪测量患者颈动脉中-内膜厚度(IMT)和粥样斑块大小,并检测血清CRP水平和总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)及高密度脂蛋白(HDL-C)水平.观察治疗24周后上述指标的变化.结果 治疗后血脂康组CRP水平、TC、TG、LDL-C明显下降,HDL-C明显升高;IMT和粥样斑块变小,且差异具有统计学意义.结论 血脂康具有抗炎,抗动脉粥样硬化,逆转粥样硬化斑块的作用,进而对脑梗死的发生起预防作用.  相似文献   

4.
目的:探讨伴发炎症性抑郁的精神分裂症患者临床特征及其影响因素。方法:来自3家医院的慢性精神分裂症患者330例中,87例精神分裂症抑郁量表(CDSS)总分≥5,诊断为伴发抑郁症状的精神分裂症;其中25例血浆超敏C反应蛋白(hs-CRP)≥3 mg/L归入炎症性抑郁组,62例血浆hs-CPR3 mg/L归入非炎症性抑郁组;比较两组人口学(性别、年龄、受教育年限、婚姻状况等)及临床资料[发病年龄、病程、体质量指数(BMI)、因精神分裂症住院次数、自杀状况、躯体疾病(冠心病、心力衰竭、高血压、糖尿病、脑卒中、肿瘤等)、用药情况等]、血液生化指标(血糖、血脂、食欲素A、瘦素)、阳性和阴性症状量表(PANSS)及失眠严重指数(ISI)评分,分析伴发炎症性抑郁的影响因素。结果:与非炎症性抑郁组相比,炎症性抑郁组BMI、血浆食欲素A及瘦素水平明显增高,服用的抗精神病药氯丙嗪等效剂明显量降低(P均0.05);二分类Logistic回归显示,高瘦素水平(OR=1.375,95%CI:1.022~1.850,P=0.035)、低氯丙嗪等效剂量(OR=0.997,95%CI:0.994~0.999,P=0.013)是炎症性抑郁的影响因素。结论:高瘦素水平及服用低剂量抗精神病药可能是精神分裂症患者伴发炎症性抑郁的危险因素。  相似文献   

5.
目的 探讨急性脑梗死患者颈动脉粥样硬化性斑块与人类软骨糖蛋白-39(YKL-40)、超敏C-反应蛋白(hs-CRP)含量的关系.方法 选取130例急性脑梗死患者和30例正常对照者检测血清YKL40、hs-CRP水平.对急性脑梗死患者结合颈动脉超声检查结果,分为颈动脉IMT正常组30例、颈动脉IMT增厚组30例、颈动脉斑块组70例,其中稳定斑块37例,不稳定斑块33例,测定并比较各组血清YKL40、hs-CRP水平.结果 急性脑梗死组血清YKL40、hs-CRP水平显著高于正常对照组(P<0.01);在急性脑梗死患者中,有颈动脉粥样硬化组血清YKL-40、hs-CRP水平较颈动脉IMT正常组明显升高(P<0.01),颈动脉IMT斑块形成组血清YKL-40、hs-CRP水平较颈动脉IMT增厚组明显升高(P<0.01),颈动脉粥样硬化不稳定斑块组血清YKL-40、hs-CRP水平显著高于稳定斑块组;线性相关分析表明YKL-40水平和hs-CRP水平无明显相关性(r=0.04,P>0.05);Logistic回归分析结果显示:YKL-40、hs-CRP是发生颈动脉粥样硬化的危险因素(OR=1.128,95%C1 1.21~1.87;OR=2.62,95% CI1.76 ~4.47).结论 YKL-40、hs-CRP可能反映急性脑梗死患者颈动脉粥样硬化斑块的炎症程度以及斑块的不稳定程度,病变越重,斑块越不稳定,YKL-40、hs-CRP水平越高,且YKL-40水平独立于hs-CRP水平.  相似文献   

6.
目的观察阿托伐他汀钙对急性脑梗死患者颈动脉粥样斑块硬化的治疗作用。方法 120例有颈动脉斑块形成的急性脑梗死患者随机分为治疗组和对照组,各组60例,均给予常规和综合性治疗,治疗组给予阿托伐他汀钙片,20 mg,1次/晚,治疗12个月,观察2组患者颈动脉斑块的内膜中层厚度(IMT)和斑块面积,血脂水平和高敏C-反应蛋白(hs-CRP)浓度。结果治疗组应用阿托伐他汀钙12个月,其颈动脉IMT斑块面积、血脂水平、hs-CRP均显著下降,治疗组治疗后的IMT与治疗前显著降低,差异有统计学意义(P<0.05)。结论阿托伐他汀钙可以显著稳定动脉斑块,并促进斑块的消退,减轻血管的炎症反应。  相似文献   

7.
目的探讨精神分裂症(schizophrenia,SZ)患者血清补体C3(complement component 3,C3)、C4(complement component 4,C4)、超敏C-反应蛋白(high sensitivity C reactive protein,hs-CRP)和尿酸(uric acid,UA)的水平变化及其临床意义。方法选择144例SZ患者为SZ组,并根据4周内有无服用抗精神病药物分为治疗组(77例)和停药组(67例),另选择同期来湘雅二医院的健康体检者147例为健康对照组。采用免疫散射比浊法、胶乳增强免疫比浊法、尿酸氧化酶法分别测定各组血清补体C3、C4、hs-CRP和UA浓度,并比较分析。结果 SZ组患者血清补体C3、C4水平低于对照组[(0.99±0.17)g/L vs.(1.03±0.17)g/L、(0.21±0.05)g/L vs.(0.23±0.05)g/L],UA水平高于对照组[(351.61±95.90)μmol/L vs.(300.28±39.57)μmol/L],差异有统计学意义(分别P0.05,P0.05,P0.001)。治疗组患者血清补体C3、C4、hs-CRP和UA水平较停药组均升高[(1.04±0.19)g/L vs.(0.95±0.15)g/L、(0.22±0.06)g/L vs.(0.20±0.05)g/L、1.08(0.33,5.04)mg/L vs.0.47(0.28,1.29)mg/L、(374.54±108.33)μmol/L vs.(331.61±79.03)μmol/L],差异均有统计学意义(P0.01)。治疗组患者血清hs-CRP和UA浓度较对照组均升高[1.08(0.33,5.04)mg/L vs.0.61(0.33,1.26)mg/L、(374.54±108.33)μmol/L vs.(300.28±39.57)μmol/L],差异有统计学意义(P0.001)。结论 SZ患者血清C3、C4、hs-CRP和UA的水平变化对SZ临床诊断和抗精神病药物疗效评估有一定指导意义。  相似文献   

8.
目的:对比症状性与无症状性颈动脉动脉粥样硬化性狭窄患者循环hs_CRP水平有无差异并探讨其意义。方法:通过数字减影脑血管造影手段筛选了48例狭窄度≥70%严重颈动脉狭窄患者,并以NASCET标准分为31例症状性与17例无症状性颈动脉狭窄两组。分别测循环血清hs_CRP水平并作对比,同时对比入院后实验室检查的血脂和纤维蛋白原水平。结果:症状性颈动脉狭窄组hs_CRP水平(6.3±5.4mg/L)高于无症状性颈动脉狭窄组(3.2±2.5mg/L),差异有统计学意义(P<0.05)。而血脂和纤维蛋白酶原水平在两组间水平对比无统计学意义差别(P>0.05)。结论:高循环hs_CRP水平可能对颈动脉病变出现相关神经缺损症状高风险性有一定的预测价值。  相似文献   

9.
10.
目的分析急性脑梗死患者颈动脉粥样硬化斑块性质与白细胞介素-6(IL-6)、C反应蛋白(CRP)表达水平的关系。方法选择急性脑梗死患者95例(观察组)为研究对象,根据颈动脉彩色多普勒超声检测结果分为不稳定斑块组(29例)、稳定斑块组(31例)及无斑块组(35例),选择同时期健康人30例为正常对照组,测定4组研究对象血清中IL-6、CRP的水平并进行比较。结果观察组CRP(4.80±2.16)mg/L和IL-6(209.54±75.60)pg/mL水平显著高于正常对照组的(2.43±0.51)mg/L和(103.34±8.99)pg/mL(P0.05)。不稳定斑块组CRP、IL-6水平均高于稳定斑块组、无斑块组和对照组(P0.05);稳定斑块组高于无斑块组和对照组(P0.05)。CRP、IL-6水平与动脉粥样硬化斑块的不稳定性呈正相关(rCRP=0.740,rIL-6=0.924,均P0.05)。结论急性脑梗死患者颈动脉粥样硬化斑块性质与IL-6、CRP表达水平密切相关,可能在预测脑血管病的发生及防治中起重要作用。  相似文献   

11.
目的:运用彩色多普勒超声检查观察脑梗死患者颈动脉粥样硬化的状况,研究颈动脉粥样硬化与各种危险因素之间的关系,探讨对脑梗死高危人群防治的策略。方法:对200例住院的脑梗死患者行彩色多普勒颈动脉超声检查,观察指标包括颈动脉内膜中层厚度(intima-mediathickness,IMT)及颈动脉粥样硬化斑块,分析这些观察指标与患者年龄、性别、入院血压、血脂、血糖、吸烟和饮酒之间的关系。结果:研究发现吸烟可能是IMT异常的独立危险因素(OR2.943,95%CI:1.253-6.912);IMT值与年龄呈正相关(r=0.23761,P=0.0007),与吸烟指数也呈正相关(r=0.14655,P=0.0409)。年龄(OR1.077,95%CI:1.043-1.111)、吸烟(OR3.424,95%CI:1.569~7.471)、糖尿病(OR3.792,95%CI:1.650-8.717)、Lp(a)异常(OR2.624,95%CI:1.112-6.193)可能是颈动脉斑块发生的独立危险因素:斑块积分与Lp(a)呈正相关(r=0.20823,P=0.0208)。结论:颈动脉IMT异常与吸烟密切相关,可能是导致脑梗死的独立危险因素,在脑梗死的发病中具有一定的影响。除年龄因素外,控制吸烟和糖尿病是预防脑梗死较为重要及可行的,而对于Lp(a)的干预方法及效果仍需要进一步研究。  相似文献   

12.
缺血性脑血管病与颈动脉粥样硬化及其危险因素的关系   总被引:17,自引:0,他引:17  
目的探讨缺血性脑血管病(ICVD)与颈动脉粥样硬化及其危险因素的关系。方法对186例ICVD患者与194例非脑血管病患者和正常体检者(对照组)行颈部血管超声检查和血液生化检查;比较两组间的颈动脉硬化程度及脑卒中危险因素的差异。结果ICVD组年龄[(69±7)岁]和患有高血压(66.1%)、糖尿病(53.4%)、代谢综合征患者(44.6%)的比率非常明显高于对照组[(61±5)岁、48.8%、15.2%、12.9%](均P<0.001)。ICVD组颈动脉粥样硬化分级计分≥2分(斑块发生率)、≥3分(血管狭窄发生率)分别为69.3%、20.4%,明显高于对照组的33.5%和5.1%(均P<0.05)。结论颈动脉粥样硬化是ICVD的危险因素之一;各种危险因素的聚集对ICVD的发生起重要作用。  相似文献   

13.
目的探讨急性脑梗死患者颈动脉粥样硬化斑块与血液炎症因子水平的关系。方法 164例急性脑梗死患者经颈动脉超声检查分为无斑块组(42例)、稳定斑块组(58例)及不稳定斑块组(64例);其中Ⅰ、Ⅱ、Ⅲ级斑块各为37、45、40例。检测各组患者血清超敏C反应蛋白(hs-CRP)及血浆肿瘤坏死因子-α(TNF-α)、白介素6(IL-6)水平,并进行比较。结果稳定斑块组及不稳定斑块组血清hs-CRP及血浆TNF-α、IL-6水平明显高于无斑块组(均P<0.05);不稳定斑块组明显高于稳定斑块组(均P<0.05)。且随着斑块严重程度的增加,其血清hs-CRP及血浆TNF-α、IL-6水平也明显增高(均P<0.05)。结论血清hs-CRP及血浆TNF-α、IL-6水平可以反映急性脑梗死患者颈动脉粥样硬化的严重程度。  相似文献   

14.
炎症因素与脑梗死患者颈动脉粥样硬化的关系   总被引:2,自引:1,他引:1  
目的 探讨炎症因素与脑梗死患者颈动脉粥样硬化的关系.方法 对244例急性缺血性脑卒中患者的颈动脉内膜中层厚度(IMT)及斑块情况和血液炎症性生化指标进行相关性分析.结果 炎症因素(单核细胞比例,纤维蛋白原,C-反应蛋白水平,血沉)和颈动脉粥样硬化相关,其中单核细胞比例(ORIMT=1.231,P<0.01;OR斑块=1.175,P<0.05)及血沉增高(ORIMT=1.024,OR斑块=1.029,均P<0.01)具有独立预测性,单核细胞比例的独立预测性最高.炎症因素和斑块稳定性之间无相关性.结论 单核细胞比例及血沉可独立预测颈动脉粥样硬化的发生.  相似文献   

15.
BACKGROUND: Some researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction. OBJECTIVE: To investigate the correlation between levels of serum high-sensitivity C-reactive protein and carotid atherosclerosis in patients with acute cerebral infarction accompanied with carotid atherosclerosis. DESIGN: Contrast observation between two groups. SETTING: Department of Neurology, Zhenzhou Hospital, Shenyang Medical College. PARTICIPANTS: A total of 102 patients with acute cerebral infarction regarded as cerebral infarction group were selected from Department of Neurology, Shenzhou Hospital Affiliated to Shenyang Medical College from February 2005 to September 2006. There were 55 males and 47 females and their ages ranged from 55 to 86 years. All patients met the variously diagnostic points of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were finally diagnosed with CT or MRI examination. Illness course was in an acute phase. A total of 96 healthy subjects were regarded as control group, including 51 males and 45 females aged from 48 to 78 years. All accepted subjects provided the confirmed consent. METHODS: ① Patients in the cerebral infarction group received carotid ultrasound Doppler examination and serum high-sensitivity C-reactive protein detection within 72 hours after onset. IMMAGE immune biochemical system and latex reinforcement particle-enhanced nephelometric immunoassay (PENIA) were used for quantitative detection of serum high-sensitivity C-reactive protein. ② Healthy subjects in the control group received the same detection. SEQUOIA512 color Doppler ultrasound (Siemens Company, USA) was used to detect carotid artery of all subjects so as to observe intima media thickness of artery and formation of artery atherosclerostic plaques. If artery atherosclerostic plaques were formed, their properties and amounts were determined based on the characteristics of light-echo signals. Evaluating criteria: Intima media thickness of artery was the vertical dimension from crossed face between lumen and tunica intima to crossed face between tunica media and tunica adventitia. Intima media thickness ≤ 0.9 mm was regarded as normal; 0.9 mm < intima media thickness ≤ 1.2 mm was regarded as thickening; when local eminence thickening was processed towards to lumen, the intima media thickness was more than 1.2 mm and plaque of tunica intima was formed at the same time. Properties of plaque were classified into 4 types: steady low-echo lipid malacoplakia, equal-echo fiber plaque, strong-echo or sound-imaging calcification hard plaque and unsteady-echo ulcer mixed plaque. Fiber plaque and calcification hard plaque were steady but malacoplakia and mixed plaque were unsteady. MAIN OUTCOME MEASURES: Thickness of tunica media, characteristics of plaque and level of serum high-sensitivity C-reactive protein in carotid artery in two groups. RESULTS: All 102 patients with cerebral infarction and 96 healthy subjects were involved in the final analysis. ① Comparisons of level of high-sensitivity C-reactive protein: Level of high-sensitivity C-reactive protein in normal tunica media was higher in the cerebral infarction group [(4.66±1.55) mg/L] than the control group [(3.49±1.24) mg/L, t =2.541, P < 0.05]. In addition, level of high-sensitivity C-reactive protein in patients with thickening tunica media and plaque was not significantly different between the cerebral infarction group and the control group (P > 0.05). ② Correlation between various degrees of vascular lesion and level of high-sensitivity C-reactive protein in the cerebral infarction group: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with thickening tunica media [(8.16±2.42) mg/L] than patients with normal tunica media [(4.66±1.55) mg/L, t =4.132, P < 0.01]. In addition, level of high-sensitivity C-reactive protein was statistically significantly higher in patients with carotid plaque [(12.08±3.85) mg/L] than patients with normal tunica media (t =5.994, P < 0.01) and thickening tunica media (t =4.197, P < 0.01). ③ Levels of high-sensitivity C-reactive protein in patients with various kinds of carotid plaque: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with unsteady carotid plaque [(13.54±2.62) mg/L] than patients with steady carotid plaque [(8.61±3.71) mg/L, t =2.002, P < 0.05]. That was to say level of serum high-sensitivity C-reactive protein in patients who suffered acute cerebral infarction combined with carotid atherosclerosis especially carotid plaque was higher than that in those patients who did not have carotid lesions. This suggested that serum high-sensitivity C-reactive protein had a certain correlation with onset of carotid atherosclerosis in patients with acute cerebral infarction. CONCLUSION: Serum high-sensitivity C-reactive protein certainly correlates with onset of carotid atherosclerosis in patients with acute cerebral infarction, while inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.  相似文献   

16.
BackgroundSome researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.ObjectiveTo investigate the correlation between levels of serum high-sensitivity C-reactive protein and carotid atherosclerosis in patients with acute cerebral infarction accompanied with carotid atherosclerosis.DesignContrast observation between two groups.SettingDepartment of Neurology, Zhenzhou Hospital, Shenyang Medical College.ParticipantsA total of 102 patients with acute cerebral infarction regarded as cerebral infarction group were selected from Department of Neurology, Shenzhou Hospital Affiliated to Shenyang Medical College from February 2005 to September 2006. There were 55 males and 47 females and their ages ranged from 55 to 86 years. All patients met the variously diagnostic points of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were finally diagnosed with CT or MRI examination. Illness course was in an acute phase. A total of 96 healthy subjects were regarded as control group, including 51 males and 45 females aged from 48 to 78 years. All accepted subjects provided the confirmed consent.Methods
Patients in the cerebral infarction group received carotid ultrasound Doppler examination and serum high-sensitivity C-reactive protein detection within 72 hours after onset. IMMAGE immune biochemical system and latex reinforcement particle-enhanced nephelometric immunoassay (PENIA) were used for quantitative detection of serum high-sensitivity C-reactive protein.
Healthy subjects in the control group received the same detection. SEQUOIA512 color Doppler ultrasound (Siemens Company, USA) was used to detect carotid artery of all subjects so as to observe intima media thickness of artery and formation of artery atherosclerostic plaques. If artery atherosclerostic plaques were formed, their properties and amounts were determined based on the characteristics of light-echo signals. Evaluating criteria: Intima media thickness of artery was the vertical dimension from crossed face between lumen and tunica intima to crossed face between tunica media and tunica adventitia. Intima media thickness ≤ 0.9 mm was regarded as normal; 0.9 mm < intima media thickness ≤ 1.2 mm was regarded as thickening; when local eminence thickening was processed towards to lumen, the intima media thickness was more than 1.2 mm and plaque of tunica intima was formed at the same time. Properties of plaque were classified into 4 types: steady low-echo lipid malacoplakia, equal-echo fiber plaque, strong-echo or sound-imaging calcification hard plaque and unsteady-echo ulcer mixed plaque. Fiber plaque and calcification hard plaque were steady but malacoplakia and mixed plaque were unsteady.Main outcome measuresThickness of tunica media, characteristics of plaque and level of serum high-sensitivity C-reactive protein in carotid artery in two groups.ResultsAll 102 patients with cerebral infarction and 96 healthy subjects were involved in the final analysis.
Comparisons of level of high-sensitivity C-reactive protein: Level of high-sensitivity C-reactive protein in normal tunica media was higher in the cerebral infarction group [(4.66±1.55) mg/L] than the control group [(3.49±1.24) mg/L, t =2.541, P < 0.05]. In addition, level of high-sensitivity C-reactive protein in patients with thickening tunica media and plaque was not significantly different between the cerebral infarction group and the control group (P > 0.05).
Correlation between various degrees of vascular lesion and level of high-sensitivity C-reactive protein in the cerebral infarction group: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with thickening tunica media [(8.16±2.42) mg/L] than patients with normal tunica media [(4.66±1.55) mg/L, t =4.132, P < 0.01]. In addition, level of high-sensitivity C-reactive protein was statistically significantly higher in patients with carotid plaque [(12.08±3.85) mg/L] than patients with normal tunica media (t =5.994, P < 0.01) and thickening tunica media (t =4.197, P < 0.01).
Levels of high-sensitivity C-reactive protein in patients with various kinds of carotid plaque: Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with unsteady carotid plaque [(13.54±2.62) mg/L] than patients with steady carotid plaque [(8.61±3.71) mg/L, t =2.002, P < 0.05]. That was to say level of serum high-sensitivity C-reactive protein in patients who suffered acute cerebral infarction combined with carotid atherosclerosis especially carotid plaque was higher than that in those patients who did not have carotid lesions. This suggested that serum high-sensitivity C-reactive protein had a certain correlation with onset of carotid atherosclerosis in patients with acute cerebral infarction.ConclusionSerum high-sensitivity C-reactive protein certainly correlates with onset of carotid atherosclerosis in patients with acute cerebral infarction, while inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.  相似文献   

17.
目的 探索重复经颅磁刺激(rTMS)治疗对住院慢性精神分裂症患者认知功能的改善作用以及对患者血清C反应蛋白(CRP)水平的影响,初步探索rTMS影响患者认知功能的潜在机制.方法 选取2013年1月~2016年1月在天津市精神卫生中心住院治疗的精神分裂症患者60例,按照病情、性别、年龄等因素进行配对,随机分配每对患者接受rTMS真刺激治疗(治疗组)和伪刺激治疗(对照组)4周,应用阳性与阴性症状量表(PANSS)和可重复的成套神经心理状态测量(RBANS)在治疗前后评估患者的精神症状及认知功能.所有患者治疗前后均检测血清CRP水平.结果 (1)治疗后,治疗组患者的血清CRP水平明显下降,差异有统计学意义(P<0.05),而对照组无变化;(2)治疗组治疗后PANSS总分及阴性症状因子分较治疗前均有下降,差异有统计学意义(P<0.05),而对照组无变化;(3)治疗后,治疗组RBANS总分、视觉广度分、注意分、延时记忆分较前均有升高,差异有统计学意义(P<0.05),对照组RBANS总分及各因子分较治疗前差异均无统计学意义;(4)治疗组患者治疗前后PANSS总分差值与即刻记忆分差值、阴性量表分差值与RBANS总分差值及延时记忆分差值均呈负相关(P<0.05);(5)治疗组患者的血清CRP变化值与RBANS总分差值、即刻记忆、注意和延时记忆各因子差值均呈负相关(P<0.05).结论 rTMS可以有效改善慢性精神分裂症患者的认知功能,其机制可能与rTMS治疗缓解炎性反应有关.  相似文献   

18.
目的研究中青年脑梗死患者颈动脉粥样硬化及其血清基质金属蛋白酶-9(MMP-9)、组织基质金属蛋白酶抑制剂-1(TIMP-1)、超敏C反应蛋白(hs-CRP)水平的改变。方法应用彩色多普勒超声仪探测42例急性脑梗死患者(ACI组)、29例无症状颈动脉硬化患者(ACA组)及17名健康体检者(NC组)的双侧颈动脉粥样硬化的情况。采用酶联免疫吸附法检测各组血清MMP-9和TIMP-1水平,免疫散射比浊法检测血清hs-CRP水平。结果 NC组均未检出颈动脉粥样硬化斑块。ACI组易损斑块的比例(69.2%)及检出率(47.6%)均明显高于ACA组(46.4%,20.7%)(均P<0.05)。ACI组血清MMP-9、TIMP-1、hs-CRP水平及MMP-9/TIMP-1比值均明显高于ACA组(均P<0.05);ACA组血清MMP-9、TIMP-1、hs-CRP水平均明显高于NC组(均P<0.05)。ACI组中,易损斑块亚组血清MMP-9、TIMP-1、hs-CRP水平及MMP-9/TIMP-1比值均明显高于稳定斑块亚组(均P<0.05);稳定斑块亚组血清MMP-9、TIMP-1、hs-CRP水平均明显高于无斑块亚组(均P<0.05)。结论血清MMP-9、TIMP-1、hs-CRP可作为反映颈动脉粥样硬化及斑块稳定性的血清学指标。MMP-9/TIMP-1比值增高及颈动脉易损斑块可能提示中青年脑梗死的风险。  相似文献   

19.
目的:探讨普伐他汀对颈动脉粥样硬化(CAS)患者血浆同型半胱氨酸(Hey)水平及颈动脉粥样硬化程度的影响.方法:给100例CAS患者(≥ 60岁50例,老年CAS组;<60岁50例,中年CAS组)普伐他汀20mg/d,连续服用2个月;检测治疗前后血浆Hey水平并与50例健康体检者(正常对照组)比较;采用颈动脉超声多普勒仪检查治疗前后CAS程度.结果:两CAS组患者血浆Hey水平均明显高于正常对照组(均P<0.01).两CAS组患者治疗后血浆Hey水平及CAS程度均较治疗前明显降低(均P<0.01).结论:普伐他汀能明显降低CAS患者血浆Hey水平,并能减轻其CAS程度.  相似文献   

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