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1.
探讨动脉粥样硬化性脑梗死患者红细胞免疫粘附功能变化的特点.观察了86例动脉粥样硬化性脑梗死患者和63例正常对照者的红细胞免疫功能4项指标红细胞C3b受体花环率、红细胞免疫复合物花环率、血清中红细胞免疫粘附增强因子及红细胞免疫粘附抑制因子.动脉粥样硬化性脑梗死患者红细胞免疫功能变化的特点是红细胞C3b受体花环率降低,红细胞免疫复合物花环率升高,同时伴有血清中红细胞免疫粘附增强因子活性降低及红细胞免疫粘附抑制因子活性增强,红细胞免疫粘附功能低下.本研究提示脑梗死患者红细胞免疫功能下降,为探讨动脉粥样硬化性脑梗死的发病与防治途径提供了依据.  相似文献   

2.
探讨动脉粥样硬化性脑梗死患者红细胞免疫粘附功能变化的特点。观察了86例动脉粥样硬化性脑梗死患者和63例正常对照者的红细胞免疫功能4项指标:红细胞G3b受体花环率、红细胞免疫复合物花环率、血清中红细胞免疫粘附增强因子及红细胞免疫粘附抑制因子。动脉粥样硬化性脑梗死患者红细胞免疫功能变化的特点是红细胞G3b受体花环率降低,红细胞免疫复合物花环率升高,同时伴有血清中红细胞免疫粘附增强因子活性降低及红细胞免疫粘附抑制因子活性增强,红细胞免疫粘附功能低下。本研究提示脑梗死患者红细胞免疫功能下降,为探讨动脉粥样硬化性脑梗死的发病与防治途径提供了依据。  相似文献   

3.
目的 探讨慢性肝病患者红细胞免疫粘附功能的变化。方法 检测73例慢性乙型肝炎及肝硬化患者红细胞C_3b受体花环形成率(RBC-C_3bRR)、红细胞免疫复合物花环形成率(RBC-ICRR)及患者的循环免疫复合物(CIC)水平。结果 与正常对照组相比,RBC-C_3bRR在慢性肝炎中、重度及肝硬化患者中明显下降(P<0.01),在慢性肝炎轻度也有显著下降(P<0.05)。而RBC-ICRR在慢性肝炎中重度及肝硬化患者中明显升高(P<0.05)。各型肝病患者CIC均明显升高。结论 慢性肝炎患者的红细胞免疫粘附功能有明显改变,其意义有待进一步研究。  相似文献   

4.
本文测定了45例偏头痛患者及相应对照组的红细胞膜受体含量变化。结果表明:偏头痛发作期病人的红细胞C_(3b)受体花环率明显低于对照组,而免疫复合物受体花环率明显高于对照组。两种受体花环率间具有显著负相关性。提示红细胞免疫粘附功能异常参与了偏头痛症状的发作。  相似文献   

5.
观察不同病期老年类风湿性关节炎患者红细胞免疫功能的动态变化,并以此作为判断疗效、观察病情变化的指标。对25例老年类风湿性关节炎患者活动期与缓解期的红细胞C3b受体(C3bR)花环率及红细胞免疫复合物(IC)花环率进行了检测,结果活动期红细胞免疫功能显著低于对照组;而缓解期则有所恢复,其C3bR花环率均低于正常组。  相似文献   

6.
本文检测了59例慢性肝炎、肝硬化和肝癌病人的红细胞免疫粘附功能、白细胞介素-2及NK细胞活性等变化。结果显示这些患者的红细胞免疫复合物及循环免疫复合物增高,红细胞C_3b受体花环率降低,外周血白细胞介素-2、NK细胞活性及淋巴细胞转换率明显低于正常人,尤以HBV—DNA、HBeAg及HBsAg三者阳性者降低更为显著。提示HBV感染时白细胞介素-2、NK细胞活性等细胞免疫功能下降,以致使机体清除HBV的功能障碍。  相似文献   

7.
王培荣  时庆 《山东医药》1994,34(6):13-14
对51例原发性肾病综合征患儿进行红细胞免疫功能检测,患儿红细胞C3b受体花环显著低于正常对照组,红细胞免疫复合物花环显著高于正常对照组,表明患儿红细胞免疫粘附功能降低,清除免疫复合物功能减退,循环中免疫复合物增多,提高原发性肾病综合的发病可能与红细胞免疫功能的异常有一定关系。  相似文献   

8.
老年糖尿病患者红细胞免疫功能的研究   总被引:1,自引:0,他引:1  
本文对34例老年糖尿病患者红细胞免疫粘附功能及其调节因子活性进行了测定。结果显示,老年糖尿病患者红细胞C_3b受体花环率较正常对照组明显降低(P<0.01),免疫粘附抑制率明显升高(P<0.01),红细胞C_3b受体花环率降低和免疫粘附抑制率升高与高血糖、高血脂均呈负相关。提示老年糖尿病患者红细胞免疫功能低下,红细胞免疫粘附抑制因子降低,高血糖、高血脂可能是导致红细胞免疫功能低下的重要因素。  相似文献   

9.
用红细胞C3b受体(RBC-C3bR)花环及红细胞免疫复合物(RBC-IC)花环试验检测患者的红细胞免疫粘附功能。20例脑囊虫病患者RBC-C3bR受体花环率比正常对照组明显降低,免疫复合物花环率明显升高。吡喹酮治疗后10、30、60 d上述二项指标无明显恢复。180 d后RBC-C3b受体花环率比治疗前有所提高,而RBC-IC花环率有所下降。  相似文献   

10.
对35例中-重度支气管哮喘发作期患者的红细胞免疫粘附功能进行测定,发现中-重度支气管哮喘发作期患者红细胞C3b受体花环率明显下降,而红细胞免疫复合物花环率则明显升高。表明中-重度支气管哮喘患者的红细胞的免疫粘附功能的继发性低下。  相似文献   

11.
目的 研究尖锐湿疣患者红细胞免疫及调节因子与胸腺肽治疗前后的变化及机理。方法 按照郭峰与刘景田等建立及改进方法检测红细胞C3b受体花环率、红细胞免疫复合物花环率和红细胞免疫调节因子,并用胸腺肽治疗。结果 尖锐湿疣治疗前红细胞C3b受体花环率明显降低,红细胞免疫复合物花环率降低,红细胞免疫促进因子明显降低,而红细胞免疫抑制因子明显升高。经胸腺肽治疗后以上指标趋于正常。治疗后3个月未复发者31例。结论 提示尖锐湿疣患者存在红细胞免疫功能低下,胸腺肽治疗获较好疗效。  相似文献   

12.
AIM: To identify the hepatic vascular architecture of patients with hepatitis C virus(HCV) using superb microvascular imaging(SMI) and investigate the use of SMI in the evaluation of liver fibrosis.METHODS: SMI was performed in 100 HCV patients. SMI images were classified into five types according to the vascular pattern, and these patterns were compared with the fibrosis stage. Moreover, the images were analyzed to examine vascularity by integrating the number of SMI signals in the region of interest ROI [number of vascular trees(VT)]. The number of VT, fibrosis stage, serum parameters of liver function, and CD34 expression were investigated.RESULTS: There was a significant difference between SMI distribution pattern and fibrosis stage(P 0.001). The mean VT values in each of the fibrosis stages were as follows: 26.69 ± 7.08 in F0, 27.72 ± 9.32 in F1, 36.74 ± 9.23 in F2, 37.36 ± 5.32 in F3, and 58.14 ± 14.08 in F4. The VT showed excellent diagnostic ability for F4 [area under the receiver operator characteristic(AUROC): 0.911]. The VT was significantly correlated with the CD34 labeling index(r = 0.617, P 0.0001).CONCLUSION: SMI permitted the detailed delineation of the vascular architecture in chronic liver disease. SMI appears to be a reliable tool for noninvasively detecting significant fibrosis or cirrhosis in HCV patients.  相似文献   

13.
AIM: To study serum levels of leptin and adiponectin in patients with chronic hepatitis C virus infection genotype-4 (HCV-4) related steatosis and fibrosis. METHODS: We prospectively studied 45 untreated men with chronic HCV-4, with proven steatosis (group I, 30 patients), and fibrosis (group II, 15 patients), on liver biopsy. In addition, 15 healthy men (group III), matched for age, and body mass index were included. However, we excluded another five patients with steatohepatitis, and six patients with cirrhosis. We measured total serum leptin and adiponectin levels, as potential predictors for liver steatosis and fibrosis. Also, a correlation between these adipokines and various clinical and laboratory data were evaluated. All subjects were selected from Tropical and Internal medicine departments, Menoufiya University Hospital, Menoufiya, Egypt, during the period from February 2010 to August 2011. RESULTS: In group I, severity of hepatic steatosis was mild, moderate, and severe, in 19 patients (63.5%), 8 patients (26.5%), and 3 patients (10%), respectively. In contrast, in group II, hepatic fibrosis was found to be in stage 1, 2, and 3, in 6 patients (40%), in 6 patients (40%), and in 3 patients (20%), respectively. On comparing group I with group II, there was a significant decrease in serum adiponectin levels (131.4 ± 7.91 pg/mL vs 436 ± 9.75 pg/mL, P < 0.001), while there was no significant difference between both groups regarding serum leptin levels (34.69 ± 7.69 ng/mL vs 35.17 ± 1.06 ng/mL, P > 0.05). However, in the same group, when compared with group III, there was a significant increase in serum leptin levels (34.69 ± 7.69 ng/mL vs 10.69 ± 0.84 ng/mL, P < 0.001), while there was a significant decrease in serum adiponectin levels (131.4 ± 7.91 pg/mL vs 342.4 ± 44.48 pg/mL, P < 0.001). In contrast, in group II, when compared with group III, there was a significant increase in serum leptin and adiponectin levels (35.17 ± 1.06 ng/mL vs 10.69 ± 0.84 ng/mL, P < 0.001, and 436 ± 9.75 pg /mL vs 342.4 ± 44.48 pg/mL, P < 0.05, respectively), while there was no significant difference between both groups regarding serum creatinine (0.83 ± 0.34 vs 0.89 ± 0.24, P > 0.05). On the other hand, serum leptin was not correlated with serum adiponectin in group I and in group II (r = 0.09, P > 0.05, and r = -0.1, P > 0.05, respectively). However, serum adiponectin was significantly negatively correlated with serum aspartate transaminase in group I, but no correlation detected in group II (r =-0.39, P > 0.05, and r = -0.03, P > 0.05). CONCLUSION: In male patients with chronic HCV-4, serum adiponectin levels are elevated in hepatic fibrosis, but decreased in steatosis. Therefore, in contrast to leptin, adiponectin may be used as a non-invasive marker.  相似文献   

14.
目的 检测血清基质金属蛋白酶-1(MMP-1)、组织金属蛋白酶抑制剂-1(TIMP-1)及两者复合物(MMP-1/TIMP-1 com-plex)含量并评价其变化意义。方法 采用双抗体夹心式酶联免疫吸附法(ELISA)对10例健康对照、15例急性肝炎患者、15例慢性活动性肝炎患者;15例晚期肝硬化患者、15例肝癌手术患者、15例晚期肝癌患者以及10例胃癌入院手术患者进行检测。结果 与健康对照组相比,慢性活动对肝炎、晚期肝硬化以及晚期肝癌患者血清TIMP-1水平显著提高;慢性活动性肝炎及肝癌手术患者组血清MMP-1及MMP-1/TIMP-1复合物水平显著下降;急性肝炎及胃癌手术患者血清MMP-1、TIMP-1及MMP-1/TIMP-1复合物含量无显著变化。结论 在慢性活动性肝炎、晚期肝硬化以及肝癌患者存在严重的MMP-1和TIMP-1的失平衡,这种失平衡是这些患者肝脏细胞外基质净沉积的重要原因。MMP-1和TIMP-1在急性肝炎和胃癌患者血清含量总体变化不显著。  相似文献   

15.
目的 探讨慢性乙型肝炎病毒携带者血清高尔基体蛋白73(GP73)水平与肝组织病理学变化的关系。方法 2014年1月~2016年12月我院诊治的慢性HBV携带者150例、慢性乙型肝炎患者150例和乙型肝炎肝硬化患者150例,另选同期健康人50例,采用ELISA法检测GP73水平,对150例慢性HBV携带者进行肝穿刺活检,采用Metavir评分对肝组织炎症和纤维化进行评价。结果 慢性HBV携带者血清GP73水平为(46.5±7.8) ng/ml,慢性乙型肝炎组为(90.2±10.9) ng/ml,乙型肝炎肝硬化组为(231.6±20.1) ng/ml,均显著高于健康人组的(36.7±6.6) ng/ml,差异有统计学意义(P<0.05),肝硬化患者血清GP73水平也显著高于慢性乙型肝炎或HBV携带者(P<0.05);经肝组织检查,150例慢性HBV携带者肝内炎症活动度分级和纤维化分期表现为G0~G1 105例,G2 30例,G3~G4 15例,其血清GP73水平分别为(45.2±12.8)ng/ml、(63.8±15.0)ng/ml和(83.7±20.1)ng/ml,S0~S1 98例,S2 30例,S3~S4 22例,其血清GP73水平分别为(45.1±16.8)ng/ml、(67.3±16.4)ng/ml和(72.0±18.4)ng/ml,肝组织炎症活动度分级和纤维化分期严重的患者血清GP73水平显著升高,与分级或分期轻的人群比,差异有统计学意义(F=16.8,F=19.2,P均<0.05);Logistic回归分析发现血清GP73水平升高是慢性HBV携带者肝组织显著炎症(OR=1.1,95 % CI:1.0~1.1,P<0.05)和显著肝纤维化(OR=2.1,95% CI:0.8~1.2,P<0.05)的高危因素。结论 检测血清GP73水平可能有助于对慢性HBV携带者肝组织炎症分级和纤维化分期的判断,能否作为预测慢性HBV携带者肝组织炎症分级和纤维化分期的潜在标志物,还需要扩大验证。  相似文献   

16.
17.
目的:观察急性和慢性乙型肝炎患者急性期和恢复期外周血NK细胞和T淋巴细胞亚群的变化。方法在40例急性乙型肝炎和40例慢性乙型肝炎患者,分别在急性期和恢复期检测CD3+CD4+T细胞、CD3+CD8+T细胞和NK(CD3-CD16+CD56+)细胞占淋巴细胞的比率(%)。结果在急性乙型肝炎急性期NK细胞计数为(15.7±7.5)%,而在恢复期则上升至(21.9±8.2)%,(P<0.05);急性乙型肝炎患者在急性期CD3+CD4+T细胞为(35.5±6.8)%,到恢复期则显著下降(33.6±7.0)%,(P<0.05);急性乙型肝炎在急性期CD3+CD8+T细胞为(35.6±7.6)%,而在恢复期则显著下降(30.0±7.5)%,(P<0.05),后者仍比慢性乙型肝炎患者在病情恢复期高(19.1±7.1)%,(P<0.05)。结论在急性乙型肝炎病程中,NK细胞呈上升趋势,CD3+CD8+T细胞呈下降趋势,而在慢性乙型肝炎患者NK细胞及T淋巴细胞数量下降,致病情迁延不愈。  相似文献   

18.
本文对25例老年肺心病患的免疫指标检测结果表明,与健康老年人相比,发作期患者CD3、CD4、CD8及CD4/CD8均显著低下。提示动态观指标对判断临床状态及为患者提供免疫提供治疗有一定的价值。  相似文献   

19.
78 hospitalized patients were selected when presenting with at least one of these signs: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, splenomegaly. All had radioimmunoassays for hepatitis B surface antigen (HBsAg) and antidelta antibody (78/78). Acute or chronic hepatic disease was diagnosed in 56 patients: 7 acute viral hepatitis, 13 chronic hepatitis, 23 non alcoholic hepatic cirrhosis, and 13 hepatocellular carcinoma. Twenty-two patients with other diagnoses served as controls. Serum antidelta was present in each group: acute viral hepatitis (2/7), chronic hepatitis (2/13), non alcoholic hepatic cirrhosis (9/23), hepatocellular carcinoma (3/13), controls (2/22). Every patient with acute or chronic hepatic disease and positive serum anti-delta was positive for serum HBsAg. Amony controls, 2 patients with positive serum antidelta were negative for serum HBsAg but positive for antiHBs. Delta superinfection is present in the sahelian region; Patients with acute viral hepatitis, chronic hepatitis, non alcoholic hepatic cirrhosis, and hepatocellular carcinoma are electively infected. Patients with acute or chronic hepatitis and positive serum antidelta have hepatitis B virus evolutive infection (positive serum HBsAg).  相似文献   

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