外周血CD4+CD28+T淋巴细胞数量与阿托伐他汀对急性冠脉综合征患者干预的相关性

目的：急性冠脉综合征患者T淋巴细胞活化增殖以及细胞因子分泌增加。实验拟进一步验证阿托伐他汀干预急性冠脉综合征患者炎症细胞因子和CD4^＋D28^＋T淋巴细胞的变化。 方法：选择2006—03／2006—07在南方医科大学附属珠江医院心内科住院患者30例。患者对治疗均知情同意，并经医院伦理委员会批准。急性冠脉综合征组20例（急性心肌梗死10例，不稳定心绞痛10例），稳定性心绞痛组10例作为对照。所有患者在随访的6个月中，除按照入院前冠心病治疗常规服用阿司匹林、玻立维、硝酸酯类等药物外，加用阿托伐他汀20mg，1次/d，持续服用到随访日期。采用ELISA检测各组患者治疗前后外周血清以及培养的外周血单个核细胞上清中肿瘤坏死因子α和干扰素-γ的水平，采用流式细胞仪检测患者治疗前后CD4^＋CD28^＋T淋巴细胞的数量。 结果：30例患者均进入结果分析。阿托伐他汀治疗前后对比，急性冠脉综合征组外周血清以及培养的单个核细胞上清中肿瘤坏死因子-α和干扰素-γ的水平均明显下降（P均〈0．001），而稳定性心绞痛组无明显变化（P〉0．05），急性冠脉综合征组外周血CD4^＋CD28^＋T淋巴细胞数量明显减少（P〈0．001），稳定性心绞痛组无明显变化。 结论：急性冠脉综合征患者促炎症细胞因子以及外周血CD4^＋CD28^＋T淋巴细胞的数量接受阿托伐他汀干预可下调。     

阿托伐他汀对急性冠状动脉综合征患者外周血Th1／Th2细胞因子的干预

目的探讨阿托伐他汀对急性冠状动脉综合征患者外周血Th1／Th2细胞因子的影响。方法对30例住院行冠状动脉造影并确诊为冠心病的患者服用阿托伐他汀前和3个月后外周血Th1／Th2细胞因子水平进行检测。结果服用阿托伐他汀3个月后,急性冠状动脉综合征患者外周血Th1细胞因子水平降低（P〈0．05）,稳定型心绞痛组水平变化不明显（P〉0．05）。各组患者外周血Th2细胞因子水平无明显变化（P〉0．05）。结论在急性冠状动脉综合征中应用他汀类药物治疗能降低Th1细胞反应,改善Th1／Th2细胞功能的失衡。     

不同剂量阿托伐他汀对不稳定型心绞痛患者血管内皮功能及血小板活化的影响

目的 探讨不同剂量阿托伐他汀对不稳定型心绞痛患者血管内皮功能及血小板活化的影响.方法 78例不稳定型心绞痛患者随机分成阿托伐他汀10mg治疗组(n=39例)和阿托伐他汀20mg治疗组(n=39例).所有患者分别于入院时及用药4周后取血,行血小板胞质内α-颗粒膜糖蛋白( CD62p)、血清一氧化氮(N0)、血浆内皮素-1(ET-1)测定.另选本院同期健康体检的30例作为对照组,要求采血前2周内未服用药物.结果 不稳定型心绞痛患者血NO水平显著低于正常组,ET-1、CD62p水平明显高于正常组(P＜0.01).治疗4周后两组血清NO水平显著升高、ET-1、CD62p水平明显降低,阿托伐他汀20mg治疗组效果显著优于阿托伐他汀10mg治疗组(P＜0.01).结论 阿托伐他汀有改善不稳定型心绞痛患者内皮功能,抑制血小板活性作用,且有剂量依赖性.     

不稳定型心绞痛患者外周血CD28表达的研究

目的 研究不稳定型心绞痛(UAP)患者外周血T淋巴细胞CD28水平的变化.方法 运用流式细胞仪三色分析技术检测25例不稳定型心绞痛患者在发病期和缓解期以及20名正常健康对照外周血标本CD28、CD4的表达.结果 经统计学分析,发作期患者外周血T淋巴细胞CD4 /CD28-表达显著高于缓解期和正常健康对照,而CD4 /CD28 无显著性差异.结论 在不稳定型心绞痛患者发病过程中CD4 /CD28 -淋巴细胞发挥着非常重要的作用.     

常规剂量他汀类药物对冠心病患者血脂及炎症因子表达的影响

目的 对比经阿托伐他汀（立普妥20 mg）及瑞舒伐他汀（可定10 mg）治疗4 周后,冠心病患者LDL-C（低密度脂蛋白）、CX3CR1以及Hcy（同型半胱氨酸）水平的变化。 方 法选择经冠状动脉造影后确诊为冠心病的患者,其中80例稳定型心绞痛病例,80例不稳定型心绞痛病例,分别随机分为两组（A组和B组）;A组服用阿托伐他汀,B组服用瑞舒伐他汀。采用均相酶显色法检测LDL-C水平,利用流式细胞仪直接免疫荧光法检测不同类型患者外周血单核细胞上CX3CR1的表达,采用酶循环法检测Hcy水平。 结果经过4周的阿托伐他汀及瑞舒伐他汀治疗后各组冠心病患者LDL-C及Hcy水平较治疗前均有所下降（P＜0.05）,CX3CR1在各组患者外周血单核细胞中的表达较治疗前均减低（P＜0.05）,且治疗后LDL-C水平两组间比较有统计学差异（P＜0.05）,但治疗后CX3CR1及Hcy水平无统计学差异。 结论阿托伐他汀及瑞舒伐他汀可有效降低血脂,同时具有抗炎作用;但瑞舒伐他汀的降脂效果要强于阿托伐他汀。      

阿托伐他汀治疗冠心病前后患者血浆黏附因子浓度变化的观察

目的观察阿托伐他汀治疗冠心病前后患者血浆黏附因子浓度的变化。方法将89例研究对象分为急性冠状动脉综合征(ACS)组、稳定型心绞痛(SAP)组和对照组。ACS组又分为急性心肌梗死(AMI)组、不稳定型心绞痛(UAP)组两个亚组,ACS组和SAP组在常规治疗的基础上每日口服20 mg阿托伐他汀,共8周。对照组未服用他汀类药物。酶联免疫吸附分析(ELISA)方法分别测定研究对象入选当日和治疗8周后血浆中可溶性细胞间黏附因子-1(s ICAM-1)和可溶性血管细胞黏附因子-1(s VCAM-1)水平。结果 AMI组和UAP组的s ICAM-1s水平[(318.0±86.4)、(334.9±122.6)μg/L]明显高于SAP组[(264.8±86.6)μg/L]和对照组[(279.8±145.8)μg/L],差异有统计学意义(P0.01)。AMI组、UAP组和SAP组s VCAM-1水平[(407.8±182.1)、(446.3±160.4)、(386.5±104.2)μg/L]均显著高于对照组[(307.7±23.2)μg/L],差异有统计学意义(P0.05)。治疗后三组s ICAM-1和s VCAM-1水平较治疗前显著下降。结论急性冠状动脉综合征患者s ICAM-1水平显著升高,反映斑块的不稳定状态;阿托伐他汀具有抑制细胞黏附因子表达、稳定粥样硬化斑块的作用。     

不同剂量阿托伐他汀对急性冠状动脉综合征患者血浆B型钠尿肽水平影响

目的 测定急性冠状动脉综合征( ACS)患者应用不同剂量阿托伐他汀后血浆B型钠尿肽(BNP)及超敏C反应蛋白(hsCRP)水平的变化,探讨ACS患者住院早期应用阿托伐他汀的临床意义及最佳剂量.方法 选择ACS患者78例,随机分为3组:阿托伐他汀10 mg组28例,阿托伐他汀20 mg组28例,阿托伐他汀40 mg组22例,均于入院24小时内开始给予阿托伐他汀治疗,测定3组入院时及治疗5天后血浆BNP及hsCRP水平的变化.结果 ACS患者早期应用阿托伐他汀可明显降低血浆BNP及hsCRP水平,阿托伐他汀20 mg组及阿托伐他汀40 mg组均优于阿托伐他汀10 mg组,BNP( 543±116)ng/L,(531±112) ng/L vs(738±121)ng/L( P＜0.01); hsCRP(7.02±3.17) mg/L,(6.87±3.21)mg/L vs (9.32±3.43) mg/L(P＜0.01),阿托伐他汀40 mg组优于阿托伐他汀20 mg组,但差异无统计学意义(P＞0.05).结论 ACS患者早期应用阿托伐他汀可降低血浆BNP及hsCRP水平,阿托伐他汀40 mg、20 mg作用明显优于10 mg.     

阿托伐他汀对不稳定型心绞痛患者血脂及C-反应蛋白的影响

目的 观察阿托伐他汀对不稳定型心绞痛患者血脂及C-反应蛋白的影响.方法 选择不稳定型心绞痛患者90例,随机分为阿托伐他汀组给予睡前口服阿托伐他汀40 mg,连用12周;对照组给予常规治疗,观察两组患者治疗前后血脂和C-反应蛋白的变化.结果 阿托伐他汀组治疗12周后,血清胆固醇、甘油三酯、低密度脂蛋白胆固醇及C-反应蛋白水平明显下降,高密度脂蛋白胆固醇明显上升,对照组治疗前后上述指标无明显变化.结论 阿托伐他汀除调脂作用外,还具有抗炎作用.     

不稳定心绞痛患者早期阿托伐他汀治疗对血浆C反应蛋白、金属蛋白酶、血管性血友病因子的影响

目的观察较大剂量阿托伐他汀治疗不稳定心绞痛患者3天后C反应蛋白(CRP)、金属蛋白酶-9(MMP-9)、血管性血友病因子(vWF)变化,以了解早期应用阿托伐他汀对斑块稳定和炎症反应的影响。方法40例不稳定心绞痛患者被分为常规治疗组(未服用任何调脂药物,19例)和阿托伐他汀组(40mg/d,21例)治疗。测定治疗前后CRP、MMP-9、vWF及血脂水平的变化。结果二组治疗前后血脂各组成分的变化差异均无显著性,而阿托伐他汀治疗组治疗后CRP、MMP-9、vWF明显下降,与治疗前比较有统计学意义(P<0.05)。结论在不稳定心绞痛的早期予以3天的阿托伐他汀治疗,可明显减低血浆炎症因子的水平,改善血管内皮功能,可能有利于动脉粥样硬化斑块的稳定。     

急诊PCI术前口服阿托伐他汀对STEMI患者MCP-1、MIF及预后的影响

目的：探讨急诊PCI术前单次口服大剂量阿托伐他汀对ST段抬高性心肌梗死（STE—MI）患者外周静脉血、病变相关冠状动脉血单核细胞趋化蛋白（MCP）-1、巨噬细胞迁移抑制因子（MIF）和患者预后的影响。方法：选取稳定型心绞痛患者36例和STEMI患者69例,并将后者随机分为阿托伐他汀组（术前口服阿托伐他汀80mg,n=36）和STEMI对照组（n=33）。分别于PCI术中抽取3组患者的病变相关冠状动脉血,术后立即抽取外周静脉血,测定各组MCP—1和MIF水平;并统计术后3个月内各组心血管急性事件的发生率。结果：STEMI组外周和病变相关冠状动脉血MCP-1、MIF水平明显高于稳定型心绞痛组,阿托伐他汀组上述指标水平明显低于STEMI对照组（P〈0．05）;阿托伐他汀组和STEMI对照组患者病变相关冠状动脉血MCP-1水平明显高于静脉血（P〈0．05）,而MIF水平无明显区别;阿托伐他汀组术后3个月心血管急性事件的发生率明显低于STEMI对照组。结论：STEMI患者术前单次大剂量应用阿托伐他汀可以降低外周血和病变相关冠状动脉血MCP-1和MIF水平及3个月内急性心血管事件的发生率。     

阿托伐他汀对急性冠脉综合征患者血清炎性指标的影响

目的：观察阿托伐他汀对急性冠脉综合征（ACS）患者血清炎性指标水平的影响。方法：将69例ACS患者随机分为阿托伐他汀10mg.d-1治疗组（35例）和40mg.d-1治疗组（34例）,并设正常对照组34例。治疗前和治疗2周后分别测定血清可溶性CD40配体（sCD40L）和高敏C-反应蛋白（hs-CRP）水平。结果：治疗前ACS组血清sCD40L、hs-CRP水平均较健康对照组明显增高（P〈0.01）。阿托伐他汀治疗2周后sCD40L和hs-CRP水平有明显降低（P〈0.01）,阿托伐他汀40mg.d-1组较10mg.d-1组降低幅度大（P〈0.05）。结论：阿托伐他汀降低ACS患者血清炎症指标水平,抑制炎性反应,可能具有稳定斑块的作用。     

急性冠脉综合征患者高表达的CD40L和炎症因子相关性

目的 检测急性冠脉综合征(ACS)患者CD4+T细胞CINOL的表达率、其血清可溶性CD40配体(sCD40L)和高敏C反应蛋白(hsCRP)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)的浓度,分析CD40L(sCD40L)与炎症因子的相关性,探讨CD40/CD40L在ACS发病中的作用及可能途径.方法 采用前瞻性研究方法,选取2006.10-2007.4中山大学附属第一医院急诊科、心血管医学部冠心病患者32例,包括稳定性心绞痛(SAP)7例、不稳定性心绞痛(UAP)14例、急性心肌梗死(AMI)11例.正常对照组(CON)为与患者年龄、性别相匹配的健康志愿者8例.所有受试者均排除感染、肿瘤、风湿、肝肾功能不全,未使用类固醇和免疫抑制剂等.流式细胞分析术(FCM)检测CD4+T细胞表达CD40L的阳性细胞率,ELISA法检测血清sCD40L、ICAM-1和VCAM-1浓度,免疫比浊法检测血清hsCRP浓度.所有资料使用SPSS 11.0进行统计学分析.结果 ANI、UAP、SAP、CON组CD4+T细胞中表达CD40L的阳性细胞率(%)分别为8.60±3.02、3.24±1.13、2.18±1.80、0.59±0.18,AMI组显著高于其他3组(P＜0.05),UAP组亦显著高于CON组(P＜0.05);4组血清sCD40L浓度分别为14.47±8.00、8.06±6.96、7.32±3.58、4.48±1.49(ng/mL),ANI组明显高于其他3组(P＜0.05);4组血清:hsCRP浓度分别为20.30±7.57、14.04±8.03、3.78±4.99、O.93±0.77(mg/L),AMI组显著高于其他3组(P＜0.05),UAP组亦显著高于SAP组与CON组(P＜0.05);4组血清ICAM-1浓度分别为418.09±222.19、212.86±128.43、165.04±32.12、108.62±62.27(ng/mL),AMI组显著高于其他3组(均P＜O.05),UAP组亦高于CON组(P＜0.05);4组血清VCAM-1浓度分别为5540.02±2614.65、3760.95±1915.01、4167.27±2084.48、2405.65±870.45(ng/mL),AMI组显著高于CON组(P＜0.01);AMI组CD4+T细胞中表达CD40L的阳性细胞率与VCAM-1呈明显正相关性(r=0.730,P=0.011),其血清sCD40L与hsCRP、ICAM-1、VCAN-1呈明显正相关性(r=0.677,P=0.011;r:0.901,P=0.000;r=0.714,P=0.014).结论 急性冠脉综合征患者CD4+T细胞CINOL的表达率和血清sCINOL浓度升高,且与血清hsCRP、ICAN-1、VCAM-1呈明显正相关;在ACS发生中起作用,此和hsCRP、ICAM-1、VCAN-1等有关,而CD40L/sCD40L可望作为冠心病危险性的预测因子.     

肺癌患者血浆CD62P、血清sCD40/sCD40L水平的检测及临床意义

目的：通过测定肺癌患者血清中可溶性CD40（sCD40）、可溶性CD40L（sCD40L）、血浆CD62P的含量,探讨血小板源性CD40/CD40L在肺癌外周血中的表达及其临床意义。方法体外分离85例肺癌患者（肺癌组）和25名健康志愿者（对照组）的血清和血浆。用酶联免疫吸附试验（ELISA）法对血清sCD40、sCD40L、血浆CD62P的含量进行测定。结果（1）肺癌组血清sCD40、sCD40L、血浆CD62P含量明显高于健康对照组（P均＜0.01）。（2）不同病理类型肺癌患者血清sCD40、sCD40L含量、血浆CD62P含量差异均无统计学意义（P均＞0.05）。（3）肺癌患者sCD40、sCD40L、CD62P的含量随临床分期的进展而呈升高趋势。（4）有远处转移肺癌患者sCD40、sCD40L、CD62P的含量明显高于无远处转移患者（P均＜0.05）。（5）肺癌患者术后2周时血浆CD62P、血清sCD40L的含量均较术前下降,但血清sCD40含量与术前相比差异无统计学意义。且其CD62P、sCD40L的表达水平成正相关关系（r=0.300,P＜0.05）。结论（1）肺癌患者血清sCD40、sCD40L、血浆CD62P含量增加,且表达水平与肺癌的进展程度相关,血小板源性CD40/CD40L系统在肺癌的发病中具有重要作用。（2）检测血小板源性CD40L、CD62P表达水平对研究肺癌的临床分期、预后判断有一定的参考价值。     

Influence of pre-analytical and analytical factors on soluble CD40L measurements

The soluble form of CD40L (CD40 ligand), a pro-atherogenic mediator, has emerged as a diagnostic and prognostic marker for cardiovascular events. However, as platelets can shed CD40L upon activation, accurate measurement has proved challenging. The present study addresses the controversy regarding the appropriate specimen and preparation for laboratory evaluation of blood sCD40L (soluble CD40L). Serum and plasma (collected in EDTA, citrate or heparin) were collected from healthy volunteers (n=20), and sCD40L was analysed by ELISA immediately or after one to three freeze-thaw cycles and at different centrifugation speeds. Urine sCD40L levels were measured in subjects with low- and high-plasma sCD40L levels. Serum sCD40L levels (5.45+/-4.55 ng/ml; P<0.001) were higher than in citrate, EDTA or heparin plasma (1.03+/-1.07, 1.43+/-1.03 or 1.80+/-1.25 ng/ml respectively), with no significant differences between plasma preparations. Increasing g values (200-13000 g), which gradually deplete plasma of platelets, yielded lower sCD40L levels. Repeated freeze-thaw cycles significantly (P<0.05) increased sCD40L concentrations in platelet-rich, but not platelet-depleted, plasma (up to 2.4-fold). Bilirubin and haemoglobin interfered positively, and triacylglycerols (triglycerides) and cholesterol quenched CD40L signalling. No sCD40L was detected in urine samples. In conclusion, serum yields higher sCD40L concentrations than plasma; accurate measurements of sCD40L require exclusion of platelets and avoiding their post-hoc activation. Samples with high concentrations of bilirubin, haemoglobin and/or triacylglycerols should be excluded, as these substances interfere with the assay.     

Increased levels of CD40-CD40 ligand system in patients with essential hypertension

BACKGROUND: Although it has been hypothesized that hypertension is in part an inflammatory disorder, clinical data linking inflammation with incident hypertension are scarce. There is evidence that have shown that CD40-CD40L interaction plays a pathogenic role in inflammatory disorders. We assessed whether CD40 system expressions were altered in patients including 30 with hypertension grade 1, 80 with hypertension grade 2 and 40 with hypertension grade 3. METHODS: Twenty normal controls and 150 patients with essential hypertension were investigated. The expression of CD40 and CD40L on platelet was analyzed by indirect-immunofluorescence flow cytometry and soluble CD40L level was determined by a commercially available ELISA. C-reactive protein was also measured by ELISA. RESULTS: All patients with hypertension showed a significant increase of CD40 (67.1+/-9.6 Mean Fluorescence Intensity, MFI) and CD40L (15.3+/-5.0 MFI) coexpression on platelets as well as sCD40L levels (12.8+/-3.9 ng/ml ) compared with controls (p<0.0001). We found that CRP levels related to CD40-CD40L system. We also observed a slight correlation between sCD40L level and blood pressure. During 3 months follow-up, patients with enhanced levels of sCD40L (>15 ng/ml) indicated a tough control of blood pressure. CONCLUSION: Patients with essential hypertension show increased coexpression of CD40 system, which suggests that hypertension is in part an inflammatory disorder.     

Relationship between CD40 ligand expression and B type natriuretic peptide levels in patients with chronic heart failure

BACKGROUND: Inflammation plays a pathogenic role in the development of chronic heart failure (CHF). Increasing evidence shows that CD40-CD40 ligand (CD40L) interaction plays a pathogenic role in inflammatory disorders. We assessed whether CD40 ligand expression was abnormal in patients with CHF. METHODS: Twenty normal controls and 86 patients with CHF were investigated. The expression of CD40L on platelets was analyzed by indirect-immunofluorescence flow cytometry, and the soluble CD40L (sCD40L) level was determined by a commercially available enzyme-linked immunosorbent assay (ELISA). B type natriuretic peptide (BNP) was measured by radioimmunoassay. RESULTS: All patients with CHF showed a significant increased expression of CD40L (32.3+/-13.9 MFI) on platelets and sCD40L levels (20.5+/-8.6 microg/l) compared with controls(p<0.0001). CD40L expression on platelets and sCD40L levels positively correlated with New York Heart Association (NYHA) functional class, left ventricular ejection fraction and BNP levels in CHF. CONCLUSIONS: Patients with CHF showed increased expression of CD40L system, which may create a pathogenic role in the development and progression of CHF.     

Association between serum soluble CD40 ligand levels and mortality in patients with severe sepsis

Introduction

CD40 Ligand (CD40L) and its soluble counterpart (sCD40L) are proteins that exhibit prothrombotic and proinflammatory properties on binding to their cell surface receptor CD40. The results of small clinical studies suggest that sCD40L levels could play a role in sepsis; however, there are no data on the association between sCD40L levels and mortality of septic patients. Thus, the aim of this study was to determine whether circulating sCD40L levels could be a marker of adverse outcome in a large cohort of patients with severe sepsis.

Methods

This was a multicenter, observational and prospective study carried out in six Spanish intensive care units. Serum levels of sCD40L, tumour necrosis factor-alpha and interleukin-10, and plasma levels of tissue factor were measured in 186 patients with severe sepsis at the time of diagnosis. Serum sCD40L was also measured in 50 age- and sex-matched controls. Survival at 30 days was used as the endpoint.

Results

Circulating sCD40L levels were significantly higher in septic patients than in controls (P = 0.01), and in non-survivors (n = 62) compared to survivors (n = 124) (P = 0.04). However, the levels of CD40L were not different regarding sepsis severity. Logistic regression analysis showed that sCD40L levels >3.5 ng/mL were associated with higher mortality at 30 days (odds ratio = 2.89; 95% confidence interval = 1.37 to 6.07; P = 0.005). The area under the curve of sCD40L levels >3.5 ng/mL as predictor of mortality at 30 days was 0.58 (95% CI = 0.51 to 0.65; P = 0.03).

Conclusions

In conclusion, circulating sCD40L levels are increased in septic patients and are independently associated with mortality in these patients; thus, its modulation could represent an attractive therapeutic target.     

系统性红斑狼疮患者sCD40L水平变化及临床意义

目的对系统性红斑狼疮（SLE）患者血清中可溶性CD40配体（sCD40L）的含量变化及临床意义进行讨论。同时分析血小板减少组SLE患者与血小板正常组SLE患者血清中sCD40L的含量差别。初步探讨血清和血浆中sCD40L浓度有无差异。分析SLE患者血清中sCD40L的含量与系统性红斑狼疮疾病活动度评分（SLEDAI评分）有无相关性。方法用酶联免疫吸附法检测25例SLE患者和15例正常人血清中及18例正常人血浆中sCD40L的浓度。结果①血小板正常组SLE患者血清中的sCD40L浓度明显高于正常对照组和血小板减少组SLE患者。②SLE患者血清sCD40L浓度、血小板正常组SLE患者血清中sCD40L浓度、血小板减少组SLE患者血清中sCD40L浓度与SLEDAI评分均无相关性。③SLE患者血清中sCD40L浓度与血小板计数呈正相关。④发现正常人血清中sCD40L的浓度明显高于血浆中的sCD40L的浓度。结论 SLE患者血清中sCD40L浓度较正常人高可能参与SLE的发生发展过程。血小板计数对血清中sCD40L浓度有一定程度的影响,且SLE患者血清中sCD40L与SLEDAI评分无相关性,在临床上sCD40L不适合作为监测SLE疾病的活动度的指标。     

Association of low-grade inflammation and platelet activation in patients with hypertension with microalbuminuria

Increased levels of sCD40L (soluble CD40 ligand) have been associated with enhanced in vivo platelet activation, and may represent a molecular link between inflammation and a prothrombotic state. The aim of the present study was to analyse the relationship between platelet activation, endothelial dysfunction, low-grade inflammation and sCD40L in patients with hypertension with or without MA (microalbuminuria). A cross-sectional comparison of sCD40L levels was performed in 25 patients with MH (essential hypertension with MA) pair-matched for gender and age with 25 patients with EH (essential hypertension) and 25 HS (healthy subjects with normotension). Circulating levels of CRP (C-reactive protein), a marker of inflammation, sP-selectin (soluble P-selectin), a marker of in vivo platelet activation, and ADMA (asymmetric dimethylarginine) and vWF (von Willebrand factor), markers of endothelial dysfunction, were analysed in each subject. sCD40L levels were increased in patients with MH compared with either patients with EH (P<0.001) or HS (P<0.0001). A highly significant correlation between plasma sCD40L and sP-selectin (P<0.0001), vWF (P<0.001) or CRP levels (P<0.05) was observed in patients with MH. Multivariate regression analysis showed that sP-selectin was the strongest independent predictor of sCD40L levels (P<0.0001) in patients with MH. Patients with hypertension with both vWF and CRP levels above the median had the highest sCD40L levels (P<0.0001). Factorial ANOVA of all of the patients with hypertension confirmed that only patients with MH with low-grade inflammation had elevated levels of sCD40L. In conclusion, sCD40L levels appear to discriminate a subset of patients characterized by MA and low-grade inflammation, suggesting that inhibition of the CD40/CD40L system may represent a potential therapeutic target in subjects with hypertension at a high risk of cardiovascular events.     

CD40-1C/T单核苷酸多态性与缺血性脑卒中易感性的研究进展

缺血性脑卒中发病受多种遗传和环境因素的影响。动脉粥样硬化是缺血性脑卒中的重要病理、生理基础,目前研究发现CD40/CD40配体（CD40L）系统及血清可溶性CD40配体（sCD40L）参与动脉粥样硬化等炎性反应过程进而影响缺血性脑卒中的发生、发展。而CD40-1C/T单核苷酸多态性可通过调控该系统及血清sCD40L影响缺血性脑卒中的疾病易感性。本文对CD40-1C/T单核苷酸多态性与缺血性脑卒中易感性的研究进展进行综述。