氯吡格雷抑制急性冠状动脉综合征患者血小板释放可溶性CD40配体

目的探讨在非ST段抬高急性冠状动脉综合征（non—ST-segment elevation acute coronary syndromes，NSTEACS）患者短期应用氯吡格雷是否有抑制ADP诱导血小板释放可溶性CD40配体（sCD40L）的作用。方法NSTEACS42例，患者服用氯吡格雷6—8d，治疗前后采静脉血。提取富含血小板血浆（platelet rich plasma，PRP）并用二磷腺苷诱导血小板聚集和释放sCD40L，在不同时间点终止反应，用酶联免疫法测量sCD40L浓度，进行自身前后对照。结果治疗前后血浆sCD40L分别为（0．20±0．16）μg／L和（0．19±0．18）μg/L（P〉0．05）；治疗前后PRP受ADP诱导后20min释放的sCD40L浓度分别为（4．3±2．5）μg／L和（2.8±1．9）μg／L（P〈0．001），诱导后40min释放的sCD40L浓度分别为（5．3±3．1）μg／L和（2．9±1．6）μg／L（P〈0．001）。结论短期应用氯吡格雷可能对非sT段抬高急性冠状动脉综合征患者血小板炎症因子sCD40L释放具有抑制作用，提示氯吡格雷很可能具有抗炎效应．     

氯吡格雷的负荷量越大越好吗?

法国学者Montalescot等研究发现,与300mg负荷量相比,口服更大负荷剂量(600mg或900mg)氯吡格雷有更好的抑制血小板凝集(IPA)作用。作者选择了103例非ST段抬高的急性冠状动脉综合征(NSTEACS)患者,在包括阿司匹林在内的常规治疗基础上,将其随机分3组,分别口服300mg、600mg和900mg负荷量的氯吡格雷,主要监测结果是抑制二磷酸腺苷(ADP)诱导的血小板聚集。在患者口服氯吡格雷后的第0·5、1、2、3、4、5、6及24小时取血,所有样本平均分为两大组,分别加入5μmol/L(第1大组)和20μmol/L(第2大组)的ADP。在第1大组中,口服氯吡格雷600mg组和90…     

超负荷量氯吡格雷对急诊冠状动脉介入治疗患者心肌微循环再灌注的影响

目的:观察急性ST段抬高型心肌梗死患者急诊经皮冠状动脉介人治疗(PCI)术前应用大负荷量氯吡格雷对术后心肌微循环灌注及心脏功能的影响.方法:64例成功接受急诊PCI的STEMI患者随机分为氯吡格雷300 mg组和600 mg组.比较两组间的基础临床状况和造影情况、结果以及术后心肌呈色显像(Blush)3级获得率、ST抬高总和回落百分比(sumSTR%)、心功能以及胎盘生长因子(PIGF)、可溶性CD40配体(sCD40L)的变化.结果:术后氯吡格雷600 mg组的Blush 3级获得率明显高于300 mg组(50.0%∶21.88%,P<0.05),ST段抬高总和回落百分比显著下降[(70.90±9.51)∶(60.70±15.06)%,P<0.05],左室射血分数(LVEF%)明显增加[(70.96±9.51)∶(65.27±9.85)%,P<0.05],PIGF较300 mg组显著下降[(14.37±1.32)∶(15.85±1.71)ng/L,P<0.05],sCD40L较300 mg组显著下降[(4.93±0.71)∶(5.68±0.77)μg/L,P<0.05].结论:急性ST段抬高型心肌梗死患者急诊PCI术前给予超负荷量氯吡格雷可以改善PCI术后的心肌微循环灌注,改善心功能状况.     

氯吡格雷对早期急性冠状动脉综合征血清sCD40配体的影响

目的观察用氯吡格雷(clopidogrel)治疗早期急性冠状动脉综合征(acute coronary syndrome,ACS)对病人血清可溶性CD40配体(soluble CD40ligand,sCD40L)的影响,了解该药对ACS斑块稳定性和免疫炎症抑制的作用。方法128例初次确诊为ACS病人分为常规治疗组62例和氯吡格雷治疗组66例,用酶联免疫吸附测定ACS病人治疗前后血清sCD40L水平的变化。结果氯吡格雷治疗组66例ACS病人治疗后血清sCD40L水平从(11.8±3.1)μg/L下降至(5.7±3.0)μg/L,与常规治疗组比较,差异有统计学意义(P<0.01)。结论使用氯吡格雷治疗早期ACS,可明显降低病人sCD40L水平。     

急性冠脉综合征患者氯吡格雷抵抗的影响因素

目的评价急性冠状动脉综合征(ACS)患者氯吡格雷抵抗的发生情况及其可能的影响因素。方法所有入选患者均给予阿司匹林100mg/d,氯吡格雷负荷剂量300mg及维持量75mg/d,于服氯吡格雷前、服药后24h分别测定二磷酸腺苷(ADP,浓度25#mol/L)诱导的血小板聚集率,计算血小板聚集抑制率〔△A〕。△A≤10%(包括负值)时考虑存在氯吡格雷抵抗。结果102例ACS患者,其中△A≤10%(包括负值)者43例(42.2%),急性非ST段抬高心肌梗死及置入支架患者氯吡格雷抵抗的发生率高。结论ACS和冠状动脉介入治疗后的抗血栓治疗中,部分患者存在氯吡格雷抵抗。其发生与患者的疾病状态及是否置入支架明显相关。     

氯吡格雷联合阿司匹林对老年不稳定性心绞痛患者血小板聚集的影响

目的观察氯吡格雷联合阿司匹林对老年不稳定性心绞痛患者血小板聚集功能的影响。方法选择老年不稳定性心绞痛患者120例,随机分为阿司匹林组、低剂量联合组(氯吡格雷25 mg)、中剂量联合组(氯吡格雷50mg)、高剂量联合组(氯吡格雷75 mg),每组30例。观察时间为8周,治疗前后测患者血小板颗粒膜蛋白140(GMP-140)浓度及分别用二磷酸腺苷(ADP)和花生四烯酸(AA)为诱导剂的血小板聚集率,记录临床疗效及不良反应发生情况。结果与治疗前比较,治疗8周后,阿司匹林组、低、中和高剂量联合组GMP-140浓度、ADP介导的血小板聚集率显著降低[(15.3±2.9)μg/L vs(9.7±1.5)μg/L、(16.7±3.4)μg/L vs(8.9±2.3)μg/L、(14.9±3.0)μg/L vs(5.1±1.4)μg/L、(16.4±3.5)μg/L vs(7.8±2.2)μg/L,(43.5±9.8)%vs(24.3±8.9)%、(41.0±7.8)%vs(20.3±8.1)%、(44.3±9.2)%vs(21.5±8.7)%、(43.9±7.6)%vs(20.6±8.0)%,P0.05];AA介导的血小板聚集率4组治疗后较治疗前明显降低[(28.7±9.1)%vs(16.1±7.4)%、(29.2±9.3)%vs(17.2±8.5)%、(30.1±10.1)%vs(17.9±9.4)%、(28.8±8.5)%vs(25.7±8.6)%,P0.05],4组比较无显著差异(P0.05)。低、中、高剂量联合组总有效率均高于阿司匹林组(93.33%、96.67%、96.67%vs 86.67%,P0.05)。仅高联合组出现2例不良反应。结论应用氯吡格雷50mg联合阿司匹林对老年不稳定性心绞痛患者双联抗血小板聚集治疗最为适合。     

国产氯吡格雷与进口氯吡格雷在冠状动脉支架术后抗血小板治疗的疗效对比

目的对比分析国产氯吡格雷与进口氯吡格雷在冠状动脉支架术后抗血小板治疗的疗效。方法选取2015年4月13日至2016年4月13日期间我院收治的100例冠状动脉支架术患者,将其抽签化分组,两组各有50例,对照组和观察组分别采用国产氯吡格雷治疗和进口氯吡格雷治疗。结果观察组ALT为(48.74±29.52)μ/L,ALP为(74.69±25.22)μ/L,TG为(1.39±0.22)g/L,AFP为(6.61±2.42)μmg/L,血小板计数为(270.69±10.96)×109/L,粒细胞计数为(8.65±1.78)×109/L,总不良反应发生率为(4.00%),随访一年后不良事件发生率为(10.00%);而对照组ALT为(48.97±29.54)μ/L,ALP为(74.61±24.43)μ/L,TG为(1.32±0.62)g/L,AFP为(6.23±1.51)μmg/L,血小板计数为(270.18±10.43)×109/L,粒细胞计数为(8.41±1.33)×109/L,总不良反应发生率为(6.00%),随访一年后不良事件发生率为(8.00%),两组对比各项指标均不存在差异性(P0.05)。结论国产氯吡格雷与进口氯吡格雷疗效相当,均可提高冠状动脉支架术患者治疗安全性。     

冠状动脉介入术前高负荷量氯吡格雷预治疗的近期疗效

目的:对比观察拟行冠状动脉(冠脉)介入术患者术前服用高负荷剂量氯吡格雷600 mg与常规负荷剂量300 mg预治疗的有效性及安全性.方法:选取100例拟行冠脉介入术的患者,术前随机分别给予600 mg(50例)或300 mg(50例)负荷剂量氯吡格雷预治疗.分别检测2组服药前、服药后16、36 h二磷酸腺苷(ADP)诱导的血小板最大凝集率(MPAR),随访术后30 d和6个月主要临床心血管事件(包括死亡、心肌梗死、紧急靶血管血运重建、脑卒中等)和出血事件的发生情况.结果:服药后16 h,氯吡格雷600 mg组较之300 mg组对ADP(5μmol/L和20μmol/L)诱导的MPAR产生更大的抑制作用[ADP 5μmol/L,(21.83±18.04)%:(14.79±9.18)%,P＜0.05];[ADP 20μmol/L,(22.12±14.81)%:(15.67±10.15)%,P＜0.05)].而服药后36 h,2组ADP(5μmol/L和20μmol/L)诱导的MPAR率分别降低[ADP5μmol/L.(16.70±15.42)%:(12.94±10.34)%,P＞0·05]和[20μmol/L :(14.14±13.16)%:(10.19±9.49)%,P＞0.05].氯吡格雷600 mg组30d和6个月主要临床心血管事件发生率较300 mg组显著减少(P＜0.05,P＜0.01).2组30 d和6个月出血事件差异均无统计学意义.结论:冠脉介入术患者术前服用高负荷剂量氯吡格雷600 mg较之常规负荷剂量300 mg预治疗能更大程度抑制血小板凝集.同时可显著改善临床预后.     

DISPERSE-2研究：NSTEACS患者中，首个口服AZD6140与氯吡格雷的安全性、耐受性和初期有效性比较

已有研究证实，首个口服可逆性ADP受体拮抗剂AZD6140在稳定型冠心病患者中所获得的平均血小板抑制水平高于氯吡格雷。美国学者Cannon等的DISPERSE-2研究主要比较非ST段抬高急性冠脉综合征（NSTEACS）患者使用氯吡格雷与AZD6140的安全性、耐受性和初期有效性。     

血栓弹力图评价老年患者抗血小板治疗的临床意义

目的应用血栓弹力图观察我院老年患者服用抗血小板药物后血小板抑制率的变化情况。方法选择我院门诊和住院的62例抗血小板治疗的老年患者,并将患者分成阿司匹林组、氯吡格雷组、阿司匹林+氯吡格雷组,16例未服用抗血小板药物的患者为对照组,应用血栓弹力图仪分别测得4组花生四烯酸(AA)和二磷酸腺苷(ADP)途径诱导的血小板抑制率值,并进行比较分析。结果阿司匹林组AA诱导的血小板抑制率为(78.93±11.73)%,氯吡格雷组ADP诱导的血小板抑制率为(53.4±21.5)%,阿司匹林+氯吡格雷组AA诱导和ADP诱导的血小板抑制率分别为(93.27±5.73)%和(55.8±24.6)%,血小板抑制率均显著高于对照组(P0.01)。结论血栓弹力图能客观反映老年患者服用抗血小板药物后血小板抑制率的变化。阿司匹林能起到较好的抗血小板作用,其抗血小板作用优于氯吡格雷,同时服用阿司匹林和氯吡格雷能起到更有效的抗血小板作用。     

Comparison of platelet function and morphology in patients undergoing percutaneous coronary intervention receiving bivalirudin versus unfractionated heparin versus clopidogrel pretreatment and bivalirudin

We hypothesized that direct thrombin inhibition could attenuate platelet activation and release of soluble CD40 ligand (sCD40L), a marker of inflammation, during percutaneous coronary intervention (PCI). To assess platelet function under flow conditions with bivalirudin versus unfractionated heparin (UFH), we employed the cone and plate(let) analyzer (CPA) assay in drug-spiked blood samples from volunteers (n = 3) in vitro, and then in PCI patients who received bivalirudin alone (n = 20), UFH alone (n = 15), and clopidogrel pretreatment plus bivalirudin (n = 15). Scanning electron microscopy was employed to image bivalirudin or UFH-treated platelets to determine whether platelet function observations had a morphologic explanation. Enzyme immunoassay was used to measure sCD40L levels in PCI patients. In vitro, bivalirudin decreased platelet surface coverage; UFH increased platelet surface coverage. In PCI patients, bivalirudin alone decreased platelet surface coverage, UFH alone increased platelet surface coverage, and clopidogrel pretreatment plus bivalirudin additively reduced platelet surface coverage. Unlike UFH, bivalirudin did not activate platelets in SEM studies. Bivalirudin alone or coupled with clopidogrel significantly reduced plasma sCD40L in PCI patients. In conclusion, our findings suggest that under flow conditions, bivalirudin alone or coupled with clopidogrel may have an antiplatelet effect versus UFH alone during PCI. These data suggest that bivalirudin and UFH may confer an anti-inflammatory effect by reducing sCD40L during PCI.     

Clopidogrel-mediated reduction of circulating tissue factor in patients with stable coronary artery disease

BACKGROUND: Tissue factor (TF), the initiator of coagulation, circulates in blood and contributes to thrombosis in patients with coronary artery disease (CAD). TF is present in the alpha-granules of platelets. Therapy with clopidogrel results in inhibition of platelet degranulation. Whether clopidogrel affects circulating TF is unknown. This study examined the effect of clopidogrel on TF level in the blood of patients with stable CAD and ST-elevation myocardial infarction (STEMI) as well as healthy controls. METHODS: Thirty-three patients with CAD and twenty with STEMI were studied pre and post clopidogrel therapy (loading dose 300 mg, then 75 mg daily). All were treated with aspirin 100 mg/d. The control groups consisted of thirty healthy male volunteers also treated with clopidogrel and ten patients with CAD treated with aspirin only. TF concentration in blood drawn pre and 96 h post clopidogrel administration was measured by enzyme-linked immunosorbent assay. RESULTS: Patients with CAD and STEMI had significantly more TF in blood than healthy controls. Clopidogrel reduced TF in stable CAD patients to levels seen in healthy controls. No alterations in TF were found in controls and patients with STEMI post clopidogrel therapy. Clopidogrel reduced sCD40L level in stable CAD patients, but not in STEMI patients. A correlation between TF and sCD40L was found for the combined CAD and control, but not STEMI group. CONCLUSION: Clopidogrel leads to a reduction of not only sCD40L but also TF in stable CAD. The reduction of TF may lead to a reduced thrombogenicity, contributing to the benefits of clopidogrel therapy.     

Cilostazol could ameliorate platelet responsiveness to clopidogrel in patients undergoing primary percutaneous coronary intervention.

BACKGROUND: Cilostazol increases the cyclic adenosine monophosphate levels in platelets and might ameliorate the antiplatelet activity of clopidogrel. This study investigated the additional effect of cilostazol on platelet aggregation measured by a VerifyNow analyzer and soluble CD40 ligand (sCD40L) as a marker of activated platelet in patients undergoing primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: Sixty cases of primary PCI were randomly assigned to dual (aspirin and clopidogrel) or triple (dual plus cilostazol) therapy. The antiplatelet effects of aspirin and clopidogrel were evaluated by VerifyNow tests. The plasma sCD40L levels at admission, 24 h and 21 days were measured by the ELISA method. The arachidonic acid induced platelet aggregation was similar in both groups. However, the triple group had a significantly lower P2Y12 reaction unit (dual 208.8+/-69.0 vs triple 168.2+/-79.2, p=0.041) and higher % inhibition of adenosine diphosphate (ADP)-induced platelet aggregation (dual 23.8+/-21.4% vs triple 40.5+/-21.0%, p=0.004). In the multivariate analysis, cilostazol was a negative predictor for low responders to clopidogrel (95% confidence interval 0.067-0.711). The plasma sCD40L levels were not significantly different between the 2 groups at the same point of time. CONCLUSIONS: The addition of cilostazol to the combination of aspirin plus clopidogrel significantly increases the inhibition of ADP-induced platelet aggregation. However, there was no additive effect on aspirin-induced antiplatelet activity or lowering of sCD40L.     

Relationship between plasma inflammatory markers and platelet aggregation in patients with clopidogrel resistance after angioplasty

We evaluated the relationship between plasma inflammation markers and clopidogrel resistance in patients after stent implantation. The plasma levels of C-reactive protein (CRP), P-selectin, platelet soluble CD40 ligand (sCD40L), interleukin 6 (IL-6) and platelet aggregation were measured in 352 patients undergoing percutaneous coronary intervention (PCI) at baseline and after 6 months. The plasma levels of CRP, P-selectin, sCD40L, IL-6 was higher in 65 (18.5%) patients with clopidogrel resistance than in those with normal responsiveness at 6 months after PCI. There was a significant positive correlation between soluble CD40L levels and platelet aggregation (r = .28, P < .05). Diabetes (DM) and sCD40L level were independent predictors for unresponsiveness after stent implantation according to stepwise multivariate analyses. The hazard ratio (HR) for sCD40L level was 3.02 (95% CI = 1.28 to 3.25; P = .036) and for DM 2.53 (95% CI = 1.28 to 6.55, P = .03). We conclude that sCD40L and DM may influence clopidogrel resistance.     

Impact of clopidogrel on suppression of circulating levels of soluble CD40 ligand in patients with unstable angina undergoing coronary stenting

This study investigated whether a regimen that comprised a loading dose of 300 mg of clopidogrel followed by 75 mg/day could significantly suppress circulating levels of soluble CD40 ligand (sCD40L) in patients who had unstable angina and underwent coronary stenting. Study results showed that the clopidogrel loading dose substantially decreased the circulating level of sCD40L at 24 hours after stenting (p <0.0001). Combined with aspirin, 75 mg/day of clopidogrel continuously decreased sCD40L levels after coronary stenting.     

高负荷剂量氯吡格雷对急性冠脉综合征患者介入治疗后血清sCD40L和hs-CRP浓度的影响

目的探讨高负荷剂量氯吡格雷对急性冠脉综合征(acute coronary syndrome,ACS)患者介入治疗后血清sCD40L和高敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)水平的影响。方法选择ACS患者190例分为高负荷剂量组94例(首剂负荷剂量600 mg,以后每天氯吡格雷150 mg,共用7 d,而后以每天氯吡格雷75 mg维持治疗)和标准剂量组96例(首剂负荷剂量300 mg,以后每天氯吡格雷75 mg维持治疗)。于服氯吡格雷前,经皮冠状动脉介入(percutaneous coronary intervention,PCI)治疗前,术后第1天,术后第7天,术后第30天血清sCD40L和hs-CRP的浓度,并记录患者术后1、3、6个月发生主要心血管事件、出血事件的情况。结果高负荷剂量组PCI治疗后不同时间点血清可溶性CD40配体(sCD40L)、hs-CRP浓度均低于标准剂量组,差异有统计学意义(P<0.05)。sCD40L与hs-CRP的变化趋势的相关性检验结果显示两者呈正相关(皮尔森相关系数r=0.128,P<0.001)。结论高剂量氯吡格雷比标准剂量氯吡格雷对sCD40L、hs-CRP的抑制作用更强;当氯吡格雷抑制炎症反应产物hs-CRP产生的同时也会抑制炎症产物sCD40L的产生。     

Analysis of serum soluble CD40 ligand (sCD40L) in the patients undergoing allogeneic stem cell transplantation: platelet is a major source of serum sCD40L

CD40 ligand (CD40L) is expressed not only on activated T cells but also on activated platelets. A soluble CD40 ligand (sCD40L) is released from the activated T cells and platelets by ill-defined proteolytic process in vitro. It has been reported that sCD40L is elevated in the serum of patients with systemic lupus erythematosus, unstable angina, essential thrombocythemia, and autoimmune thrombocytopenic purupura. However, source of sCD40L in vivo remains to be elucidated. We investigated the serial sCD40L in the serum in patients undergoing allogeneic stem cell transplantation and compared with the platelets number and soluble IL2R, which is a marker of activated T cells. The value of sCD40L was well correlated with platelet number or thrombopoiesis. In cases of severe graft vs. host disease with markedly increased sIL2R, sCD40L was not increased in vivo. These results indicate that sCD40L in vivo is released mainly from the platelets or in the process of platelet production but not from the activated T cells.     

Activated platelets are the source of elevated levels of soluble CD40 ligand in the circulation of inflammatory bowel disease patients

BACKGROUND: The CD40/CD40L system, a key regulator and amplifier of immune reactivity, is activated in inflammatory bowel disease (IBD) mucosa. AIMS: To determine whether plasma levels of sCD40L are elevated in Crohn's disease (CD) and ulcerative colitis (UC) patients compared with normal controls, to investigate the cellular source of sCD40L, and to explore CD40L induction mechanisms. PATIENTS: CD, UC, and normal control subjects were studied. METHODS: The concentration of sCD40L in plasma and supernatants of freshly isolated platelets and autologous peripheral blood T cells (PBT) was measured by ELISA. Surface CD40L expression level was measured by flow cytometry in resting and thrombin activated platelets, and unstimulated and CD3/CD28 stimulated PBT before and after coculture with human intestinal microvascular endothelial cells (HIMEC). RESULTS: Compared with normal controls, plasma sCD40L levels were significantly higher in both CD and UC patients and proportional to the extent of mucosal inflammation. Platelets from IBD patients displayed a significantly higher surface CD40L expression than those from control subjects, and released greater amounts of sCD40L than autologous PBT. Contact with IL-1beta activated HIMEC induced significant upregulation of CD40L surface expression and release by platelets. CONCLUSIONS: Elevated levels of sCD40L in the circulation of IBD patients reflect enhanced surface expression and release of CD40L by platelets. This phenomenon translates to an increased platelet activation state apparently induced by passage through an inflamed mucosal microvascular bed, a conclusion supported by the positive correlation of plasma sCD40L levels with the extent of anatomical involvement by IBD. These results suggest that platelet-endothelial interactions critically contribute to activation of the CD40 pathway in IBD.     

Enhanced levels of soluble CD40 ligand and C-reactive protein in a total of 312 patients with metabolic syndrome

The metabolic syndrome (MS) is associated with a systemic inflammatory response that plays an important pathogenetic role in atherothrombotic disease. Increasing evidence indicates that CD40-CD40 ligand interactions constitute an important mediator for vascular inflammation. The purpose of this study was to assess whether high-sensitivity C-reactive protein (hs-CRP) and soluble CD40 ligand (sCD40L) levels were increased in patients with MS. During the study period from January 2004 to August 2004, 312 patients with MS and 98 control subjects were included. Anthropometric measurements, blood pressure assessment, electrocardiography, and blood measurements including fasting blood glucose, postprandial blood glucose, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, glycated hemoglobin, white blood cell (WBC), platelets, hs-CRP, and sCD40L were performed. Patients with MS were divided into 3 groups based upon their glucose tolerance (group 1, normal glucose tolerance; group 2, prediabetic group; and group 3, diabetes mellitus). Patients with MS showed a significant increase of WBC, hs-CRP, and sCD40L levels compared with control subjects. The levels of both hs-CRP and sCD40L were positively correlated with body mass index (BMI). High-sensitivity CRP levels were also positively correlated with waist circumferences, fasting blood glucose, postprandial blood glucose, and glycated hemoglobin, and negatively correlated with high-density lipoprotein cholesterol. In patients with MS, both hs-CRP and sCD40L levels were positively correlated with WBC count. We found a positive correlation between sCD40L and platelets. Among the subgroups of patients with MS, the mean levels of WBC, hs-CRP, and sCD40L did not show any significant differences. In conclusion, elevated levels of WBC, hs-CRP, and sCD40L in MS patients provide further insight into the relationship between MS and inflammation. In our study, positive correlations between BMI and both hs-CRP and sCD40L levels suggest that BMI is an important determinant of a chronic inflammatory state in patients with MS. Moreover, this study reports significantly increased levels of WBC, hs-CRP, and sCD40L not only in diabetic subjects with MS but also in prediabetic subjects and nondiabetic subjects with MS compared with control subjects. Our data suggest that MS patients have proinflammatory state independent of their glucose tolerance status. In our study, the positive correlation between the levels of sCD40L and platelets in patients with MS supports previous reports indicating that sCD40L are derived predominantly from platelets.