血管内皮损伤标志物在肾移植患者中的应用价值

目的 :通过对肾移植患者血浆可溶性血栓调节蛋白 (solublethrombomdulin ,sTM)、可溶性血管内皮细胞蛋白C受体 (endothelialproteinCreceptor ,sEPCR)、血管性血友病因子 (vonWillebrandfactor,vWF)含量水平的动态检测分析 ,探讨其在肾移植及移植排斥反应中的应用价值。方法 :采用双抗体夹心ELISA法检测 4 2例肾移植患者手术前后、排斥反应治疗过程中的sTM、sEPCR、vWF含量。结果 :肾移植术后sTM、sEPCR、vWF含量水平较术前明显增高 (P <0 0 5 )、与正常对照组比较有显著性差异 (P <0 0 1) ;发生移植排斥反应者较无排斥者有明显差异 (P <0 0 5 ) ;肾移植术前、排斥反应有效治疗后与正常对照组比较无显著差异 (P >0 0 5 ) ;肾移植患者sTM、sEPCR、vWF各指标间呈正相关 (r =0 5 95 ,P <0 0 1,r =0 5 81,P <0 0 1,r =0 6 0 6 ,P <0 0 1)。结论 :sTM、sEPCR、vWF均可作为肾移植患者血管内皮的免疫损伤标志物 ,联合动态监测sTM、sEPCR、vWF的含量在观察肾移植手术创伤程度、排斥反应的早期诊断和治疗效果的监测等方面均有重要的临床应用价值。     

2型糖尿病血管并发症患者血清可溶性细胞粘附分子-1和C-反应蛋白的检测分析

目的:测定2型糖尿病(T2DM)患者血清可溶性细胞间粘附分子-1(sICAM-1)及C-反应蛋白(CRP)水平,分析两者在T2DM血管并发症发生、发展中的作用。方法:检测25例T2DM并血管并发症患者空腹血糖(FBS)、甘油三酯(TG)、糖化血红蛋白(HbA1c)、sICAM-1和CRP水平,并与33例无血管并发症患者和50例正常对照组比较。结果:T2DM患者组FBS、TG、HbA1c、sICAM-1和CRP等均显著高于正常对照组(P<0.01),T2DM血管并发症组TG、sICAM-1和CRP显著高于非血管并发症组(P<0.01)。HbA1c与sICAM-1和CRP呈正相关(P<0.01),TG、FBS与sI-CAM-1和CRP水平无相关性。结论:ICAM-1和CRP参与血管内皮细胞的炎症损伤,并在T2DM血管并发症发生发展中起重要作用。     

糖尿病并发大血管病变患者sCD163与oxLDL-Ab检测的临床价值

目的:探讨老年2型糖尿病(DM2)患者血清可溶性单核-巨噬细胞血红蛋白清道夫受体(sCD163)和抗氧化型低密度脂蛋白抗体(oxLDL-Ab)与大血管病变的关系。方法:测定189例DM2患者及50例正常对照者sCD163和oxLDL-Ab水平,189例DM2患者分为大血管病变组(120例)与无大血管病变组(69例),比较三组间sCD163和oxLDL-Ab水平,并进行相关性分析。结果:与正常对照组比较DM2组sCD163与oxLDL-Ab水平较高、DM合并大血管病变组sCD163与oxLDL-Ab水平高于DM无血管病变组,各组间有显著性差异(P<0.05,P<0.05),且sCD163与oxLDL-Ab水平呈正相关(r=0.45,P<0.05)。结论:sCD163与oxLDL-Ab与DM2大血管病变的发生发展密切相关,且联检可对早期动脉硬化的诊断具有重要的指导意义。     

Ⅱ型糖尿病患者血浆可溶性凝血酶调节蛋白的变化及临床意义

目的 评价血浆可溶性凝血酶调节蛋白与Ⅱ型糖尿病患者凝血和纤溶系统之间的关系。方法 我们检测了50例Ⅱ型糖尿病患者血浆中可溶性凝血酶调节蛋白、蛋白C(PC)(由凝血酶-TM复合物诱导产生的抗凝物质)、凝血酶原片段F1+2(一种凝血酶生成的直接标志物)、纤溶酶-α2-抗纤溶酶复合物(PAP)和D二聚体(DD)。结果 患者血浆中的sTM(P<0.01)、PAP(P<0.01)、PC(P<0.05)和F1+2(P<0.05)较50例正常对照组明显增高,糖尿病肾病患者的sTM和PAP升高更加显著。在糖尿病患者中,sTM与PC呈负相关(r=-0.50,P<0.001),而与PAP呈正相关(r=0.47,P=0.01)。结论 结果表明糖尿病患者的凝血和纤溶系统均是活化的,血浆中的可溶性凝血酶调节蛋白升高与糖尿病患者凝血和纤溶系统活化相关。     

血清HGF、VEGF、sP-selectin和LTB4水平的波动与DM2大血管病变

目的:探讨2型糖尿病(DM2)大血管病变发生及病程进展过程中相关多肽生长因子水平测定的临床意义。方法:本文将40例DM2患者按不同的病情分为大血管病变组和非血管病变组进行研究。同时设置体检健康人40名作为正常对照组。血清血管内皮生长因子(vascular endothelial growth factor,VEGF)采用RIA测定;血清肝细胞生长因子(hepatocyte growth factor,HGF)、血清可溶性P-选择素(soluable P-selectin,sP-selectin)、白三烯B4(leukotrieneB4,LTB4)水平均采用ELISA测定。并将测定结果进行统计学分析。结果:两组DM2患者血清VEGF水平均显著地高于正常对照组(P<0.05,P<0.01),大血管病变组则显著高于非血管病变组(P<0.01)。HGF水平显示大血管病变组显著高于非血管病变组及正常对照组(P均<0.01),大血管病变组与非血管病变组比较差异不显著(P>0.05)。sP-selectin含量大血管病变组显著地高于非血管病变组及正常对照组(P均<0.01),大血管病变组则显著地高于非血管病变组(P<0.01)。LTB4水平的变化为两组DM2患者血清VEGF水平均显著地高于正常对照组(P<0.05,P<0.01),大血管病变组则显著高于非血管病变组(P<0.01)。结论:四项指标的变化与患者的病情关系密切,其测定对DM2大血管病变的早期诊断具潜在的临床价值。     

辛伐他汀对急性冠脉综合征患者CRP、vWF、血脂水平及凝血系统的影响

目的观察辛伐他汀对急性冠脉综合征(ACS)患者C反应蛋白(CRP)、血管性假性血友病因子(v WF)、血脂水平及凝血系统指标的影响,探讨其非调脂作用。方法随机选取48例ACS患者,其中23例高脂血症患者为血脂紊乱组,口服辛伐他汀40mg/天,治疗12周,25例血脂正常患者为正常对照组,测定血脂紊乱组治疗前后CRP、v WF、血脂和凝血系统指标的变化。结果与治疗前比较,治疗后的CRP、v WF、TC、TG、LDL-C、Fib均显著降低(P<0.01),HDL-C、PT明显升高(P<0.05),TT、APTT显著延长(P<0.01)。且治疗后v WF、TT、APTT与正常对照组有显著性差异(P<0.05)。结论辛伐他汀治疗ACS患者,在有效调脂的同时可显著降低CRP和v WF水平,改善凝血系统功能,有利于动脉粥样硬化斑块的稳定。     

sEPCR、VEGF、MVD、KDR在早发型子痫前期胎盘中的表达

目的 研究sEPCR、VEGF、MVD、KDR在早发型子痫前期胎盘中的表达情况.方法 选取2016年3月至2017年4月我院收治的早发型子痫前期患者50例为研究对象,以同期入院体检的50例健康产妇为对照组,测定入组对象胎盘组织中可溶性血管内皮细胞蛋白C受体(sEPCR)、血管内皮生长因子(VEGF)、胎盘微血管密度(MVD)、含有激酶插入区的受体(KDR)及可溶性血管内皮生长因子受体(sFlt-1)水平,同时比较子痫前期病情轻度、中重度患者上述指标,分析PE患者sEPCR、VEGF、MVD、KDR及sFlt-1的相关性,评价上述指标联合诊断PE的效能.结果 早发型组胎盘组织VEGF(30.25 ±1.87)％、MVD(37.11 ±1.54)条低于对照组(P＜0.05),而其sEPCR(156.34±1.25) ng/mL、KDR(70.34±1.38)％、sFlt-1 (80.32±1.67)％较对照组升高(P＜0.05);重度子痫前期患者VEGF(30.18±1.30)％、MVD(36.20±1.31)条与轻度组比较明显降低,而sEPCR(154.22±1.05)％、KDR(71.20±1.66)％、sFlt-1 (81.11±1.56)升高(P＜0.05);sEPCR、VEGF、MVD、KDR联合诊断早发型PE患者灵敏度为98.05％,特异性为93.11％,准确度为96.20％,均高于上述指标单项诊断;相关分析显示子痫前期患者胎盘组织中VEGF、MVD与sFlt-1呈负相关(P＜0.05).结论 sEPCR、VEGF、MVD、KDR在早发型子痫前期胎盘中呈异常表达,随病情加重VEGF、MVD表达降低,sEPCR、KDR表达增多,其中VEGF、MVD表达水平与sFlt-1高表达有关.     

2型糖尿病合并心血管病患者B型尿钠肽水平变化及与超敏C反应蛋白和脂蛋白(a)的关系

目的:分析2型糖尿病(T2DM)合并心血管病患者血浆B型尿钠肽(BNP)水平变化及与血清超敏C反应蛋白(hs-CRP)和脂蛋白(a)[Lp(a)]浓度的关系。方法:将49例T2DM患者分为单纯T2DM组(n=28)和T2DM合并心血管病组(n=21),同时选择30例健康体检者作为健康对照组。采用化学免疫发光法检测血浆BNP,采用透射比浊法检测血清hs-CRP,采用胶乳比浊法检测Lp(a);比较各组以上指标水平变化,并分析T2DM合并心血管病患者BNP水平与hs-CRP和LP(a)浓度的相关性。结果:T2DM合并心血管病组BNP、hs-CRP及Lp(a)水平均显著高于健康对照组和单纯T2DM组(P<0.05);单纯T2DM组BNP和hs-CRP的检测结果显著高于健康对照组(P<0.05),而Lp(a)在此两组间无显著性差异(P>0.05)。T2DM合并心血管病组血浆BNP与血清hs-CRP水平呈显著正相关(r=0.467,P<0.05),而与Lp(a)无明显相关性;hs-CRP与Lp(a)亦无明显相关性。结论:血浆BNP水平显著升高可提示T2DM患者合并心血管病变。     

糖尿病肾病时血浆基质金属蛋白酶3及血栓前体蛋白的变化

目的： 探讨基质金属蛋白酶3（MMP-3）和血栓前体蛋白（TpP）在2型糖尿病肾病（DN）中的变化。方法: 用ELISA双抗体夹心法测定57例DN患者及35例正常对照者的血浆MMP-3和TpP水平,DM组根据24 h尿白蛋白排泄量（UAE）分DN0(UAE＜30 mg/24 h)、DN1（30 mg/24 h≤UAE＜300 mg/24 h）、DN2（UAE≥300 mg/24 h）3组。 结果: DN0组血浆MMP-3和TpP水平与正常对照组间无显著差异。DN1组血浆MMP-3水平高于正常对照组（P＜0.05）,但TpP水平无显著差异。DN2组血浆MMP-3水平显著高于正常对照组（P＜0.01）、DN0组（P＜0.05）及DN1组（P＜0.05）,TpP水平也高于正常对照组（P＜0.01）。DN患者血浆MMP-3和TpP水平呈正相关（P＜0.01）。 结论: MMP-3及TpP可能参与DN发生,MMP-3水平变化与DN病变程度相关。     

DM2患者血脂、尿酸和CRP测定的临床分析

目的:为了探讨2型糖尿病(DM2)患者血脂、尿酸(SUA)和C-反应蛋白(CRP)测定的临床意义.方法:采用生化法测定了78例DM2患者和66例正常对照组的血脂(TC、TG、HDL-C和LDL-C)水平,过氧化物酶免疫分析测定了SUA水平以及免疫比浊法测定了CRP水平,并与66例正常对照组进行了对比性分析.结果:78例...     

罗格列酮对改善糖尿病大鼠心肌微血管内皮细胞功能的影响

目的探讨罗格列酮对糖尿病大鼠心肌微血管内皮细胞功能的影响。方法腹腔注射小剂量链脲佐菌素结合高能量饲料制备2型糖尿病大鼠模型，随机分为未治疗组与治疗组：罗格列酮4mg／（kg·d）。16周后定量测定血管内皮损伤标志物：可溶性血管内皮细胞蛋白C受体（sEPCR）、可溶性血栓调节蛋白（sTM）、血管性血友病因子（VWF）和一氧化氮（NO）的血浆浓度。分光光度法及免疫组化法分别测定心肌组织内NO浓度、NO合酶（NOS）的活性及内皮型NO合酶（cNOS）在微血管内皮细胞的表达。结果罗格列酮治疗组血糖及血浆中sEPCR、sTM、vWF显著低于未治疗组，但高于非糖尿病对照组。与未治疗组比较，罗格列酮治疗组心肌组织中NO、结构型NOS（cNOS）含量增高，eNOS阳性反应产物量增多，而诱导型NOS（iNOS）含量降低。结论罗格列酮可以降低糖尿病大鼠血糖，减轻内皮细胞损伤与改善心肌微血管内皮细胞功能，有助于减少糖尿病时心肌微血管病的发生与发展。     

Plasma levels of soluble endothelial cell protein C receptor in patients with Wegener's granulomatosis

Elevated soluble thrombomodulin (sTM) levels are an accepted marker of endothelial damage. The physiological significance of plasma endothelial protein C receptor (sEPCR) levels is not known. To assess the relevance of this plasma protein in Wegener's granulomatosis (WG), sEPCR levels were measured in sera obtained from WG patients and related to disease activity, sTM levels, and other known markers of disease activity. In total, 129 sera (37 at active disease, 92 during follow-up) from 31 WG patients were tested. During active disease, eight (22%) and 17 (46%) out of 37 active sera had elevated levels of sEPCR and sTM, respectively (NS); sEPCR (r = 0.39; P = 0.02) and sTM (r = 0.53; P <0.01) levels correlated with disease activity (Birmingham Vasculitis Activity Score). Analysis of longitudinal sera revealed a significant increase in sEPCR (P = 0.01) and sTM (P = 0.04) levels prior to the moment of a relapse. Corrected for renal function, the increase in sEPCR remained significant (P =0.04) whereas sTM did not (NS). Levels of sEPCR correlated with sTM levels (r = 0.32; P < 0.001).Plasma levels of sEPCR respond to changes in the disease in patients with WG.     

Serum levels of adhesion molecules and thrombomodulin as indicators of vascular injury in severe Plasmodium falciparum malaria

Severe Plasmodium falciparum malaria is characterized by multiple organ involvment due to sequestration of infected erythrocytes in small vessels. Endothelial cell adhesion molecules play an important role in this interaction. During the course of a severe cerebral P. falciparum malaria infection we found very markedly elevated levels of the soluble adhesion molecules intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1, with a maximum increase of nine, seven, and eight times, respectively. These very high levels of soluble adhesion molecules point to an endothelial cell injury as an additional cause to physiological release or shedding due to receptor interactions. Soluble thrombomodulin (sTM) levels showed an extremely marked elevation up to 332 ng/ml (up to 13 times the normal value) as well. Malaria patients without severe organ involvement/cerebral manifestation showed only a mild elevation of sTM levels. TM is a parameter independent of the immunological system. It is regarded as a marker of vasculitis and endothelial cell destruction. Therefore, markedly elevated sTM levels document a substantial endothelial cell injury in severe malarial infection and may be of diagnostic and prognostic importance.Abbreviations VCAM-1 vascular cell adhesion molecule-1 (CD106) - ICAM-1 intercellular adhesion molecule-1 (CD54) - IL-2R interleukin-2 receptor (CD25) - TM thrombomodulin     

高血压病和2型糖尿病患者血清损伤ECV-304细胞的比较研究

目的:以高血压病和2型糖尿病为例进行血瘀证血管内皮细胞损伤模型的比较研究,为中医学"异病同证"理论提供实验依据。方法:取对数生长期ECV-304细胞,分组如下:空白对照组(无血清的DMEM组)、糖尿病血瘀证组(糖尿病血瘀证患者血清)和高血压病血瘀证组(高血压病血瘀证患者血清)。采用噻唑蓝比色法(MTT法)观察细胞活性;在倒置相差显微镜、扫描电镜和透射电镜下观察细胞形态的变化;应用放免法测定内皮素(ET)含量;硝酸还原酶法测定一氧化氮(NO)含量;利用双抗夹心酶联免疫法(ELISA)检测各组细胞培养上清液中内皮细胞蛋白C受体(EPCR)、血管内假性血友病因子(vWF)和血栓调节蛋白(sTM)的含量;应用激光扫描共聚焦显微镜,采用Fluo-3/AM作为荧光指示剂观察细胞内游离钙([Ca2+]i)浓度的变化;并采用荧光探针标记的鬼笔环肽染色法观察细胞肌动蛋白微丝分布的差异。结果:(1)MTT结果显示,10%血清作用下,高血压病血瘀证组的细胞活力低于对照组(P0.05),糖尿病血瘀证组的细胞活力也低于对照组(P0.05),但高血压病血瘀证组的细胞活力与糖尿病血瘀证组差异无显著(P0.05);(2)高血压病血瘀证组的ET水平高于对照组(P0.05),糖尿病血瘀证组也高于对照组(P0.05),且高血压病血瘀证组的ET水平低于糖尿病血瘀证组(P0.05);高血压病血瘀证组的NO水平低于对照组(P0.05),糖尿病血瘀证组也低于对照组(P0.05),且高血压病血瘀证组的NO水平高于糖尿病血瘀证组(P0.05);(3)高血压病血瘀证组的EPCR、vWF和sTM含量高于对照组(P0.05),糖尿病血瘀证组也高于对照组(P0.05),且高血压病血瘀证组的EPCR水平低于糖尿病血瘀证组(P0.05);而高血压病血瘀证组的vWF和sTM含量与糖尿病血瘀证组之间差异无显著(P0.05);(4)高血压病血瘀证组[Ca2+]i高于对照组(P0.05),糖尿病血瘀证组[Ca2+]i高于对照组(P0.05),高血压病血瘀证组胞浆内荧光分布不均匀,[Ca2+]i高于糖尿病血瘀证组(P0.05);(5)高血压病血瘀证组可见细胞骨架微丝减少但排列较为规则,糖尿病血瘀证组的微丝断裂且排列紊乱,二者微丝分布差异显著。结论:高血压病患者血清和糖尿病患者血清对ECV-304细胞骨架、[Ca2+]i及ET、NO和EPCR表达的影响不同,但均能造成ECV-304细胞损伤,这可能是中医学"异病同证"的病理学基础。     

Impact of chemotherapy on thrombin generation and on the protein C pathway in breast cancer patients

Although thromboembolism is a problematic complication of chemotherapy, the pathogenic mechanisms by which chemotherapeutic agents exert prothrombotic effects in vivo are unclear.The objective of this study was to examine the effects of adjuvant chemotherapy on thrombin generation, the protein C anticoagulant pathway, and microparticle tissue factor (MP TF) activity in 26 breast cancer patients (stages I to III). The patients received cyclophosphamide, 5-fluorouracil, and methotrexate, epirubicin, or doxorubicin. Plasma samples were collected on day 1 (baseline), day 2, and day 8 for the first 2 cycles of chemotherapy. Levels of thrombin-antithrombin (TAT) complexes, MP TF activity, and components of the protein C anticoagulant pathway, including protein C, activated protein C (APC), soluble thrombomodulin (sTM), and soluble endothelial protein C receptor (sEPCR), were measured. Compared to prechemotherapy baseline levels, plasma TAT, protein C, and APC were significantly different following the administration of chemotherapy (p < 0.01 for each). Plasma TAT was higher in cycle 1, day 2, and cycle 2, day 8, compared to baseline. Plasma protein C levels were lower in cycle 2, day 8, whereas plasma APC levels were lower in cycle 2, day 1, and cycle 2, day 8. No significant changes were found in plasma sEPCR, sTM, or MP TF activity. This study suggests that adjuvant chemotherapy in women with breast cancer increases thrombin generation and impairs the endothelium-based protein C anticoagulant pathway.     

类风湿关节炎患者血清炎性因子、ANCA水平与血管内皮损伤标志物的相关性分析

目的:探讨类风湿关节炎(RA)患者血清炎性因子及抗中性粒细胞胞浆抗体(ANCA)水平与血管内皮损伤的相关性。方法:106例RA患者,分为活动组(83例)和缓解组(23例),55例健康人群作为对照,采用ELISA检测各组血清炎性因子白介素-1β(IL-1β)、白介素-6(IL-6)、白介素-17(IL-17)、肿瘤坏死因子-α(TNF-α)及血管内皮损伤标志物-血管性血友病因子(vWF)、可溶性细胞间黏附分子-1(sI-CAM-1)及血管内皮黏附分子-1(sVCAM-1)水平;采用间接免疫荧光法(IIF)检测各组血清ANCA阳性率。比较各组上述指标水平差异,分析两组RA患者炎性因子水平、ANCA阳性率与血管内皮损伤标志物水平的相关性。结果:RA活动组IL-6、TNF-α、vWF、sICAM-1、sVCAM-1血清水平均高于对照组(P<0.05);RA缓解组IL-6、vWF水平均低于RA活动组(P<0.05),但vWF、sVCAM-1水平仍显著高于对照组(P<0.01);RA患者IL-6、IL-1β、IL-17与血管内皮损伤标志物有不同程度的相关性;RA患者活动组ANCA阳性率为32.5%,显著高于对照组(P<0.01);ANCA阳性患者vWF水平高于ANCA阴性患者(P<0.05)。结论:RA活动期患者存在较明显血管内皮损伤,这种损伤与高水平的炎性因子及ANCA阳性表达有关。     

Cerebral endothelial damage after severe head injury.

We demonstrate that in head injuries the degree of cerebral endothelial activation or injury depends on the type of brain injury and the patients age, and that in severe head injuries measuring the serum levels of thrombomodulin (TM) and von Willebrand factor (vWF) is useful in evaluating cerebral endothelial injury and activation. The values of vWF in the cases of focal brain injury were significantly higher than in the cases of diffuse axonal injury. The serum levels of TM in focal brain injuries were higher than in diffuse axonal injuries, but the differences were not statistically significant. In patients with delayed traumatic intracerebral hematoma (DTICH), vWF levels were much higher than in patients without DTICH. The values of TM and vWF in elderly patients were significantly higher than in younger patients. These findings indicate that: 1) the degree of endothelial activation in focal brain injury is significantly higher than in diffuse brain injury; 2) the degree of cerebral endothelial injury in patients with DTICH is much higher than in those without DTICH; and 3) the degree of cerebral endothelial activation and injury in elderly head injury patients is significantly higher than in younger patients.     

Effects of percutaneous lower-extremity arterial interventions on endothelial function and inflammation response in patients with both type 2 diabetes and lower-extremity peripheral arterial disease

Background: The high incidence and damage of PAD in people with diabetes has aroused wide attention. We aimed to examine effects of percutaneous lower-extremity arterial interventions (PLEAIs) on endothelial function and inflammation response in type 2 diabetes (T2D) patients with lower-extremity peripheral arterial disease (PAD). Methods: 78 T2D inpatients with PAD were selected into the treatment group. Their venous levels of von Willebrand Factor (vWF) and high sensitivity C reactive protein (hsCRP) were measured. Blood samples were collected from the arterial sheath for vWF and hsCRP tests. Venous levels of vWF and hsCRP were monitored at 24 hours, 48 hours, 1 week, and 2 weeks post PLEAIs. Results: Prior to PLEAIs, venous levels of vWF and hsCRP in the treatment group were significantly higher than the control group. The arterial levels of vWF and hsCRP were 117.9%±15.1% and 5.19±0.76 mg/L in the control group, while those levels in the treatment group before intervention were also significantly higher than in the control group. In the treatment group prior to inventions, vWF and hsCRP levels of arterial ischemic regions were significantly higher than the non-ischemic regions. The vWF level of arterial ischemic regions after treatment was significantly higher than that prior to treatment. Conclusions: PLEAIs applied to those patients may lead to worse endothelial dysfunction and activated inflammatory response during treatment and 1 week after treatment, which indicates an emerging necessary of early protection or care on endothelial function and inflammatory reaction during and post PLEAIs.     

Systemic Inflammation and Disseminated Intravascular Coagulation in Early Stage of ALI and ARDS: Role of Neutrophil and Endothelial Activation

To determine the existence of a close link between inflammation and coagulation in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) and to examine their prognostic value in the development of ARDS and clinical outcome, we made a prospective cohort study. The study subjects consisted of 57 patients: 19 patients with ARDS and 38 patients with ALI as defined by a Lung Injury Score of > or =2.5 and 1.0 to less than 2.5, respectively. According to the outcome, the patients were subdivided into the survivors and the nonsurvivors. Ten normal healthy volunteers served as control subjects. Plasma levels of soluble L-, P-, and E-selectins, intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), thrombomodulin (sTM), and neutrophil elastase were measured within 24 h after the diagnosis of ALI or ARDS. The number of systemic inflammatory response syndrome (SIRS) criteria being met by the patients and the disseminated intravascular coagulation (DIC) scores were determined simultaneously. The number of SIRS criteria and the DIC scores of the patients with ALI or ARDS showed high values, and more than half of the patients were complicated by DIC. The levels of sL-selectin in both groups of the patients were significantly lower than those of the control subjects. All other soluble adhesion molecules, neutrophil elastase, and sTM in the patients with ALI and ARDS were markedly elevated than those in the control subjects. The levels sICAM-1, sVCAM-1, and sTM in the ARDS patients significantly increased compared with the ALI patients. The number of SIRS criteria and the DIC scores in the nonsurvivors showed higher values than those in the survivors. In addition, we found significant differences in the levels of soluble adhesion molecules, neutrophil elastase, and sTM between the survivors and the nonsurvivors. In conclusion, we found a concurrent activation of both inflammation and coagulation in the patients with ALI or ARDS. The results also suggest that systemic activation of inflammation and coagulation associated with endothelial injury has prognostic value for the development of ARDS and poor outcome.