尼可地尔对急性冠状动脉综合征患者PCI术后炎性因子及血管内皮功能的影响

目的:探讨尼可地尔对急性冠状动脉综合征患者冠状动脉介入术(percutaneous coronary intervention,PCI)术后炎性因子及血管内皮功能的影响.方法:选取2018年7月至2020年7月于我院接受PCI治疗的急性冠状动脉综合征患者94例,随机分为对照组和研究组(n=47).对比两组炎性因子[C反应蛋白(C-reactive protein,CRP)、肿瘤坏死因子-α(Tumor necrosis factor,TNF-α)、白介素-6(Interleukin-6,IL-6)]、血管内皮功能[内皮素-1(endothelin-1,ET-1)、一氧化氮(nitric oxide,NO)、血管性血友病因子(Von Willebrand factor,VWF)]、预后.结果:各组术后CRP、TNF-α、IL-6水平均呈先升后降趋势,其中研究组术后1个月CRP、TNF-α、IL-6水平均低于对照组(P<0.05);各组术后VWF、ET-1均呈先升后降趋势、NO呈先降后升趋势,其中研究组术后1个月VWF、ET-1均低于对照组、NO高于对照组(P<0.05);研究组心血管事件及再狭窄发生率低于对照组(P<0.05).结论:尼可地尔可有效缓解急性冠状动脉综合征患者PCI术后炎性反应,改善血管内皮功能,改善预后.     

Solitaire AB支架取栓术对急性脑梗死患者血管内皮功能及炎性因子的影响

目的:探究急性脑梗死患者使用Solitaire AB支架取栓术对患者血管内皮功能以及炎性因子的影响。方法:回顾性分析2019年1月至2020年7月医院收治85例急性脑梗死患者治疗资料,依据治疗方式不同分为对照组(n=40)和观察组(n=45),对照组患者接受保守治疗,观察组在对照组基础上加用Solitaire AB支架取栓术治疗。比较两组患者治疗前后血管内皮功能指标(内皮素-1(Endothelin-1,ET-1)、血栓素B2(Thromboxane B2,TXB2)、一氧化氮(Nitric oxide,NO)),炎性因子(肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、白细胞介素-6(Interleukin-6,IL-6)及C反应蛋白(C-reactive protein,CRP))、神经功能损伤(美国国立卫生研究院卒中量表(the National Institutes of Health Stroke Scale,NIHSS)评分以及中国卒中量表(Chinese Stroke Scale,CSS))、生活能力(Barthel指数)、治疗效果及不良反应。结果:两组患者治疗后血管内皮功能指标,炎性因子以及神经功能损伤评分、Barthel指数较治疗前明显改善(P<0.05)。治疗后观察组患者ET-1、TXB2明显低于对照组,NO明显高于对照组(P<0.05),治疗后观察组患者炎性因子下降水平明显高于对照组(P<0.05),治疗后观察组患者NIHSS评分、CSS评分明显低于对照组(P<0.05),Barthel指数和总有效率明显高于对照组(P<0.05)。观察组患者治疗后不良反应发生率略低于对照组(6.67%vs 15.00%),但是差异无统计学意义(P>0.05)。结论:急性脑梗死患者使用Solitaire AB支架取栓术可以有效修复血管内皮功能,下调炎性因子水平,临床应用价值较高。     

三种血管内皮损伤指标血清水平与冠心病病变范围的关系

目的:探讨血清可溶性血管细胞黏附分子-1(sVCAM-1)、可溶性细胞间黏附分子-1(sICAM-1)、血管性血友病因子(vWF)水平与冠心病(CHD)病变范围的相关性。方法:根据冠脉造影结果将87例患者分为CHD组(63例)和对照组(24例)。采用ELISA平行检测两组血清sVCAM-1、sICAM-1和vWF水平,酶法测定血脂水平,比较两组患者sVCAM-1、sICAM-1、vWF及血脂水平的差异,并进行相关性分析;以冠脉狭窄支数作为判断CHD病变范围的依据,探讨不同病变范围患者血清sVCAM-1、sICAM-1和vWF的水平变化。结果:CHD组血清sVCAM-1、sI-CAM-1、vWF水平显著高于对照组(P<0.01);血清sVCAM-1、sICAM-1和vWF水平与血脂水平之间无明显相关性(P>0.05);单支冠脉狭窄组血清sVCAM-1、sICAM-1水平显著低于多支冠脉狭窄组(P<0.05)。结论:CHD患者血清sV-CAM-1、sICAM-1和vWF水平升高,sVCAM-1、sICAM-1水平与CHD病变范围有关。     

补阳还五汤对颈动脉粥样硬化患者炎性因子及血管内皮功能的影响

目的:探讨补阳还五汤对颈动脉粥样硬化(CAS)患者血脂、血清炎性因子和血管内皮功能的影响。方法:90例颈动脉粥样硬化患者，随机分为对照组和治疗组(各45例),在常规治疗基础上，对照组加用瑞舒伐他汀，治疗组加用补阳还五汤，疗程12周。对比两组患者治疗前后血脂四项、炎性因子、血管内皮功能及颈动脉超声影像指标的变化。结果:治疗前，两组各有关指标差异均无统计学意义(P>0.05)。治疗后两组患者高密度脂蛋白胆固醇(HDL-C)均升高，总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)均降低(P<0.05),各炎性因子水平均降低(P<0.05),内皮素-1(ET-1)、血管性血友病因子(vWF)和纤维蛋白原(FIB)均下降，一氧化氮(NO)升高(P<0.05);颈动脉IMT、斑块面积、Crouse斑块积分均降低(P<0.05)。且治疗组以上各项指标改善均明显优于对照组(P<0.05)。结论:补阳还五汤能通过改善CAS患者血脂水平、降低血清炎性因子、调节血管内皮功能，达到减小CAS斑块的作用。     

代谢综合征患者血管内皮损伤标志物、C反应蛋白与胰岛素抵抗的关系

目的:观察代谢综合征(MS)患者血管内皮损伤标志物血管性假性血友病因子抗原(vWF:Ag)、凝血酶调节蛋白(TM)及超敏C反应蛋白(Hs-CRP)的水平变化及其与胰岛素抵抗的关系。方法:测定67例MS患者(其中合并冠心病31例)及35例健康对照组TM、vWF:Ag、Hs-CRP、空腹胰岛素(Fins)水平,计算胰岛素抵抗指数(IR)。结果:单纯MS组(B组)TM、vWF:Ag、Hs-CRP水平明显高于对照组(A组),P<0.05;MS合并冠心病组(C组)TM、vWF:Ag、Hs-CRP水平均高于A组和B组,差异有显著性统计学意义(P<0.05)。单因素直线相关分析表明TM、vWF:Ag、Hs-CRP与IR显著正相关(r分别为0.32、0.36、0.38)。结论:MS患者血管内皮损伤标志物、CRP水平升高,且与IR抵抗有关。     

黄芪汤联合负压封闭引流治疗对糖尿病足溃疡患者临床疗效、炎性因子及血管内皮功能的影响分析

目的分析黄芪汤联合负压封闭引流治疗对糖尿病足溃疡患者临床疗效、炎性因子及血管内皮功能的影响。方法回顾性分析2018年6月~2020年6月我院收治的60例糖尿病足溃疡患者作为研究对象,根据治疗方法的不同分为联合组(黄芪汤联合负压封闭引流术)和基础组(负压封闭引流术),每组各30例。比较两组患者临床疗效,治疗前后炎性因子水平及血管内皮功能。结果治疗后,联合组患者临床总有效率为(96.67%),显著高于基础组的(83.33%),差异具有统计学意义(P<0.05);治疗后两组患者CRP、TNF-α和IL-6水平均较治疗前呈明显下降趋势,且联合组上述指标下降程度明显高于基础组(P<0.05);治疗后两组患者vWF和ET-1均明显低于术前,NO明显高于术前,联合组上述指标变化程度明显大于基础组(P<0.05)。结论黄芪汤联合负压封闭引流术治疗能够提升糖尿病足溃疡患者的临床疗效,抑制炎症反应,改善血管内皮功能,有利于患者预后,值得临床推广。     

炎性因子在2型糖尿病冠脉循环障碍中作用的研究进展

糖尿病(DM)是一种内分泌代谢障碍性疾病,其中以2型糖尿病(T2DM)最为常见,主要发病机制是胰岛素抵抗(IR)伴胰岛素分泌不足,疾病后期多种并发症并存,尤其心血管并发症是DM患者致残、致死的主要原因。现越来越多的证据表明T2DM是炎性因子介导的血管内皮炎症反应,炎性因子可通过IR、胰岛β细胞损伤或干扰信号传导等多途径参与T2DM的发生、发展。本文回顾了各炎性因子对T2DM的作用,将目前研究较多的炎性因子如:C反应蛋白(CRP)、肿瘤坏死因子(TNF-α)、白介素-6(IL-6)、核转录因子(NF-κB)、白介素-8(IL-8)、白介素-12(IL-12)、白介素-18(IL-18)以及白介素-10(IL-10)在T2DM冠脉循环、微循环中的作用作一综述,提出既然是炎性因子介导的炎症发应,就应针对相应炎性因子及其信号传导途径等发生机制给予对应抗炎治疗及阻碍信号传导,延缓或阻止T2DM心血管并发症发生,改善T2DM冠脉循环、微循环,降低T2DM心血管死亡率,提高T2DM患者预后。     

类风湿关节炎患者抗血管内皮细胞抗体、血管内皮生长因子和白细胞介素-17的检测及意义

目的 通过对类风湿关节炎(RA)患者血清抗血管内皮细胞抗体(AECA)、血浆血管内皮生长因子(VEGF)和白细胞介素-17(IL-17)的检测,旨在探讨AECA、VEGF、IL-17在RA患者发病、病情进展中的相关性及其内在联系.方法 采用间接免疫荧光法(IIF)和双抗体夹心酶联免疫吸附试验(ELISA)法检测86例RA、45例骨关节炎(OA)、30例健康对照AECA的阳性率和VEGF、IL-17水平,VEGF、IL-17水平与红细胞沉降率(ESR)、超敏C反应蛋白(hs-CRP)、类风湿因子(RF)等指标进行相关性分析.结果 RA患者AECA阳性率为8.1%,高于OA患者的阳性率2.2%(t:2.133,P<0.05)和健康对照的阳性率0(t=2.562,P<0.05);RA活动期AECA阳性率为16.7%,高于RA缓解期的阳性率3.6%(t=2.105,P<0.05);RA患者血浆IL-17和VEGF水平显著高于OA组(t=2.02、t=2.106,P<0.05)和健康对照组(t=2.413、t=2.469,P<0.05);RA患者活动期血浆IL-17和VEGF水平明显高于RA缓解组(t=2.315、t=2.232,P<0.05)及健康对照组(t:2.985、t=2.753,P<0.01);RA缓解组与健康对照组无明显差异(t=1.475、t=1.326,P>0.05);RA患者AECA滴度、血浆IL-17、VEGF水平与ESR、hs-CRP、RF的指标呈正相关.结论 AECA、VEGF、IL-17三者与RA的发病、病情活动存在一定的关系,IL-17、VEGF水平变化及AECA的滴度可作为临床观察RA病情活动、判断疗效及预后等方面的参考指标.     

类风湿关节炎患者抗血管内皮细胞抗体、血管内皮生长因子和白细胞介素-17的检测及意义

目的 通过对类风湿关节炎(RA)患者血清抗血管内皮细胞抗体(AECA)、血浆血管内皮生长因子(VEGF)和白细胞介素-17(IL-17)的检测,旨在探讨AECA、VEGF、IL-17在RA患者发病、病情进展中的相关性及其内在联系.方法 采用间接免疫荧光法(IIF)和双抗体夹心酶联免疫吸附试验(ELISA)法检测86例RA、45例骨关节炎(OA)、30例健康对照AECA的阳性率和VEGF、IL-17水平,VEGF、IL-17水平与红细胞沉降率(ESR)、超敏C反应蛋白(hs-CRP)、类风湿因子(RF)等指标进行相关性分析.结果 RA患者AECA阳性率为8.1%,高于OA患者的阳性率2.2%(t:2.133,P<0.05)和健康对照的阳性率0(t=2.562,P<0.05);RA活动期AECA阳性率为16.7%,高于RA缓解期的阳性率3.6%(t=2.105,P<0.05);RA患者血浆IL-17和VEGF水平显著高于OA组(t=2.02、t=2.106,P<0.05)和健康对照组(t=2.413、t=2.469,P<0.05);RA患者活动期血浆IL-17和VEGF水平明显高于RA缓解组(t=2.315、t=2.232,P<0.05)及健康对照组(t:2.985、t=2.753,P<0.01);RA缓解组与健康对照组无明显差异(t=1.475、t=1.326,P>0.05);RA患者AECA滴度、血浆IL-17、VEGF水平与ESR、hs-CRP、RF的指标呈正相关.结论 AECA、VEGF、IL-17三者与RA的发病、病情活动存在一定的关系,IL-17、VEGF水平变化及AECA的滴度可作为临床观察RA病情活动、判断疗效及预后等方面的参考指标.     

高血压对急性心肌梗死患者血清IL-1β、IL-6及IL-8水平的影响

为探讨高血压对急性心肌梗死（AMI）患者血清白介素-1β（IL-1β）、白介素-6（IL-6）及白介素-8（IL-8）的影响。AMI患者67例,根据高血压病史分为非高血压组37例,高血压组30例,对照组28名,采用ELISA测定各组患者入院第24h、第14d及对照组的血清IL-1β、IL-6及IL-8水平。结果表明非高血压组患者的炎性因子水平于AMI发病第24h显著高于对照组（P〈0．001）,发病第14天炎症因子水平与对照组相比无显著性差异,高血压组患者AMI发病第24h、第14d血清炎症因子水平均显著高于非高血压组和对照组（P〈0．001）。结果显示,IL-1β、IL-6及IL-8参与了AMI的发病,但高血压对炎性因子的升高起到了关键作用。     

Soluble cell adhesion molecules and von Willebrand factor in children with Kawasaki disease.

Fifty-nine children with acute Kawasaki disease (KD), a childhood vasculitis, were compared with 35 children with fever due to infection and 48 healthy children. Levels of soluble E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1) in the healthy children were double those found in adults. All three soluble cell adhesion molecules and von Willebrand factor (vWF) were higher in the children with KD than in the healthy children, but only sE-selectin, a marker for activated endothelial cells, and sICAM-1 were higher than in the febrile children. The high levels of vWF in KD appear to reflect the prominent acute-phase reaction. This information can help us to understand further the complex interactions between cytokines, circulating inflammatory cells and the vascular endothelium, and may lead to new therapeutic avenues in KD and other inflammatory diseases and vasculitides.     

Levels of soluble VCAM-1, soluble ICAM-1, and soluble E-selectin during disease exacerbations in patients with systemic lupus erythematosus (SLE); a long term prospective study.

Active SLE is characterized by immune deposits and subsequent vascular inflammation in many organs. Expression and up-regulation of adhesion molecules is basic to migration of inflammatory cells into the tissues. Recently, soluble isoforms of these molecules have been described which might be an expression of their up-regulation in the tissues and, as such, of disease activity. The purpose of this study was to evaluate whether changes in levels of soluble adhesion molecules reflect disease activity. We analysed serial sera in a 6-month period preceding 22 consecutive exacerbations of SLE for levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and sE-selectin. Levels were related to clinical disease activity (SLEDAI), and levels of anti-dsDNA and complement. At the time of maximal disease activity, levels of sVCAM-1 in patients with SLE were higher than those in controls (P < 0.0001), levels in patients with renal involvement being higher than in those without (P < 0.02). Levels of sVCAM-1 correlated with SLEDAI scores (P < 0.05) and, inversely, with levels of C3 (P = 0.01). In addition, in the presence of anti-dsDNA, levels of sVCAM-1 tended to correlate with levels of these autoantibodies (P < 0.1). Levels of sICAM-1 were normal and sE-selectin levels even decreased compared with controls. Levels of sVCAM-1 were higher at the moment of relapse (P = 0.001) than at 6 months before this time point. This rise correlated with the rise in SLEDAI score (P < 0.02). Levels of sICAM-1 and sE-selectin did not rise, and remained in the normal range in all exacerbations studied. In conclusion, in contrast to sICAM-1 and sE-selectin, levels of sVCAM-1 are increased, rise parallel to disease activity during exacerbations in SLE, and are associated with decreasing levels of complement factors. This favours the hypothesis of immune deposit formation, activation of the complement cascade and activation of endothelial cells. Concurrent up-regulation of vascular adhesion molecules may thus result in transmigration of activated inflammatory cells inducing tissue damage.     

Increased plasma concentrations of sICAM-1, sVCAM-1 and sELAM-1 in patients with Plasmodium falciparum or P. vivax malaria and association with disease severity.

Increased serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), soluble endothelial leucocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were detected in Danish malaria patients infected with sequestering Plasmodium falciparum or non-sequestering P. vivax parasites, as well as in patients with sepsis or meningitis. Levels of soluble adhesion molecules remained elevated in the P. falciparum patients for several weeks after initiation of treatment. Plasma concentrations of sICAM-1, sVCAM-1 and sELAM-1 were higher in Gambian children with severe P. falciparum malaria than in children with mild malaria. Plasma levels of sVCAM-1 and sELAM-1 were significantly correlated. Plasma levels of sELAM-1 and sVCAM-1 may reflect endothelial inflammatory reactions and these reactions may be harmful for humans infected with malaria parasites.     

Evaluation of the association of serum levels of hyaluronic acid,sICAM-1, sVCAM-1, and VEGF-A with mortality and prognosis in patients with Crimean-Congo hemorrhagic fever

BackgroundCrimean-Congo hemorrhagic fever (CCHF) is a tick-borne viral hemorrhagic disease. Pathogenesis of the disease has not been well described yet. A well-known pathogenic feature of CCHF virus is its capability to damage endothelium. Increased hyaluronic acid (HA) levels indicate liver sinusoidal endothelial damage. Soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and vascular endothelial growth factor-A (VEGF-A) play a role in the inflammatory process, vascular damage and plasma leakage.ObjectivesTo investigate whether or not there is a relationship between HA, sICAM-1, sVCAM-1 and VEGF-A serum levels and fatality in CCHF.Study designSixty-one patients who were confirmed by RT-PCR and serological tests for CCHF, included in the current study. HA, sICAM-1, sVCAM-1, VEGF-A levels in serum samples were analyzed by ELISA.ResultsThere were statistically significant differences between fatal and non-fatal CCHF patients in terms of HA, sICAM-1, sVCAM-1, and VEGF-A levels. In addition, AST and ALT levels were positively correlated with HA, sICAM-1, sVCAM-1, and VEGF-A levels.ConclusionHA, sICAM-1, sVCAM-1, and VEGF-A levels of the patients that died during hospitalization were statistically significantly higher than the patients that survived, and this finding suggests that the level of these molecules could be used as a prognostic marker in CCHF.     

Levels of soluble vascular cell adhesion molecule-1 and soluble intercellular adhesion molecule-2 in plasma of patients with hemorrhagic fever with renal syndrome, and significance of the changes in level

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease characterized by endothelial dysfunction. Vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-2 provide costimulatory signals for the activation of T lymphocytes; these adhesion molecules play key roles in leukocyte adherence and propagation of inflammatory responses. They may be involved in the immunologic response that leads to vascular endothelial cell (VEC) and kidney damage of HFRS patients, and increased levels of soluble (s)VCAM-1 and sICAM-2 in plasma may indicate the severity of HFRS. We examined the presence of sVCAM-1 and sICAM-2 in 52 plasma samples collected from 52 patients. We tested these plasma samples for sVCAM-1 and sICAM-2 by double-antibody sandwich ELISA. We found variable, but persistently elevated, levels of sVCAM-1 and sICAM-2 throughout the various phases and types of the disease, which suggested sVCAM-1 may play an important role in the immunopathological lesions of HFRS and is closely correlated to the severity of HFRS and the degree of kidney damage. sICAM-2 may be associated with the hyperfunctioning of the cellular immune response.     

Unfractionated heparin is associated with a lower rise of serum vascular cell adhesion molecule-1 in acute ischemic stroke patients

We sought to assess the anti-inflammatory properties of unfractionated heparin (UFH) in patients with ischemic stroke treated within 24 h from the onset of symptoms. We studied prospectively 167 patients that received 1000 IU/h intravenous UFH (n=70) or 300 mg oral aspirin (n=97) at a mean treatment delay of 6.7 h. Repeated plasma levels of interleukin (IL)-6, IL-10, IL-4, tumor necrosis factor (TNF)-alpha, soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were compared in both groups using multivariate analyses. Whereas TNF-alpha and sICAM-1 decreased at 48 h, IL-6, IL-4, and sVCAM-1 increased compared with baseline values (P<0.01). The rise of sVCAM-1 levels at 48 h was significantly lower in patients treated with UFH (P=0.017) and a two-fold increase of baseline sVCAM-1 was an independent predictor of poor outcome (odds ratio, 2.19, 1.1-4.39). These results suggest that adjusted high-dose UFH has anti-inflammatory effects which might improve recovery if administered early after stroke onset.     

Production of soluble ICAM-1 by mononuclear cells from patients with rheumatoid arthritis patients

The present study was designed to quantify the level of the soluble form of ICAM-1 (sICAM-1) produced by mononuclear cells (MNC) of rheumatoid arthritis (RA) patients, and to correlate these levels with the disease activity and with the amounts of cytokines or rheumatoid factors (RF) produced by MNC. Unstimulated synovial fluid (SF) MNC produced higher amounts of sICAM-1 than peripheral blood (PB) MNC in RA patients (P<0.01). sICAM-1 production by PHA-stimulated MNC was higher in RA SF MNC than RA or normal PB MNC (P<0.01). The amounts of SICAM-1 produced correlated with the amounts of soluble IL-2 receptor produced (P<0.02) but not with IL-1B or the Lansbury activity index in RA PB MNC. sICAM-1 correlated with the amounts of soluble CD23 and IL-4 produced by normal PB MNC (P<0.01). The amounts of sICAM-1 correlated with IgG-RF (P <0.02) and IgM-RF (P<0.01) produced by unstimulated MNC obtained from the bone marrow (BM) of RA patients. ICAM-1 expression of T-lymphocyte subsets, B lymphocytes, and monocytes obtained from RA PB and RA BM assayed by twocolor flow cytometry ranged from 0.1 to 6%, which was not appreciably different from that of normal controls. The monocyte fraction of RA PB MNC produced significantly higher amounts of sICAM-1 than lymphocyte fraction. These results suggest that sICAM-1 produced by MNC may be a marker of cell activation in T and B lymphocytes, in contrast to the transient increase of ICAM-1 expression.     

Reduction of soluble adhesion molecules (sICAM-1, sVCAM-1, and sE-selectin) and vascular endothelial growth factor levels in serum of rheumatoid arthritis patients following multiple intravenous infusions of infliximab

INTRODUCTION: The purpose of this study was to determine the effect of repeated infusions of infliximab, a chimeric anti-tumor necrosis factor (anti-TNF)-alpha antibody, on the levels of soluble adhesion molecules and vascular endothelial growth factor (VEGF) in patients with active rheumatoid arthritis (RA). MATERIALS AND METHODS: The treatment design consisted of 9 infusions of infliximab (3 mg/kg) at weeks 0, 2, 6, and every 8 weeks thereafter. All patients had been receiving methotrexate (MTX; 7.5-20 mg/week). Serum levels of soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, E-selectin (sE-selectin), and VEGF were measured by ELISA at weeks 0, 2, 6, 14, and 38 prior to infusion, and at week 62. RESULTS: A remarkable decrease in serum sICAM-1 (p<0.001), sVCAM-1 (p<0.01), sE-selectin (p<0.01) and VEGF (p<0.001) levels was observed in RA patients after the initial dose of infliximab. The second administration of the drug was followed by an even more significant suppression of serum sICAM-1, sVCAM-1, sE-selectin, and VEGF (p<0.001 in all cases). Further infliximab infusions also significantly reduced serum soluble adhesion molecules and VEGF concentrations, although these were less effective. Infliximab treatment induced a significant decrease in the number of monocytes observed until the end of the study. CONCLUSIONS: Our study, besides a rapid suppression of disease activity, showed that serum soluble adhesion molecules and VEGF concentrations are down-regulated following anti-TNF-alpha antibody therapy combined with MTX. Repeated doses of infliximab sustained the reductions in the soluble adhesion molecules and VEGF concentrations, although they were less effective than the first and second infusions of infliximab.     

Normal levels of soluble E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1) decrease with age

sE-selectin, sICAM-1, sVCAM-1 and von Willebrand factor (vWF) were assayed in 238 samples in a longitudinal study of 81 normal children from 9.5 to 15.5 years old. Multilevel modelling was used to quantify changes with age. sE-selectin, sICAM-1 and sVCAM-1 all fell significantly over the age range (by 17%, 16%, and 10%, respectively). In contrast, levels of vWF were not age-dependent. Our findings highlight the need for age-matched controls when studying cell surface adhesion molecules in disease groups, and may imply developmental changes in expression of these molecules and their shedding from the cell surface.