60例炎症性肠病患者血小板检测的临床意义

炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),血小板参与了炎症性肠病的发病机制,血小板计数(PC)增加与疾病活动有关。血小板激活与纤维蛋白溶解系统作用的减弱参与了炎症性肠病患者高凝状态的形成[1]。血小板平均体积(MPV)变小能够反映被激活。我们对60例炎性肠病患者     

血小板功能障碍:炎症性肠病研究的一种新动向

至今,人们已意识到血小板增多是炎症性肠病(IBD)活动期的一种标志,且是发生全身性血栓栓塞的一种可能诱发因素。 作为炎症细胞的血小板,能直接引起炎症反应。将血小板提取物注入健康人皮肤,可发生强烈炎症反应,且可持续数小时,而注入中性粒细胞及嗜碱性细胞的提取物则无此反应。活化的血小板可释放一系列炎性介质,如血小板活化因子(PAF)、血栓素(Tα)12-HETE、血小板     

高血压病患者vWF检测的临床意义

目的 探讨血管性假血友病因子（vWF）检测在高血压病患者的临床意义。方法 选103例高血压病患者及30例正常者空腹取肘静脉血采用酶联免疫吸附双抗体夹心法（ELISA）,测定血浆vWF含量。按高血压病分期及年龄段分组。结果 高血压Ⅱ、Ⅲ期患者,vWF含量显著高于正常对照组（P＜0．01）,随着年龄增大,vWF的含量也增高,同时70岁以上年龄段中男性升高最明显。结果 vWF是血管内皮受损的标志物,高血压患者存在内皮细胞受损,受损程度与年龄大小,病情正相关。     

高血压病患者vWF检测的临床意义

目的探讨血管性假血友病因子(vWF)检测在高血压病患者中的临床意义。方法选103例高血压病患者及30例正常者空腹取肘静脉血采用酶联免疫吸附双抗体夹心法(ELISA),测定血浆vWF含量。按高血压病分期及年龄段分组。结果高血压Ⅱ、Ⅲ期患者vWF含量显著高于正常对照组(P<0.01),随着年龄增大,vWF的含量也增高,同时70岁以上年龄段中男性升高最明显。结论vWF是血管内皮受损的标志物,高血压患者存在内皮细胞受损,受损程度与年龄大小,病情正相关。     

炎症性肠病中的血小板异常

ＩＢＤ存在着血小板形态和功能的异常，血小板的促炎和促血栓作用及其功能失调所致的血栓形成，血管炎和多灶微循环梗塞在ＩＢＤ粘膜损伤中起重要作用，血小板抑制剂治疗ＩＢＤ的临床意义尚有待证实。     

炎症性肠病中的血小板异常

IBD存在着血小板形态和功能的异常,血小板的促炎和促血栓作用及其功能失调所致的血栓形成、血管炎和多灶微循环梗塞在IBD粘膜损伤中起重要作用,血小板抑制荆治疗IBD的临床意义尚有待证实。     

血清TNF-α、IL-35在炎症性肠病患者中的水平变化及其临床意义

【】目的：探讨血清肿瘤坏死因子-α(Tumour necrosis factor,TNF-α)、白细胞介素-35(Interleukin - 35,IL-35)在炎症性肠病(inflammatory bowel disease,IBD)患者中的水平变化及其临床意义。方法：选取2010年1月至2016年1月期间本院消化内科住院部IBD患者120例,其中60例克罗恩病(Crohn’s disease,CD)患者作为CD组,60例溃疡性结肠炎(ulcerative colitis,UC)患者作为UC组,同期选取健康体检中心的60例健康志愿者作为对照组,采用双抗夹心酶联免疫吸附试验(Double sandwich enzyme-linked immunosorbent assay,DSA-ELISA)检测血清TNF-α、IL-35水平。结果：CD组与UC组患者血清TNF-α水平明显高于对照组,血清IL-35水平明显低于对照组,P<0.05。随着CD、UC患者病情活动度增加,血清TNF-α水平逐渐增加,血清IL-35水平逐渐降低,不同病情活动度血清TNF-α、IL-35水平比较差异具有统计学意义(P<0.05)。经Pearson直线相关性分析显示,CD组患者血清TNF-α水平与血清IL-35水平呈负相关(r=-0.412,P<0.001);UC组患者患者血清TNF-α水平与血清IL-35水平呈负相关(r=-0.423, P<0.001)。结论：炎症性肠病患者血清TNF-α水平明显升高,血清IL-35水平明显降低,且改变幅度与病情活动度具有紧密的关系。     

血小板激活因子与炎症性肠病

炎症性肠病（ＩＢＤ）的病因及发病机制目前还不清楚，触发和维持结肠粘膜炎症的生化因素有待探讨。诸多研究结果表明，脂类介质是ＩＢＤ的重要参与者，对其生化通路进行调控可能是治疗ＩＢＤ的一种新策略。血小板激活因子（ＰＡＦ）是可由很多种类炎症细胞合成的一种磷脂...     

血小板参数、C反应蛋白对炎症性肠病患者活动性的评价

目的 探讨血小板参数、C反应蛋白(CRP)对炎症件肠病活动性的评价.方法 分析75例活动性和26例缓解期炎症性肠病患者的血小板参数、CRP的水平及其间的关系,比较临床严重程度对血小板参数及CRP的影响.结果 活动性炎症性肠病患者血小板计数(PLT)和CRP水平明显高丁缓解期患者,平均血小板体积(MPV)明显低于缓解期患者,两组筹异有显著性(P<0.05);重度炎症性肠病患者PUF和CRP水平明显高于中度炎症性肠病患者,MPV明显低于巾度炎症性肠病患者(P<0.05);中度炎症性肠病患者PLT和CRP水平高于轻度患者,MPV水平低于轻度患者(P<0.05).活动性炎症性肠病患者严重程度分别与PLT和CRP之间呈正相关(r=-0.83,P<0.05;r=0.89,P<0.05),与MPV水平呈负相关(r=-0.38,P<0.05).结论 血小板参数和CRP水平能反映活动性炎症性肠病患者的临床严重程度.     

系统性红斑狼疮患者血管内皮细胞损伤标志物检测及其临床意义

目的探讨血管内皮细胞损伤与系统性红斑狼疮(SLE)疾病活动、肾脏损伤的关系。方法应用酶联免疫吸附试验(ELISA)检测31例SLE患者和10例健康对照者血浆可溶性血栓调节蛋白(sTM)、血管假性血友病因子(vWF)水平。结果SLE组血浆sTM、vWF水平明显高于对照组;SLE组血浆sTM、vWF水平均与疾病活动指数(SLEDAI)呈显著正相关,与24小时尿蛋白定量呈正相关。结论血管内皮损伤可能在SLE发病机制中起重要作用,血浆sTM、vWF水平可作为判断SLE疾病活动性及肾脏损伤程度的指标。     

The role of platelet von Willebrand factor in platelet adhesion and thrombus formation: a study of 34 patients with various subtypes of type I von Willebrand disease

Summary In order to investigate the respective role of plasma and platelet von Willebrand factor (vWF) in mediating platelet adhesion and thrombus formation, we performed ex vivo perfusion studies with native blood from patients with various subtypes of type I von Willebrand disease (vWD). We studied 34 patients with type I vWD (19 'platelet normal', five 'platelet low', two 'platelet discordant', eight 'Vicenza'). Parallel studies were carried out on nine patients with severe vWD (type III). At high shear rate (2600 s^-1) we found that the defect in platelet-vessel wall interactions in patients having a normal platelet vWF content ('platelet normal' and 'Vicenza') involved thrombus formation, whereas platelet adhesion was normal. At this high shear rate, platelet adhesion and thrombus volume were significantly decreased in patients with subtypes 'platelet low' and 'platelet discordant', i.e. when platelet vWF is either low or dysfunctional. These results indicate that platelet vWF may substitute for plasma vWF to promote platelet adhesion. emphasizing the important role of platelet vWF. They also confirm the role of vWF in thrombus formation at high shear rate because an abnormal thrombus volume was observed in all patients. even when platelet adhesion was normal.     

Shear-induced platelet aggregation increases in patients with proximal and severe coronary artery stenosis

BACKGROUND: Shear stress generated in stenosed arteries promotes platelet thrombi formation at the stenosed sites by accelerating the binding of von Willebrand factor (vWF) to platelets. Shear-induced platelet aggregation (SIPA) has been studied in acute coronary syndromes, but not in chronic coronary disease. HYPOTHESIS: We investigated the effect of both the site and severity of coronary stenosis on SIPA in patients with chronic coronary artery disease. METHODS: Shear-induced platelet aggregation was measured using platelet-rich plasma in 49 patients (41 men and 8 women; mean age 61+/-10 years) with coronary artery disease to evaluate the association between the extent of SIPA and coronary angiographic findings. Stenoses > 75% were considered severe. In all, 62 healthy individuals (54 men and 18 women; mean age 45+/-7 years) served as controls. The correlation between SIPA and the site and severity of the coronary lesion, and parameters of coagulation and fibrinolysis were evaluated. RESULTS: Shear-induced platelet aggregation was increased in the stenosis group (69.0+/-10.6%) compared with the controls (57.7+/-10.3%, p < 0.0001). Patients with severe stenosis in the proximal segments had significantly increased SIPA (p< 0.0001) and vWF larger multimer concentration (p<0.0001) compared with the control group. A significant correlation existed between SIPA and the vWF larger multimer concentration in all subjects studied (r = 0.422, p < 0.0001). CONCLUSIONS: Shear-induced platelet aggregation is increased in patients with severe stenosis of the proximal coronary arteries and correlates with plasma concentrations of vWF larger multimers, suggesting that severe stenosis in the proximal segments is not only associated with an increased risk of significant myocardial ischemia, but may also generate high shear stress in the stenosed artery and increase plasma vWF larger multimers, thereby promoting the formation of platelet thrombi.     

Autosomal dominant C1149R von Willebrand disease: phenotypic findings and their implications

Background

Mutation C1149R in the von Willebrand factor (VWF) gene has been thought to cause autosomal dominant severe type 1 von Willebrand disease (VWD).

Design and Methods

Eight patients from three unrelated families with this mutation were included in the present study who had distinct VWF abnormalities, not described in earlier studies.

Results

The patients showed notably low levels of VWF antigen (VWF:Ag), VWF ristocetin cofactor activity (VWF:RCo), VWF collagen binding (VWF:CB), and a reduced ristocetin-induced platelet aggregation (RIPA). VWF:RCo/VWF:Ag and VWF:CB/VWF:Ag ratios were lower than 0.7. At basal conditions, all the VWF multimers were decreased in plasma, with a clearly lower relative proportion of the high molecular weight VWF multimers (HMWM). In high-resolution agarose gels, a large decrease in the relative proportions of the satellite bands was seen. The patients had a brief good response to desmopressin (DDAVP) administration, but the released VWF half-life was shorter than normal, indicating an accelerated clearance of their VWF. Platelet VWF was abnormal.

Conclusions

We conclude from the results obtained in these patients for plasma phenotypic data that this mutation should be classified as a VWD type 2A (IIE). DDAVP therapy may be somewhat helpful for this mutation, at least for mild to moderate bleeding. These data provide evidence that for VWD classification factors other than basal VWF, such as DDAVP response and platelet VWF, should be considered.     

Spontaneous platelet aggregation in type IIB Tampa von Willebrand disease is inhibited by the 52/48-kDa fragment of normal von Willebrand factor, which contains the GPIb binding domain

The association of Type IIB von Willebrand disease (vWD) with chronic persistent thrombocytopenia and spontaneous platelet aggregation has recently been recognized. It has been shown that IIB von Willebrand factor (vWF) can initiate platelet aggregation by binding to the platelet glycoprotein (GP) lb receptor and inducing exposure of the GpIIb/IIIa fibrinogen receptor. In this study we demonstrate the increased binding of Type IIB Tampa vWF with normal platelets when compared with nonthrombocytopenic Type IIB vWF. Studies further demonstrate that spontaneous platelet aggregation initiated by IIB Tampa vWF can be blocked by a 52/48-kDa fragment of normal vWF, which contains the binding domain.     

脑梗死患者血浆血管性血友病因子等三种因子的测定及其临床意义

目的探讨脑梗死患者血浆血管性血友病因子(vWF)、血管内皮生长因子(VEGF)和基质金属蛋白酶-9(MMP-9)在脑梗死发生、发展过程中的临床意义。方法将30例脑梗死患者按梗死体积大小分为大梗死组、中梗死组、小梗死组,每组各10例。发病后第1、3、7、15天用酶联免疫吸附试验(ELISA)双抗体夹心法检测脑梗死患者和对照组20名体格检查健康的血浆vWF、VEGF、MMP-9的浓度。结果脑梗死组vWF、VEGF、MMP-9分别为:(216±62)μg/L、(584±151)ng/L和(287±147)μg/L,显著高于对照组(96±12)μg/L、(111±17)ng/L和(102±14)μg/L,P<0.01。而且在脑梗死早期同一时间点与脑梗死体积呈正相关(r分别为0.496、0.519和0.472,P<0.01)。结论血浆vWF、VEGF、MMP-9浓度与脑梗死体积相关。     

The platelet indices in patients with rheumatoid arthritis: Mean platelet volume reflects disease activity

The present study was designed to investigate the interaction between platelet indices, inflammatory markers and disease activity in rheumatoid arthritis (RA) subjects. The effects of anti-TNF-α therapy and conventional treatment on platelet indices were also compared. We studied 97 patients with RA (19 men, 78 women: mean age 51 years) and 33 age and sex-matched healthy subjects as a control group. All RA patients were administered conventional therapy. After 3 months of therapy, 35 subjects who had high disease activity score (DAS28 > 5.1) were grouped as non-responders and were administered infliximab as a TNF-α blocker at the standard intravenous dose. Responders to the conventional therapy and non-responders were also compared. At baseline white blood cell (WBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelet count and mean platelet volume (MPV) were significantly higher in patients with RA. Mean platelet volume was positively correlated with DAS28 score (r = 0.27; p = 0.007). These markers of inflammation and platelet indices were substantially decreased after therapy. The reductions were similar in responders to conventional therapy and non-responders (TNF alpha group). In conclusion, we found that MPV was correlated with inflammatory markers and disease activity in patients with RA. Both anti-TNF-alpha and conventional therapy decreases markers of inflammation and platelet indices. MPV can reflect both disease activity and response to treatment.     

Platelet and mean platelet volume kinetics in adult patients with sepsis

Abstract

The aims of this study were to evaluate the kinetics of platelet counts and mean platelet volume (MPV) in adults with sepsis and to determine whether the responses are infection-specific. This retrospective cohort study included patients admitted to a tertiary-care teaching hospital with microbiologically proven nosocomial sepsis between January 2006 and January 2011. Platelet counts and MPV measurements were examined daily for 5 days after the onset of sepsis. During the study period, 151 of the 214 sepsis episodes were associated with thrombocytopenia. Gram-positive microorganisms were the most frequently isolated. The decrease in platelet counts was statistically significant for the first 3 days of sepsis in Gram-positive septic patients, for 4 days in Gram-negative septic patients and for all 5 days in fungal septic patients (p?<?0.001). The increase in MPV values was statistically significant for the first 3 days of sepsis in Gram-positive septic patients and for all 5 days in the other groups (p?<?0.001). We conclude that fungal sepsis has a stronger association with thrombocytopenia and increased MPV.     

Studies of multimerin in patients with von Willebrand disease and platelet von Willebrand factor deficiency

In normal platelet α-granules von Willebrand factor (VWF) is stored with multimerin and factor V in an eccentric electron-lucent zone. Because the platelet stores of VWF are deficient in 'platelet low' type 1 and type 3 von Willebrand disease (VWD), we investigated their electron-lucent zone proteins. The patients with VWD had partial to complete deficiencies of plasma and platelet VWF but normal α-granular multimerin and factor V, and normal α-granular fibrinogen, thrombospondin-1, fibronectin, osteonectin and P-selectin. In type 3 VWD platelets, α-granular electron-lucent zones lacking VWF-associated tubules were identified and multimerin was found in its normal α-granular location. These findings indicate that the formation of the electron-lucent zone and the sorting of multimerin to this region occur independent of VWF. The isolated abnormalities in VWF suggests a VWF gene mutation is the cause of 'platelet low' type 1 VWD.