特发性血小板减少性紫癜患者血小板相关抗体水平与预后的关系

目的:探讨特发性血小板减少性紫癜(ITP)与血小板相关抗体之间的相互关系,为临床诊断和治疗提供帮助。方法:回顾性分析了2000年1月～2007年4月应用流式细胞术检测140例临床确诊的ITP患者初诊时及治疗前后不同血小板相关抗体——血小板膜糖蛋白抗体(PAIg)的表达。结果:ITP患者初诊时PAIgG、PAIgA及PAIgM抗体表达水平均高于正常对照组;PAIgG、PAIgM、PAIgA表达水平与血小板数之间均呈负相关,相关系数分别为γ=-0.72、γ=-0.83和γ=-0.67。在确诊ITP后予激素等免疫治疗无效转变为慢性ITP的患者时,PAIgM抗体水平要明显高于激素治疗有效的急性ITP患者,并且PAIgM异常增高或联合PAIgG增高的比例要显著多于急性ITP患者(均P<0.05)。35例PAIgG和PAIgM同时升高的ITP患者,经治疗血小板升至正常后,PAIgG、PAIgM抗体表达水平均有显著下降。结论:ITP的发生与血小板抗体密切相关,初诊ITP患者PAIgM单独或联合PAIgG异常增高常提示预后不良,易转变为慢性ITP。     

特发性血小板减少性紫癜患者血小板相关抗体及网织血小板检测的临床意义

目的探讨血小板相关抗体(PAIgG)和网织血小板(RP)检测在特发性血小板减少性紫癜(ITP)治疗中的临床意义。方法收集常州市第一人民医院2003-06～2004-10住院的ITP患者48例,根据疗效分为两组,其中临床有效组40例,临床无效组8例,以50例健康人为正常对照。应用流式细胞仪(FCM)测定其治疗前后血浆和(或)血清PAIgG及RP%,并常规血小板计数。结果ITP患者临床有效组治疗后较治疗前血小板计数明显升高、PAIgG和RP%显著降低(P<0.01)。临床无效组治疗前后血小板计数、PAIgG和RP均无明显变化(P>0.05)。两组治疗前3项指标与对照组比较差异有显著性意义(P<0.01)。结论PAIgG和RP动态检测将是ITP患者血小板治疗效果的预测指标之一。     

血浆置换与血小板洗涤对ITP患者血小板及相关抗体影响的研究

目的：探讨血浆置换（PE）和血小板洗涤（PW）对特发性血小板减少性紫癜（ITP）患者体内血小板相关抗体（PAIg）水平及血小板计数（BPC）变化的影响。方法：对各组测定PAIg和BPC的变化并作统计学处理比较。结果：PE加PW治疗组PAIg含量的递减速度均明显快于普通治疗组（P〈0．01）,普通治疗组BPC的回升速度明显慢于PE加PW组（P〈0．01）。结论：血浆置换及血小板洗涤治疗ITP可迅速降低患者体内PAIg水平、促进体内BPC的回升;BPC的回升与PAIg水平的递减呈负相关,动态监测PAIg和BPC的变化有助于及时评估患者病情转归情况和指导临床治疗方案。     

特发性血小板减少性紫癜无效输注原因分析

目的:探讨特发性血小板减少性紫癜(ITP)患者血小板无效输注的原因.方法:90例确诊的ITP患者中对输注血小板的48例计算血小板计数增高指数(CCI),评价输注的效果并分析与感染、脾脏肿大、血小板抗体、骨髓巨核细胞数和免疫指标等因素的关系.结果:18例应用血小板和激素治疗的患者,44.4%有效输注,30例应用血小板、激素和丙种球蛋白患者,53.3%有效输注.24例无效输注患者中在感染组与非感染组、脾脏肿大组与正常组、血小板相关抗体升高组与正常组,有效输注率有显著性差异.骨髓巨核细胞数升高组与正常组、调节性T细胞低表达组与正常组,有效输注率差异无统计学意义.结论:ITP患者输注血小板50%存在无效输注,其原因可能与感染、脾脏肿大、血小板相关抗体有关.因此控制感染和抑制免疫应作为首选治疗,而血小板的输注应严格把握指征.     

流式细胞术研究特发性血小板减少性紫癜患者血小板相关抗体

目的：探讨特发性血小板减少性紫癜（ITP）患者血小板表面相关抗体（PAIg）在诊断及预后的价值。方法：应用流式细胞术（FCM）检测84例ITP患者及20例正常人PAIgG、PAIgM、PAIgA。结果：初发ITP和复发ITP患者组与正常对照组比较，PAIgG、PAIgA差异有统计学意义（P〈0．01），PAIgM差异无统计学意义（P〉0．05）。PAIgM与PAIgA之间有显著相关性，r=0．451（P〈0．01）。结论：①PAIg增高可作为诊断初发ITP的重要指标之一；②FCM检测ITP患者血小板表面PAIg敏感性好、特异性高，适用于临床，对ITP的诊断及预后评价有较好的实用价值；③初发型ITP患者以PAIgG和PAIgA增高为主，预后较好；复发型以PAIgM增高为主，预后较差，易复发。     

慢性特发性血小板减少性紫癜患者PAIgG、ACAIgG的测定及意义

应用ELISA法对 41例慢性特发性血小板减少性紫癜 (ITP)患者和 2 5例健康对照者进行血浆和 (或 )血清血小板相关抗体 (PAIgG)、抗心磷脂抗体 (ACAIgG)测定 ,并常规血小板计数。发现ITP患者治疗有效组治疗后血小板计数明显升高、PAIgG含量显著降低 ,治疗前较治疗后及对照组均有显著性差异 (P <0 .0 1 ) ,且血小板计数与PAIgG之间呈显著性负相关 (r =- 0 .738,P <0 .0 0 1 )。而治疗无效组血小板计数、PAIgG均无明显变化。ACAIgG治疗前后无明显变化 ,且未发现与血小板及PAIgG相关。PAIgG、ACAIgG含量增高提示ITP患者针对血小板磷脂及其他糖类蛋白等不同抗原产生了自身免疫反应 ,为免疫抑制剂的应用提供了理论依据     

血液光量子疗法对急性白血病患者血小板输注效果的影响

目的　探讨血液光量子疗法对急性白血病患者血小板输注效果的影响。方法　将 5 4例血小板减少的急性白血病患者随机分为两组 ,治疗组采用血液光量子疗法行血小板输注 ,对照组单纯行血小板输注。两组均采用酶联免疫吸附法 ,在血小板输注前后定量测定血小板表面相关抗体 (PAIg G和 PAIg M) ;计数血小板 ,计算1、2 4小时血小板增值 (CCI) ;观察其临床效果和非溶血性输血反应 (NHFTR)。结果　血小板输注前两组 PAIg M及 PAIg G值无显著性差异 ,输注后两组 PAIg M无显著性差异 ,而治疗组 PAIg G值明显低于对照组 (P<0 .0 5 )。两组 1小时 CCI无显著性差异 ,治疗组 2 4小时 CCI和临床效果明显优于对照组 (P<0 .0 5 ) ;治疗组的 NHFTR低于对照组 (P<0 .0 5 ) ,其临床效果优于对照组 (P<0 .0 5 )。结论　血液光量子疗法可减少血小板输注无效     

122例特发性血小板减少性紫癜血小板输注疗效观察

目的:探讨特发性血小板减少性紫癜(ITP)患者临床血小板输注的指征.方法:比较122例ITP患者输注血小板和未输注血小板的临床转归;比较血小板输注前及输注24 h后血小板计数.参照PAIg,分析抗体与血小板输注疗效的相关性.结果:67例未输注血小板的患者中,有2例PLT＜10×109/L的患者发生严重出血危及生命,55例输注血小板的惠者,有17例(31%)PLT较输注前降低,其中7例输注后PLT＜10×109/L,未发生严重出血;ITP患者血小板输注无效率86%,PAIg升高患者血小板输注无效率升高,有统计学差异.结论:如无明显的出血症状,ITP血小板输注指征建议PLT＜10×109/L,应输注少白细胞同型单采血小板制荆.     

ITP患者血清血小板生成素水平与临床治疗效果的关系

目的 探讨血小板生成素（TPO）对特发性血小板减少性紫癜（ITP）临床治疗效果的影响。方法 将25例初治ITP患者按治疗效果分为有效组和无效组,另设正常对照组22例。采用ELISA法和放免法分别检测治疗前后血清TPO水平,取治疗前骨髓涂片计数巨核细胞数量。结果 无效组TPO水平明显高于有效者及对照组（P均〈0．05）,有效者与对照组间无显著性差异;无效者巨核细胞计数则显著低于有效者（P〈0．01）。结论 血清高水平TPO可能预示ITP治疗困难;TPO治疗有效与无效者的发病机理可能存在差异。     

环孢菌素Ａ治难性特发性血小板养活性紫癜的疗效

特发性血小板减少性紫癜 ( ITP)是常见的出血性疾病 ,传统的治疗方法能使大多数患者缓解 ,经治疗无效的即所谓“难治性 ITP”。有文献报告用环孢菌素 ( Cs A)治疗难治性 ITP取得良好效果〔1〕。我院自 1 990年以来采用 Cs A治疗难治性 ITP 1 5例 ,并随访 1年 ,现将疗效报告如下。1　资料与方法1 .1　临床资料1 5例均为住院患者 ,男 4例 ,女 1 1例 ,年龄 1 7～ 47岁 ,平均 31 .5岁。其诊断均符合 1 986年 1 2月首届全国血栓与止血学术会议所制定的诊断标1山东东营市人民医院血液科 (山东东营 ,2 5 70 91)2山东东营市东营区机关门诊部…     

特发性血小板减少性紫癜患者外周血淋巴细胞亚群和血小板相关抗体变化及临床意义

用流式细胞术直接免疫法检测l72例早期特发性血小板减少性紫癜(ITP)患者外周血淋巴细胞亚群(CD3、CD4、CD8、CD19、C16、CD56)，ELISA法检测血小板表面血小板相关抗体(PAIgG、PAIgA、PAIgM)。结果显示，ITP组与正常对照组比较CD3、CD4／CD8显著降低(P＜0.01)，CD8增高(P＜0．05)，CD19增高极为显著(P＜0．01)；ITP血小板表面PAIgG、PAIgA、PAIgM显著高于对照组；CD19升高和CD4/CD8下降与PAIgG、PAIgA、PAIgM增高有显著的相关性。认为淋巴细胞亚群功能和比例失常、T细胞免疫调节机制紊乱在ITP的发病机制中起非常重要的作用。     

Study of platelet-associated immunoglobulins of IgG,IgM, IgA,and IgE classes and platelet kinetics in 33 patients with idiopathic thrombocytopenic purpura

Summary The role of platelet-associated immunoglobulins (PAIg) of four different immunoglobulin classes -IgM, IgG, IgA, and IgE- and their relation to platelet count and platelet kinetics was studied in 33 patients with idiopathic thrombocytopenic purpura (ITP). During the course of 1 year, repeated determinations of PAIg were made. The results indicate that PAIgG, PAIgM, and PAIgA are present in all ITP patients, and that autoantibodies of all three Ig classes show highly significant correlations to the platelet counts (p< 0.0001). Double logarithmic negative correlations have been found between PAIgG and platelet count (r=–0.71), PAIgM and platelet count (r=–0.84), and PAIgA and platelet count (r=–0.79). Statistical analyses using partial correlation and multiple regression methods showed that PAIgM is predominantly related to the platelet count, whereas PAIgG and PAIgA are only of secondary importance. Accordingly, a relation of PAIgM (and PAIgA) to increased liver destruction of platelets was found in kinetic studies using¹¹¹indium-labeled platelets. Taken together, these results suggest a predominant role of PAIgM in the pathogenesis of ITP.     

Platelet-associated immunoglobulins IgG, IgM, IgA and complement C3 in immune and nonimmune thrombocytopenic disorders

A two-stage radioactive antiglobulin test--using unlabelled antisera specific for IgG, IgA, IgM and C3 followed by binding of 125I-staphylococcal protein A--was applied to determine platelet-associated immunoglobulins (PAIg) and complement (PAC3) in thrombocytopenias of various etiologies. One hundred and one patients with immune thrombocytopenia (chronic autoimmune, 48; acute autoimmune, 37; Evans syndrome, nine; connective tissue diseases, seven) and 20 patients with presumed nonimmune thrombocytopenia (bone marrow aplasia or malignancy, six; septicemia, five; hypersplenism, five; cirrhosis of liver, three; others, one) were studied. Increased levels of PAIg/C3 were found in 76% of patients with immune thrombocytopenia. PAIgG was raised in 66%, PAIgM in 57%, PAIgA in 44%, and PAC3 in 29%. Isolated elevation of PAIgG and of PAIgM was found in four and three cases, respectively; PAIgA and PAC3 were elevated in one case each. PAIgG was associated with PAIgM in 56%, with PAIgA in 34%, and with PAC3 in 27%. Both patients with Evans' syndrome and patients with connective tissue diseases had significantly higher PAIgM levels than the other patients with immune thrombocytopenia. In patients with nonimmune thrombocytopenia, increased rates of PAIg/C3 were also encountered. Positive test results were found in 88% (PAIgG 88%, PAIgM 47%, PAIgA 35%, and PAC3 24%). In immune-mediated thrombocytopenia, we observed a significant inverse correlation between platelet counts and PAIgG, PAIgA, and PAC3, but not with PAIgM. In contrast, no such correlation was found in patients with nonimmune thrombocytopenia. Our data indicate that the evaluation of neither parameter alone nor the combination of PAIg/C3 will discriminate between immune and nonimmune thrombocytopenia. Preferential coating with certain immunoglobulins, however, may be present in some subgroups of immune thrombocytopenias.     

Platelet-associated immunoglobulins IgG, IgM, IgA and complement C3c in chronic idiopathic autoimmune thrombocytopenia: relation to the sequestration pattern of 111indium labelled platelets

Levels of platelet-associated immunoglobulins (PAIg) IgG, IgM, IgA and complement C3c were related to parameters of 111Indium-labelled platelet kinetics in 17 patients with chronic idiopathic autoimmune thrombocytopenia (cAITP). Elevated levels of PAIg/C3c were found in 14 patients (82%) (PAIgG n = 13, PAIgM n = 11, PAIgA n = 1, PAC3c n = 5). Only PAIgG correlated with platelet counts (RS = -0.71, p less than 0.01). Mean platelet life span (MLS) was shortened in all patients (median 12.0 h, range 0.3-45.6 h) and correlated with the platelet counts (RS = 0.49, p less than 0.05). MLS was correlated with PAIgG (RS = -0.52, p less than 0.05), but not with PAIgM, PAIgA, or PAC3c. The site of sequestration was splenic in 10 patients and splenic-hepatic in 7 patients. Although no significant correlation between either site of platelet sequestration and any of the investigated PAIg/C3c was demonstrable, platelets coated with higher PAIgG levels were more readily sequestrated in the spleen, while elevations of PAC3c were found in 4 out of 7 patients with hepatic involvement.     

Pattern of platelet-associated immunoglobulin (classes and IgG subclasses) in childhood immune thrombocytopenic purpura

Platelet-associated Ig classes and IgG subclasses were studied by a semiquantitative platelet ELISA test in 17 children with immune thrombocytopenic purpura (ITP). An elevation of PAIg was found in 94% of the children. In nearly all cases increased amounts of PAIgG of subclass G1 was seen, and in half of the cases increased amounts of PAIgM were also seen. No statistical difference in the composition of PAIg classes and PAIgG subclasses in acute and in chronic ITP was found. However, a correlation of increased amount of PAIgG3 and very low platelet count (20 x 10(9)/l) was observed.     

病毒性肝炎血小板减少症影响因素的研究

目的探讨病毒性肝炎血小板减少症的发病机制.方法 84例病毒性肝炎患者和20名健康志愿者分为3组,A组(48例病毒性肝炎并血小板减少症患者)、B组(36例病毒性肝炎血小板正常患者)和C组(20名健康志愿者),分别采用酶联免疫吸附法、流式细胞术、腹部彩色B超检测3组血清血小板生成素(TPO)水平、血小板相关免疫球蛋白(PAIg)及其类别PAIgG、PAIgA、PAIgM水平、脾脏大小,采用骨髓穿刺术对其中74例行骨髓细胞学检查.结果血清TPO水平A组低于C组(P<0.01)和B组(P<0.05),严重肝病血清TPO水平与血小板数相关(r=0.374,P<00.01).PAIg、PAIgG水平A组明显高于B组(P<0.001)和C组(P<0.01),血小板数与PAIg水平呈负相关(r=0.446,P<0.01),血小板数与PAIgG水平亦呈负相关(r=-0.462,P<0.01).脾脏肿大发生率A组(77.1%)明显高于B组(47.2%,P<0.01),C组无脾脏肿大发生,血小板数与脾脏大小呈负相关(r=-0.5 81,P<0.01).74例骨髓象显示A组有4例呈骨髓抑制象改变,B组和C组无一例有上述改变.结论严重肝功能受损时血清TPO水平下降,与血小板数减少直接相关.PAIg介导的自身免疫机制在病毒性肝炎血小板减少症中可能起重要作用.脾脏肿大是引起病毒性肝炎血小板减少的因素.初步发现慢性肝病有骨髓抑制现象,可能成为引起病毒性肝炎血小板减少的因素之一.     

Platelet-associated immunoglobulins in patients with primary Sj?gren's syndrome

Ten patients with primary Sj?gren's syndrome (7 females) were examined in order to evaluate whether in vivo-bound platelet-associated immunoglobulins (PAIg) and/or in vitro binding of circulating Ig to normal platelets influences platelet function. With an ELISA technique it was found that 9/10 patients had increased amounts of in vivo PAIgG, 4/10 patients of in vivo PAIgA and 5/10 patients of in vivo PAIgM. There was no correlation between patients platelet aggregability and the presence of in vivo PAIg. Incubation of platelets from a healthy person with plasma from the 10 patients caused in vitro binding of IgG in 7/10 cases, of IgA in 0/10 cases and of IgM in 1/10 cases. Adenosine diphosphate (ADP)-induced aggregability of the normal platelets was impaired in 7/10 incubation experiments (no correlation to in vitro PAIg) and unchanged in 3/10 cases. Epinephrine- and collagen-induced platelet aggregability was unchanged in all cases. It is concluded that increased amounts of in vivo and in vitro PAIg seem to occur frequently in patients with primary Sj?gren's syndrome, but do not influence platelet aggregability.     

Flow cytometry detection of platelets autoantibodies in children with idiopathic thrombocytopenic purpura

Abstract  

Immune thrombocytopenic purpura is an acquired disorder, in which accelerated platelet consumption is due to platelet autoantibodies. The aim of this study was to investigate the clinical value of platelet autoantibodies assay in children with ITP and to evaluate flow cytometry in the detection of platelet autoantibodies in comparison with monoclonal antibody specific immobilization of platelet antigen (MAIPA) assay. We measured platelet autoantibodies by flow cytometry and MAIPA in 18 children with ITP (6 acute, 7 chronic and 5 in remission), in addition to 5 healthy children with matched age and sex as a control group. Significant elevation of platelet-associated immunoglobulin G (PAIgG), PAIgM and PAIgA was demonstrated in children with acute ITP compared to controls and children with chronic ITP (P < 0.05). There was significant elevation of PAIgG and PAIgM in children with acute ITP compared to children with ITP in remission (P < 0.05). There was significant negative correlation between platelet count and PAIgG levels in ITP children (r = −0.717; P = 0.001). Flow cytometry found PAIgG in 94.4% of ITP children. MAIPA has detected platelet specific IgG autoantibodies in 83.3% of ITP children. ROC analysis revealed sensitivity of 94%, specificity of 57% with overall accuracy of 83% for detection of PAIgG by flow cytometry compared to MAIPA.     

Platelet-associated IgM elevated in patients with chronic hepatitis C contains no anti-platelet autoantibodies

Abstract: We investigated whether thrombocytopenia in patients with chronic hepatitis C is due to anti-platelet autoantibodies. Platelet-associated IgG (PAIgG) and platelet-associated IgM (PAIgM) were measured by direct immunofluorescent flow cytometric analysis. Elevation of PAIgM level was detected in 70% of chronic hepatitis C patients, while only a mild elevation of PAIgG level was detected in 32% of the cases. The elevation of PAIgM values in these patients was comparable to that in patients with chronic immune thrombocytopenic purpura (ITP). However, elevated PAIgM was also found in both patients with and without thrombocytopenia, and no correlation was found between PAIgM and platelet count. Eluted PAIgM did not react with normal platelets in all cases with a positive PAIgM value, indicating that eluted PAIgM contained no detectable anti-platelet antibodies. During alpha-interferon therapy, the level of PAIgM increased in association with the decrease in platelet counts in 75% of the cases; however, eluted PAIgM at any day point never reacted with platelets from normal donors. PAIgM was elevated in patients with chronic hepatitis C, but contained no detectable anti-platelet autoantibodies. Thrombocytopenia in these patients is not due to anti-platelet autoantibodies.     

Antiplatelet antibodies and their correlation with clinical findings in childhood immune thrombocytopenic purpura

The demonstration of antiplatelet antibodies (PAIgG, PAIgM) and decreased detection of platelet surface antigens (CD41, CD61, CD42b) in children with immune thrombocytopenic purpura (ITP) have a diagnostic role. This study was conducted to determine whether these parameters differed in acute and chronic ITP. Chronic ITP was defined as thrombocytopenia persisting for more than 6 months from the onset of illness. A total of 80 subjects were divided into three groups: group 1 included 39 patients with acute ITP; group 2 included 31 patients with chronic ITP, and group 3 included 10 healthy children. At diagnosis, blood samples were obtained for platelet count, mean platelet volume, plateletcrit and platelet distribution width along with platelet surface antigens and antiplatelet immunoglobulins. We found that platelet surface antigens were significantly decreased in both acute and chronic ITP when compared to the control group (p = 0.001). In contrast, PAIgG was increased in acute and chronic ITP patients compared to the control group. PAIgM was significantly higher in acute ITP. We conclude that decreased platelet surface antigens and increased antiplatelet antibodies are observed in both acute and chronic ITP. In patients with chronic progress, a relatively lower level of PAIgM can be identified.