细胞免疫及体液免疫在ITP发生发展中的作用及其机制探讨

目的用ELISA法检测60例特发性血小板减少性紫癜(ITP)患者(观察组)血小板相关抗体PAIgG、PAIgA、PAIgM,免疫比浊法(ITM)测定补体C3、C4,流式细胞仪直接免疫法检测外周血淋巴细胞亚群(CD3、CD4、CD8、CD 16 CD56)水平,并与30例健康人(对照组)比较。结果与对照组比较,观察组血小板相关抗体PAIgG、PAIgA、PAIgM均显著升高,补体C3显著降低,C4无明显变化;外周血淋巴细胞亚群CD3显著降低,CD8增高,CD4/CD8下降,CD16 CD56降低。证实T细胞免疫调节机制紊乱、淋巴细胞功能和比例失调在ITP的发生中起非常重要的作用。     

特发性血小板减少性紫癜患者血小板抗体等四项参数测定的价值

目的　探讨特发性血小板减少性紫癜 (ITP)患者血小板抗体 (PAIgG)、血小板膜蛋白(CD62P)、网织血小板 (RP)及淋巴细胞亚群变化及意义。方法　应用流式细胞术检测 5 8例ITP组及 2 0例正常对照组外周PAIgG、血CD62P、RP、淋巴细胞亚群的表达。结果　ITP组的血小板数明显低于正常对照组 (P <0 .0 1) ,PAIgG、CD62P、RP均明显高于正常对照组 (P <0 .0 1)。在淋巴细胞亚群中 ,ITP组CD3、CD4、CD4/CD8比值明显低于正常对照组 (P <0 .0 1) ,CD8、CD19细胞则显著高于正常对照组 ,而CD16+ 5 6与正常对照组无明显差异。结论　PAIgG、CD62P、RP及淋巴细胞亚群的变化可较好地反映ITP这一病理过程 ,对提高诊断水平及指导临床有一定实用价值。     

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。     

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。     

CD28/CTLA-4:B7在特发性血小板减少性紫癜患者外周血淋巴细胞中的表达及意义

目的:探讨特发性血小板减少性紫癜(ITP)患者外周血淋巴细胞CD28、CTLA-4(CD152)、B7-1(CD80)及B7-2(CD86)的表达及意义。方法:采用免疫荧光标记和流式细胞术检测41例ITP患者和40例健康对照者外周血CD3+CD28+细胞、CD3+CD152+细胞、CD80+CD19+细胞和CD86+CD19+细胞分别占淋巴细胞的比例及血小板表面相关抗体水平,进行2组对比、分析。结果:与正常对照组相比,急性ITP患者外周血CD3+CD28+细胞和CD3+CD152+细胞差异无统计学意义(P0.05),CD80+CD19+细胞增多(P0.05),CD86+CD19+细胞显著增多(P0.01),慢性ITP患者CD86+CD19+细胞增多(P0.05);急性ITP患者外周血CD86+CD19+细胞较慢性ITP患者增多(P0.05);与正常对照组相比,急性ITP患者PAIg's、PAIgG和PAIgM水平显著增高,慢性ITP患者PAIgG水平增高;CD80、CD86表达与PAIgG水平之间存在显著的相关性(均P0.01)。结论:ITP患者外周血B淋巴细胞上CD86和CD80表达均异常,可能与其发病相关。     

ITP血小板特异性抗体和T淋巴细胞亚群及NK细胞变化的意义探讨

目的：检测特发性血小板减少性紫癜（ITP）患者抗血小板膜糖蛋白（GPⅡb／Ⅲa、GPⅠb／Ⅸ）特异性抗体表达、T淋巴细胞亚群及NK细胞的变化,探讨相关因素在ITP发病机制中的作用。方法：应用改良血小板抗原单克隆抗体固相化检测技术（MAIPA）、流式细胞术分别检测52例ITP和24例正常对照组抗血小板膜糖蛋白（GPⅡb／Ⅲa、GPⅠb／Ⅸ）特异性抗体表达、T淋巴细胞亚群及NK细胞变化。结果：ITP组的血小板计数明显低于正常对照组（P〈0．05）;抗GPⅡb／Ⅲa及GPⅠb／Ⅸ抗体A值均高于正常对照组（P〈0．05）;相关分析表明ITP组血小板计数与两种特异性抗体水平均呈负相关关系;在T淋巴细胞亚群变化中,ITP组CD3^＋T淋巴细胞百分比、CD4^＋T淋巴细胞百分比及CD4^＋／CD8^＋的比值均明显低于正常对照组（P〈0．05）,CD8^＋T淋巴细胞百分比则显著高于正常对照组（P〈0．05）;NK细胞百分比明显低于正常对照组（P〈0．05）。结论：血小板特异性抗体及T淋巴细胞亚群的变化可较好地反映ITP这一病理过程,对提高诊断水平及指导临床有一定的实用价值。     

淋巴细胞亚群在成人特发性血小板减少性紫癜中的变化及临床意义

目的:探讨淋巴细胞亚群与成人特发性血小板减少性紫癜(ITP)的关系及临床意义。方法:采集52例成年ITP患者和21例正常对照者外周血标本,分离单个核细胞后,应用流式细胞术检测淋巴细胞亚群,并将ITP患者与对照组比较。结果:ITP组较对照组CD3、CD4降低,CD8升高,CD4/CD8降低,CD19升高,CD16+56降低,2组间差异有统计学意义(P<0.05或P<0.01)。结论:ITP的发病机制与细胞免疫和体液免疫均密切相关,纠正患者免疫紊乱有益于ITP的治疗,外周血淋巴细胞亚群变化对ITP的疗效评价及预后判断也有一定价值。     

特发性血小板减少性紫癜患者免疫相关指标的检测及其临床意义

目的 检测特发性血小板减少性紫癜(ITP)患者免疫相关指标的变化,探讨其在ITP发病机制中的作用及其临床意义.方法 应用酶联免疫斑点技术(ELISPOT)、改良血小板抗原单克隆抗体固相化检测技术(MAIPA)、流式细胞术及夹心法ELISA分别检测64例1TP患者及31例正常对照者分泌GPⅡb/Ⅲa抗体B细胞、血小板特异性抗体(抗GPⅡb/Ⅲa抗体、抗GP I b/Ⅸ抗体)、T淋巴细胞亚群、网织血小板(RP)及血小板生成素(TPO)的变化.结果 ITP患者分泌GPⅡb/Ⅲa抗体B细胞频数[急性ITP组患者为7.6±4.6/105个外周血单个核细胞(PBMC),慢性ITP组患者为5.3±3.0/105个PBMC]、血小板特异性抗体(抗GPⅡb/Ⅲa抗体、抗GPI b/Ⅸ抗体)的吸光度值(急性ITP组患者为0.51±0.11、0.48±0.06,慢性ITP组患者为0.49±0.10、0.46±0.09)、CD8+T淋巴细胞百分比[(27.09±9.86)%]、RP百分比[巨核细胞增多组为(24.85±19.18)%,巨核细胞正常组为(23.89±18.90)%]明显高于正常对照组[1.3±0.5/105个PBMC,0.33±0.06,0.41±0.03,(22.08±4 54)%,(8.19±2.46)%,P值均＜0.05],其中急性ITP患者分泌GPⅡb/Ⅲa抗体B细胞高于慢性ITP患者(P＜0.05).ITP组CD3+T淋巴细胞百分比、CD4+T淋巴细胞百分比及CD4+/CD8+比值[(60.88±14.59)%、(28.41±10.55)%、1.18±0.59]均低于正常对照组[(69.89±6.43)%、(35.38±5.05)%、1.64±0.29,P值均＜0.05].ITP患者巨核细胞增多组TPO水平(72.09±41.64)明显低于ITP患者巨核细胞正常组(118.60±70.72,P＜0.05),与正常对照组(75.37±26.32)之间差异无统计学意义(P＞0.05).结论 分泌GPⅡb/Ⅲa抗体B细胞、血小板特异性抗体、T淋巴细胞亚群、RP%及TPO在ITP诊断及指导定向干预治疗中有一定的意义.     

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     

人微小病毒B19感染与小儿ITP的关系

采用PCR检测41例特发性血小板减少性紫瘢（ITP）患儿和22例健康儿童的血清人微小病毒B19（HPVB19）DNA，并用酶联免疫法（ELISA）检测血小板相关抗体。结果ITP组患儿血清中HPVB19DNA阳性率39．0％（16／41）显著高于对照组；ITP组中急性型HPVB19DNA阳性率50．0％（14／28）显著高于慢性型15．4％（2／13）；病毒感染阳性患儿的血小板相关抗体PAIgG、PAIgA明显高于病毒感染阴性患儿。ITP患儿血清中HPVB19DNA阳性率高，病毒感染可导致血小板相关抗体升高而致血小板减少。     

免疫抑制治疗无效的特发性血小板减少性紫癜患者血小板相关免疫球蛋白的亚型分析

目的分析糖皮质激素、环孢菌素A治疗无效的特发性血小板减少性紫癜(ITP)患者血小板相关免疫球蛋白(PAIg)的亚型。方法采用酶联免疫法(ELISA)对19992004年绵阳市中心医院收治的17例激素治疗无效、4例激素 环孢菌素A治疗无效以及30例激素治疗有效ITP患者的PAIg亚型进行检测。结果17例激素治疗无效的患者PAIg各亚型抗体较之激素治疗有效ITP患者差异有显著性(P<0·01),激素治疗无效组PAIg各亚型水平均明显增高;激素 环孢菌素A治疗无效组PAIgM较之激素治疗有效ITP患者有所增高(P<0·05)。结论激素治疗无效的ITP患者PAIg各亚型均显著增高,提示PAIg在介导ITP患者异常免疫反应过程中起重要作用,PAIg各亚型水平的增高可能有助于预测ITP患者对激素治疗的敏感性。     

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.     

ITP患儿的白细胞介素2受体及NK细胞的研究

采用双抗夹心ELISA、APAAP桥联酶标法、MTT比色法检测了34例ITP患儿的血清可溶性白介素2受体（sIL-2R）外周血单个核细胞（PBMC）经PHA刺激后膜白介素2受体（mIL－2R）的表达、T淋巴细胞亚群以及自然杀伤（NK）细胞活性。结果：ITP患儿血清sIL－2R水平升高，mIL－2R的表达和NK活性显著降低；血清sIL－2R水平与NK活性、CD4 ／CD8 比值是负相关，与疾病严重程度和疗效密切相关。提示sIL－2R可作为监测病情、观察疗效的敏感指标；在纠正ITP的免疫调节紊乱中应充分考虑到细胞因子受体异常这个环节。     

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.     

免疫性血小板减少性紫癜35例患者外周血免疫细胞亚群的检测及其临床意义

目的 探讨免疫细胞亚群的变化在免疫性血小板减少性紫癜(ITP)发病机制中的作用及其临床意义.方法 应用流式细胞术检测35例ITP患者治疗前、后及20例正常对照者免疫细胞亚群各指标的变化,包括CD3+、CD4+、CD8+、CD56+、CD19+淋巴细胞及CD4+/CD8+比值.结果 ITP患者CD3+ T淋巴细胞百分比(61.58±6.45)%、CD4+ T淋巴细胞百分比(28.38±4.89)%、CD4+/CD8+比值(0.99±0.22)较对照组[(67.85±4.68)%、(38.00±3.37)%、1.54±0.13]均减低(P值均＜0.05),治疗后3项指标[(69.41±5.03)%、(38.17±3.18)%、1.60±0.15]均升高至正常水平;CD8+ T淋巴细胞百分比(29.20±4.50)%及CD19+ B淋巴细胞百分比(17.74±4.14)%较对照组[(24.82±2.93)%、(12.09±3.51)%]升高(P值均＜0.05),治疗后2项指标[(24.06±3.02)%、(10.90±3.55)%]均降至正常水平;ITP患者CD56+细胞百分比治疗前(15.80±2.85)%、治疗后(15.16±2.77)%与对照组(16.36±2.75)%差异无统计学意义(P＞0.05).结论 免疫细胞亚群紊乱参与了ITP的发病,对其检测可作为ITP的辅助诊断,在指导治疗方面可能有一定的意义.

Abstract：

Objective To explore the clinical significance of immunocyte subsets before and after immunosuppressive therapy in the peripheral blood of patients with immune thrombocytopenic purpura (ITP).MethodsThe percentages of immunocyte subsets in the peripheral blood of 35 patients with ITP and 20 healthy controls were detected by flow cytometry,including CD3+,CD4+,CD8+,CD56+,CD19+ lymphocytes and CD4+/CD8+.Results The percentages of CD3+ T lymphocyte (61.58 ± 6.45 ) %,CD4+ T lymphocyte (28.38 ±4.89)% and the ratio of CD4+/CD8+ 0.99 0.22 in patients with ITP were lower than those in healthy controls[( 67.85 ± 4.68 ) %,( 38.00 ± 3.37 ) %,1.54 ± 0.13,all P ＜ 0.05].After immunosuppressive therapy,the percentages of CD3+ T lymphocyte ( 69.41 ± 5.03 ) %,CD4+ T lymphocyte (38.17 ±3.18)% and the ratio of CD4+/CD8+ 1.60 ±0.15 recovered to control levels.The percentages of CD8+ T lymphocyte (29.20 ±4.50)% and CD19+B lymphocyte ( 17.74 ±4.14)% were higher than those in healthy controls[( 24.82 ± 2.93 ) % and ( 12.09 ± 3.51 ) %,all P ＜ 0.05].After the immunosuppressive therapy,the percentages of CD8+ T lymphocyte ( 24.06 ± 3.02 ) % and CD19+ B lymphocyte ( 10.90 ± 3.55 ) %recovered to control levels.There were no significant difference of the percentage of CD56+ lymphocyte among ITP patients ( 15.80 ± 2.85 )%,ITP patients after immunosuppressive therapy ( 15.16 ± 2.77 )% and healthy controls ( 16.36 ± 2.75 ) %.ConclusionThe aberrant immunocyte subsets are involved in the pathogenesis of ITP,and detection of immunocyte subsets might be helpful for the diagnosis and determination of therapeutic outcome of ITP.     

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.     

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.     

慢性肾炎患者外周血共刺激分子CD28和CD137水平变化研究

目的　研究慢性肾炎患者外周血共刺激分子CD2 8和CD1 37的表达特点及其在慢性肾炎免疫病理机制中的作用。方法　采用免疫荧光标记和流式细胞仪分析 ,对 5 2例慢性肾炎患者外周血共刺激分子CD2 8、CD1 37和T淋巴细胞亚群的表达进行检测。结果　慢性肾炎患者T细胞亚群明显失衡 ,表现为CD4减少 ,CD8增加 ,CD4 CD8比值显著降低。共刺激分子CD2 8表达显著低于正常对照组 (P <0 0 1) ,且CD+4 CD+2 8T细胞和CD+8CD+2 8T细胞均显著减少 (P <0 0 1)。共刺激分子CD1 37表达显著高于正常对照组 (P <0 0 1)。结论　慢性肾炎患者外周血T细胞亚群失衡和T细胞活化所必需的共刺激分子CD2 8、CD1 37异常表达 ,可能在慢性肾炎发生和病变进展中起着重要作用     

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.     

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.