部分脾动脉栓塞术治疗原发性肝癌合并脾功能亢进的临床疗效观察

目的:探讨部分性脾动脉栓塞术(PSE)治疗原发性肝癌合并脾功能亢进的临床疗效及安全性。方法:选择2008年5月至2013年4月我科收治的160例原发性肝癌合并有脾功亢进患者为研究对象,患者在行肝动脉化疗栓塞术(TACE)的同时进行PSE,PSE栓塞面积在30%~60%之间,观察治疗后3天、7天、1个月、3个月、6个月患者白细胞(WBC)计数和血小板(PLT)计数的动态变化情况。结果:以外周血白细胞计数达到4.0~13×109/L、血小板达计数到50×109/L为治疗有效,160例患者术后3个月时外周血白细胞治疗有效为151例(94.38%),血小板治疗有效为155例(96.88%),术后6个月时白细胞治疗有效136例(85%),血小板治疗有效125例(78.13%)。所有患者术后6个月均未发生严重并发症。结论:PSE联合TACE治疗原发性肝癌合并有脾功亢进患者具有良好的疗效,且安全性较高。     

术前DSA损伤分级在外伤性脾破裂行脾动脉栓塞治疗中的价值分析

摘要 目的：分析术前DSA损伤分级在外伤性脾破裂行脾动脉栓塞治疗中的价值。方法：选取2020年1月～2022年12月本院收治的95例外伤性脾破裂患者进行研究,根据随机数字表法将其分为常规手术组（45例）和DSA引导下脾动脉栓塞组（50例）,常规手术组行开腹脾全切术,DSA引导下脾动脉栓塞组在DSA引导下行脾动脉栓塞术,分析两组与DSA引导下脾动脉栓塞组不同DSA分级的手术相关指标、T淋巴细胞（CD3⁺、CD4⁺、CD8⁺、CD4⁺/CD8⁺）、免疫球蛋白（IgG、IgA、IgM）、白细胞（WBC）和血小板（PLT）含量及血清白介素6（IL-6）、血清白介素10（IL-10）、促吞噬素因子（Tuftsin）水平。结果：与常规手术组比较,DSA引导下脾动脉栓塞组手术时间、下床时间、住院时间较短,术中出血量较少（P＜0.05）。术后14 d,与常规手术组比较,DSA引导下脾动脉栓塞组CD3⁺、CD4⁺、CD4⁺/CD8⁺水平较高,CD8⁺水平较低（P＜0.05）。术后14 d,与常规手术组比较,DSA引导下脾动脉栓塞组IgG、IgA、IgM水平较高（P＜0.05）。术后14 d,与常规手术组比较,DSA引导下脾动脉栓塞组PLT含量较低;与DSA Ⅲ级比较,DSA Ⅰ～Ⅱ级PLT含量较低（P＜0.05）。术后14 d,与常规手术组比较,DSA引导下脾动脉栓塞组血清IL-6水平较低,血清IL-10、Tuftsin水平较高（P＜0.05）。结论：于DSA损伤分级指导下对外伤性脾破裂患者开展脾动脉栓塞术,对机体免疫功能造成的影响较小,且术中不会出现大量出血的情况,不仅能降低患者的血小板含量,还能促使患者尽快恢复。     

脾动脉栓塞术后出现严重粘连的脾切除手术体会

目的:探讨脾动脉栓塞术后严重脾粘连脾切除手术技巧,为临床实践提供可借鉴的方法。方法:收集我院2005年4月-2013年6月收治的18例脾动脉栓塞术后严重脾粘连行脾切除术的患者临床资料,分析手术时间、术中出血、术中特殊处理及术后恢复情况等。结果:18例患者均顺利恢复出院,无围手术期死亡,开腹后到脾切除完成平均耗时55 min、出血550 mL。术后并发症为腹水(8例)、肺部感染(1例)、胰瘘(1例)及腹腔内出血(1例)。结论:脾动脉栓塞术后出现严重脾粘连行脾切除术,手术风险较大,手术时间、术中出血较常规脾切除术明显延长、增多。规范手术操作,细致分离脾周粘连,合理处理脾蒂,是安全、有效完成此类脾切除术的关键。     

脾动脉介入栓塞治疗外伤性脾破裂的临床效果及对患者免疫功能的影响

目的:探讨脾动脉介入栓塞治疗外伤性脾破裂的临床效果及对患者免疫功能的影响。方法:选择2013年4月到2017年2月在中国人民解放军第九七医院进行急诊治疗的116例外伤性脾破裂患者,根据治疗方法的不同将其分为观察组60例与对照组56例,对照组接受脾脏切除手术,观察组给予脾动脉介入栓塞治疗,记录和比较两组的术后下床活动时间、术后住院时间、术后肛门排便时间、术后肛门排气时间、术中输血量、手术时间与治疗前后CD4~+/CD8~+、CD8~+、CD4~+、CD3~+的变化及不良反应的发生情况。结果:所有患者都完成治疗并抢救成功,观察组的术后下床活动时间、术后住院时间、术后肛门排便时间、术后肛门排气时间、术中输血量、手术时间都少于对照组(P0.05)。观察组围手术期间的急性肠梗阻、急性胰腺炎、肺炎等并发症发生率为3.33%,对照组为17.86%,观察组低于对照组(P0.05)。术后14天,两组白细胞与血小板含量均显著高于术前1天(P0.05),而观察组血小板含量显著低于对照组(P0.05),但两组白细胞含量比较差异无统计学意义(P0.05)。观察组术后14天与术后1个月的CD4+/CD8+、CD4+、CD3+值均明显高于对照组(P0.05),两组CD8+对比差异无统计学意义(P0.05)。结论:脾动脉介入栓塞治疗外伤性脾破裂能提高治疗的临床效果,减少术后并发症的发生,促进患者免疫功能的恢复。     

脾动脉结扎联合肝癌切除术治疗肝癌并门静脉高压症临床研究

目的:探讨脾动脉结扎联合肝癌切除术对肝癌并门静脉高压症的治疗效果和临床应用的价值。方法:对2008年10月至2013年10月期间我院收治的84例肝癌并门静脉高压症患者的资料进行回顾性分析,其中脾动脉结扎联合肝癌切除手术的患者50例为研究组,患者34例行肝癌切除及脾切断流术为对照组。比较两组治疗效果及患者术前、术后情况。结果:研究组术前白细胞计数、血小板计数、红细胞计数为(3.1±0.9)×109/L、(58.6±12.7)×109/L、(3.4±0.4)×109/L,术后2周白细胞计数、血小板计数、红细胞计数分别为(5.9±1.5)×109/L、(140.3±50.1)×109/L、(3.6±0.7)×109/L;对照组为术前白细胞计数、血小板计数、红细胞计数为(2.8±1.2)×109/L、(45.8±20.5)×109/L、(3.4±0.4)×109/L,术后2周白细胞计数、血小板计数、红细胞计数为(6.2±0.7)×109/L、(172.5±32.7)×109/L、(3.6±0.3)×109/L。研究组与对照组相比,术后2周白细胞计数、红细胞计数相比差异无统计学意义(P0.05),但术后2周血小板计数研究组低于对照组,差异有统计学意义(P0.05)。研究组术前与术后的白细胞计数、血小板计数、红细胞计数相比,差异均有统计学意义(P0.05)。研究组有17例患者出现术后并发症,占16.0%;对照组有20例患者出现术后并发症,占38.2%;两组对比差异有统计学意义(P0.05)。结论:根据病情合理选择使用脾动脉结扎联合肝癌切除术治疗肝癌并门静脉高压症,可以有效治疗肝癌和脾功能亢进,促进肝功能恢复,对延长原发性肝癌合并肝硬化脾功能亢进患者的生存时间,提高生活质量,具有重要意义。     

部分性脾动脉栓塞术治疗脾功能亢进的护理体会

目的：总结部分性脾动脉栓塞术（PSE）治疗肝硬化脾功能亢进的护理方法。方法对28例脾功能亢进行PSE术的患者给予围手术期护理。结果28例患者均发生不同程度的不良反应,包括脾区疼痛、发热及恶心呕吐等,经积极治疗及护理后均好转出院。结论加强病情观察,并采取积极有效的护理措施,可减轻PSE术后不良反应,提高治疗效果和病人的生活质量。     

支气管动脉灌注化疗与栓塞治疗中晚期肺癌的疗效观察

目的：对比分析支气管动脉灌注化疗与支气管动脉灌注化疗十栓塞术治疗中晚期肺癌的临床疗效。方法：将我院2011年1月-2013年1月期间收治的76例中晚期肺癌患者随机分为两组,即观察组38例,对照组38例。观察组患者行支气管动脉灌注化疗联合栓塞术治疗,对照组患者行单纯支气管动脉灌注化疗治疗。分别对两组患者治疗后的临床治疗效果进行评价,同时观察两组患者治疗后的不良反应及并发症的发生情况。结果：观察组患者临床治疗的总有效率为84．21％,对照组为64．78％．两组比较,差异具有统计学意义（P〈0．05）。两组患者治疗后,观察组患者总不良反应率为23．67％,对照组为21．04％,两组比较．差异无统计学意义（P〉0．05）。且经对症处理后,均得到有效改善。结论：支气管动脉灌注化疗联合栓塞术治疗中晚期肺癌的,临床疗效明显优于单纯支气管动脉灌注化疗,且无明显不良反应及并发症的发生,安全性好,值得临床推广与应用。     

脾功能亢进患者行脾切除术与部分脾动脉栓塞术前后免疫功能的对比研究

目的:研究脾切除术与部分脾动脉栓塞术对脾功能亢进患者的影响。方法:选取我院外科确诊为乙型病毒性肝炎后肝硬化伴脾功能亢进症患者38例,通过随机数表法将所有患者平分为观察组和对照组,观察组给予部分脾动脉栓塞术,对照组给予脾切除术。检测术前术后血细胞计数、细胞免疫指标和体液免疫指标。结果:术后7天,对照组的红细胞略低于实验组(X~2=0.118,P=0.906);对照组的白细胞高于实验组(X~2=6.095,P0.001);对照组的血小板显著低于实验组(X~2=17.263,P0.001);术后28天,对照组的红细胞显著低于实验组(X~2=7.981,P0.001);对照组的白细胞明显高于实验组,差异有统计学意义(X~2=4.862,P0.001);对照组的血小板低于实验组(X~2=2.165,P=0.037);术后7天,对照组的CD3略低于实验组(t=0.606,P=0.548),对照组的CD4明显低于实验组,CD8显著高于实验组,CD4/CD8低于实验组,差异均有统计学意义(P0.001);术后28天,对照组的CD3略低于实验组(t=0.948,P=0.349);对照组的CD4略低于实验组(t=2.742,P=0.009);对照组的CD8显著高于实验组,CD4/CD8低于实验组,差异均无统计学意义(P0.05);术后7天,对照组的IgM高于实验组,对照组的IgG略高于实验组,IgA低于对照组,但差异无统计学意义(P0.05);术后28天,对照组的IgM高于实验组,对照组的IgG略高于实验组,但差异无统计学意义(P0.05);对照组的IgA为(2.76±1.37)g/L,明显低于实验组的(3.79±1.69)g/L(t=2.063,P=0.046)。结论:部分脾动脉栓塞术能有效改善脾亢症状,调节脾脏功能,提升全身性免疫功能,值得在临床中推广。     

剖宫产疤痕妊娠30例临床分析

摘要目的：探讨子宫剖宫产疤痕妊娠（CSP）的诊断和最佳治疗方法,为后续的临床研究工作提供理论依据和临床资料。方法：回顾性分析我院2010年2月．2012年2月收治的30例CSP患者的临床资料。结果：30例患者中,有25例行双侧子宫动脉栓塞（UAE）＋MTX灌注术后,再行清宫术,手术均获得成功,术后无任何并发症出现;另外5例患者因误诊为宫内妊娠后行人工流产术时发生大出血转至我院进行抢救,其中,4例成功实施了子宫动脉栓塞术,达到了止血目的,1例因子宫破裂直接行全子宫切除术。结论：对子宫剖宫产疤痕妊娠（CSP）患者实施双侧子宫动脉栓塞术＋MTX灌注术后,借助B超监测,再行刮宫术,是治疗剖宫产切口妊娠的有效方法。     

逆转录-聚合酶链反应技术诊断丙型肝炎病毒感染

本文采用逆转录－聚合酶链反应（ＲＴ-ＰＣＲ）技术对２１２例住院及门诊病人其中肝病患者９８例（慢性肝炎４３例、肝炎后肝硬化４７例、原发性肝细胞癌８例）进行ＨＣＶ－ＲＮＡ检测。结果９８例慢性肝病患者血清中ＨＣＶ-ＲＮＡ-ＰＣＲ阳性２７例（２７．６％）,１１４例非肝病患者血清中ＨＣＶ-ＲＮＡ-ＰＣＲ阳性９例（７．９％）,两组间差异非常显著（Ｐ（０．０１）,各种肝病患者的ＨＣＶ-ＲＮＡ-ＰＣＲ阳性率均高于非肝病组。６８例患者同时进行了ＨＣＶ-ＲＮＡ-ＰＣＲ检测和抗－ＨＣＶ检测,２５例抗－ＨＣＶ阳性的患者中ＨＣＶ－ＲＮＡ-ＰＣＲ,２１例阳性（８４％）,４３例抗－ＨＣＶ阴性的患者中ＨＣＶ-ＲＮＡ-ＰＣＲ,９例阳性（２０．１％）、有输血及血制品史者４８例,其中ＨＣＶ-ＲＮＡ-ＰＣＲ阳性１６例（３３．３％）,１６４倒无输血史者中ＨＣＶ-ＲＮＡ-ＰＣＲ阳性２０例（１２．２％）,两组间差异非常显著（Ｐ（０．０１）。结果表明：１．ＨＣＶ感染与慢性肝病有密切联系,说明ＨＣＶ感染是慢性肝炎、肝硬化、肝癌的致病因素;２．ＨＣＶ-ＰＣＲ法具有特异性好、灵敏度高、简便快速等特点,弥补了抗－ＨＣＶ检测的不足之处,是目前确定ＨＣＶ感染的主要手段;３．ＨＣＶ感染与输血关系密切,因此对献血员进行常规ＨＣＶ检测对预防由输血所致ＨＣＶ感染有着极其重要的临床意义。     

Mesenchymal stem cells improve platelet counts in mice with immune thrombocytopenia

Immune thrombocytopenia (ITP) is a common autoimmune bleeding disorder. The breakdown of immune tolerance (regulatory T [Treg] cells and suppressor cytokines) plays an important role in ITP pathophysiology, especially in refractory ITP. Bone marrow–derived mesenchymal stem cells (BM-MSCs) show immunomodulatory properties and have been extensively utilized for autoimmune diseases. However, it has not been fully elucidated how BM-MSCs affect ITP. In this study, we explore the therapeutic mechanism of BM-MSCs on ITP in mice. Dose-escalation passive ITP mice were inducted by injection of MWReg30. BALB/c mice were randomly divided into two groups: ITP with BM-MSC transplantation and ITP controls. The serum levels of cytokines (interleukin 10 [IL-10] and transforming growth factor-β1 [TGF-β1]) were examined by enzyme-linked immunosorbent assays. The frequency of Treg cells in both peripheral blood and spleen mononuclear cells was analyzed by flow cytometry, and the forkhead box P3 (Foxp3) messenger RNA (mRNA) level was measured by real-time polymerase chain reaction. After BM-MSC treatment, the platelet (PLT) counts were significantly elevated. Meanwhile, cytokines (TGF-β1 and IL-10), the ratios of Treg cells, and the Foxp3 mRNA expression level were significantly higher in the BM-MSC group. Our results show that BM-MSCs can improve PLT counts mainly by secreting suppressive cytokines and upregulating Tregs, which may provide new therapeutic potential for human ITP.     

The humoral regulation of megakaryocytopoiesis and platelet production in vivo

We examined the effects of the urinary extracts from aplastic anemia (AA) patients, idiopathic thrombocytopenic purpura (ITP) patients, and normal subjects on murine megakaryocyte/platelet production in vivo and in vitro. In the first study, single doses of AA urinary protein (65%-90% ethanol precipitate) were individually injected intraperitoneally into rats and mice. Blood platelet counts in rats increased significantly 24 hours after the injection. Total megakaryocyte colony-forming units (CFU-Meg) in mouse spleens increased by 24 hours postinjection, peaked at 48 hours and returned to normal levels at 96 hours. Changes in the number of megakaryocyte colonies showed similar patterns of increasing, peaking and returning to normal levels postinjection. In the second study, we compared the effects of some urinary extracts on murine megakaryocyte/platelet production. These observations provided the evidence that AA urinary extracts contain a factor that directly stimulates megakaryocyte progenitor cell proliferation in mouse spleen in vivo as well as the release of platelets from megakaryocytes, and ITP urinary extracts do not contain increased levels of Meg-CSF and/or some other factor that directly stimulates CFU-Meg in vivo, and the decreased blood platelet mass that is clinically characteristic of ITP is not a primary in vivo determinant of the elaboration of these factors.     

Immunocytochemical localization of platelets in baboon hepatic sinusoids using monoclonal mouse anti-human platelet glycoprotein IIIa following induction of thrombocytopenia.

A commercially available mouse monoclonal antibody to human platelet glycoprotein IIIa was used to demonstrate sequestration of platelets in hepatic biopsies obtained from baboons following intravenous infusion of echistatin, a novel fibrinogen receptor antagonist derived from the venom of the snake Echis carinatus. Biopsies of liver and spleen were taken prior to administration of echistatin. The hepatic biopsies were either snap-frozen in Freon-22/liquid nitrogen or fixed in 10% neutral buffered formalin. Biopsies of spleen were snap-frozen. During infusion of echistatin (2.3 micrograms/kg/min), circulating platelet counts decreased from 331,000/mm3 to 167,000/mm3. Selective sequestration within the liver was confirmed using whole body gamma camera imaging to demonstrate 111Indium-oxine labeled platelet accumulation within the liver during the thrombocytopenic episode. Hepatic biopsies were again taken and either snap-frozen in Freon-22/liquid nitrogen or fixed in 10% neutral buffered formalin. Biopsies of spleen and inguinal lymph node were also snap-frozen. Platelet rich plasma smears, included as positive controls, dewaxed paraffin sections, and cryosections of liver, spleen, and lymph node were stained with monoclonal mouse anti-human platelet glycoprotein IIIa using an avidin biotinylated peroxidase complex (ABC) technique. Prior to infusion of echistatin, platelet staining within the liver was minimal. After echistatin infusion, hepatic cryosections showed prominent platelet staining within hepatic sinusoids. No localization was shown in lymph node, however, the spleen showed prominent platelet staining both before and after echistatin infusion. Platelet rich plasma smears were intensely positive. No prominent platelet staining was observed in formalin-fixed, paraffin-embedded material. Thus, this immunocytochemical technique may help localize platelets in cryosections of tissues from baboons and other primate species.     

Proof of an association between Helicobacter pylori and idiopathic thrombocytopenic purpura in Latin America

BACKGROUND: Association between Helicobacter pylori and idiopathic thrombocytopenic purpura (ITP) has been found in Japan and in some European countries. It has also been shown that eradication of H. pylori can increase platelet counts in patients with ITP. The aims of this study were to determine the prevalence of H. pylori infection in patients with ITP in Colombia, and the effect of bacterial eradication on their platelet counts. MATERIALS AND METHODS: Between December 1998 and April 2006, a total of 32 patients diagnosed with ITP were included in the study. Controls were age and sex matched. RESULTS: H. pylori infection in patients with ITP was significantly higher (p = .00006) than in control individuals (90.6% and 43.8%, respectively), as determined by (13)C-urea breath test. A significant association between H. pylori infection and ITP was found (p < .0003), with an odds ratio (OR) of 13.15 (95%CI: 3.24-53.29). Multivariate analysis for the association between H. pylori and ITP showed an OR of 20.44 (95%CI: 3.88-107.49) for women and 19.28 (95%CI: 2.03-183.42) for individuals over 50 years. All 29 H. pylori-positive patients with ITP received eradication treatment. After a median follow up of 12.2 months, 80.8% had a recovery in platelet counts. CONCLUSIONS: According to these results and others from different countries where H. pylori infection rates are high, patients with ITP should be initially tested for H. pylori status, and if present, infection should be eradicated before initiating a drastic conventional ITP treatment. An algorithm for the study and management of patients with ITP in the post-Helicobacter era is presented.     

Immunocytochemical localization of platelets in baboon hepatic sinusoids using monoclonal mouse anti-human platelet glycoprotein IIIa following induction of thrombocytopenia

Summary A commercially available mouse monoclonal antibody to human platelet glycoprotein IIIa was used to demonstrate sequestration of platelets in hepatic biopsies obtained from baboons following intravenous infusion of echistatin, a novel fibrinogen receptor antagonist derived from the venom of the snake Echis carinatus. Biopsies of liver and spleen were taken prior to administration of echistatin. The hepatic biopsies were either snap-frozen in Freon-22/liquid nitrogen or fixed in 10% neutral buffered formalin. Biopsies of spleen were snapfrozen. During infusion of echistatin (2.3 µg/kg/min), circulating platelet counts decreased from 331000/mm³ to 167000/mm³. Selective sequestration within the liver was confirmed using whole body gamma camera imaging to demonstrate ¹¹¹Indium-oxine labeled platelet accumulation within the liver during the thrombocytopenic episode. Hepatic biopsies were again taken and either snap-frozen in Freon-22/liquid nitrogen or fixed in 10% neutral buffered formalin. Biopsies of spleen and inguinal lymph node were also snap-frozen. Platelet rich plasma smears, included as positive controls, dewaxed paraffin sections, and cryosections of liver, spleen, and lymph node were stained with monoclonal mouse anti-human platelet glycoprotein IIIa using an avidin biotinylated peroxidase complex (ABC) technique. Prior to infusion of echistatin, platelet staining within the liver was minimal. After echistatin infusion, hepatic cryosections showed prominent platelet staining within hepatic sinusoids. No localization was shown in lymph node, however, the spleen showed prominent platelet staining both before and after echistatin infusion. Platelet rich plasma smears were intensely positive. No prominent platelet staining was observed in formalin-fixed, paraffin-embedded material. Thus, this immunocytochemical technique may help localize platelets in cryosections of tissues from baboons and other primate species.     

Ability of plasma from patients with immune thrombocytopenic purpura (ITP) to promote the growth of megakaryocyte progenitors from normal bone marrow.

The ability of plasma from ITP patients (before and after splenectomy) to support the growth of megakaryocyte progenitors was compared with that from healthy subjects. Plasma Factor Index-Megakaryocyte PFI-Mk (ITP) which expressed resultant colony growth was significantly lower before splenectomy, but it normalized after splenectomy. (PFI-Mk) (ITP) did not relate neither to megakaryocyte nor to platelet counts. A positive correlation has been observed between megakaryocyte and platelet numbers in healthy subjects and in ITP patients after splenectomy, but not before splenectomy. The proportion of immature megakaryocytes was markedly higher in ITP marrow before splenectomy. This study indicates, that in ITP apart from antibodies directed to platelets and megakarocytes a low plasma stimulatory activity affected megakaryocytopoiesis.     

Pathway of Toll-like receptor 7/B cell activating factor/B cell activating factor receptor plays a role in immune thrombocytopenia in vivo

Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by anti-platelet autoantibody-mediated platelet destruction. Antigen-presenting cell (APC) dysfunction is considered to play crucial roles in ITP. However, how APC affects autoreactive B cells in ITP is still unknown. Using a mouse model of immune thrombocytopenia, we demonstrated an increase in levels of TLR7 in splenic mononuclear cells (SMCs). Using both TLR7 agonist and TLR7 silencing lentivirus, we found stimulation of TLR7 decreased platelet counts and increased levels of platelet-associated IgG (PAIgG) in ITP mice, which correlates TLR7 with platelet destruction by autoantibodies. Levels of serum BAFF increased significantly in ITP mice and stimulation of TLR7 promoted secretion of BAFF. Among the three BAFF receptors, only BAFF receptor (BAFF-R) increased in ITP mice. However, activation of TLR7 showed no effect on the expression of BAFF receptors. These findings indicate that upregulation of TLR7 may augment BAFF secretion by APC and through ligation of BAFF-R promote autoreactive B cell survival and thus anti-platelet autoantibody production. The pathway of TLR7/BAFF/BAFF-R provides us with an explanation of how activation of APC affects autoantibody production by B cells in ITP and thus might provide a reasonable therapeutic strategy for ITP.     

Amelioration of Murine Passive Immune Thrombocytopenia by IVIg and a Therapeutic Monoclonal CD44 Antibody Does Not Require the Myd88 Signaling Pathway

Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by a low platelet count and the production of anti-platelet antibodies. The majority of ITP patients have antibodies to platelet integrin α_IIbβ₃ (GPIIbIIIa) which can direct platelet phagocytosis by macrophages. One effective treatment for patients with ITP is intravenous immunoglobulin (IVIg) which rapidly reverses thrombocytopenia. The exact mechanism of IVIg action in human patients is unclear, although in mouse models of passive ITP, IVIg can rapidly increase platelet counts in the absence of adaptive immunity. Another antibody therapeutic that can similarly increase platelet counts independent of adaptive immunity are CD44 antibodies. Toll-like receptors (TLRs) are pattern recognition receptors which play a central role in helping direct the innate immune system. Dendritic cells, which are notable for their expression of TLRs, have been directly implicated in IVIg function as an initiator cell, while CD44 can associate with TLR2 and TLR4. We therefore questioned whether IVIg, or the therapeutic CD44 antibody KM114, mediate their ameliorative effects in a manner dependent upon normal TLR function. Here, we demonstrate that the TLR4 agonist LPS does not inhibit IVIg or KM114 amelioration of antibody-induced thrombocytopenia, and that these therapeutics do not ameliorate LPS-induced thrombocytopenia. IVIg was able to significantly ameliorate murine ITP in C3H/HeJ mice which have defective TLR4. All known murine TLRs except TLR3 utilize the Myd88 adapter protein to drive TLR signaling. Employing Myd88 deficient mice, we found that both IVIg and KM114 ameliorate murine ITP in Myd88 deficient mice to the same extent as normal mice. Thus both IVIg and anti-CD44 antibody can mediate their ameliorative effects in murine passive ITP independent of the Myd88 signaling pathway. These data help shed light on the mechanism of action of IVIg and KM114 in the amelioration of murine ITP.     

青少年慢性粒细胞白血病急变临床分析

目的:分析青少年慢性粒细胞白血病(CGL)急变患者临床表现及实验检查特点,以提高对青少年CGL急变临床特点的认识。方法:将CGL急变患者按年龄分组,将青少年组和中老年组患者的急变时间、确诊时和急变时的脾脏大小、白细胞和血小板数目、急变时骨髓幼稚细胞的比例,以及患者的总生存时间、急变后生存时间进行对比分析。结果:青少年组和中老年组的脾脏大小、确诊时血小板数目、急变时的白细胞数目、急变时间、以及总生存时间无显著性差异;青少年组确诊时的白细胞数目较中老年组高,青少年组的急变后生存时间较长。结论:青少年CGL患者的临床表现及实验室检查结果具有CGL的普遍特征,但其确诊时白细胞数目较高,急变后生存时间较长。