病毒性肝炎患者血小板减少与脾脏肿大和血小板生成素的关系

目的研究病毒性肝炎患者血小板减少、脾脏肿大及血清血小板生成素(TPO)水平之间的关系,以探讨病毒性肝炎患者血小板减少的发病机制。方法应用腹部彩色B超测量58例病毒性肝炎并血小板减少症患者(A组)以及48例病毒性肝炎血小板正常患者(B组)和20例健康志愿者(C组)的脾脏大小,并采用酶联免疫吸附法测定其血清TPO水平。结果A组脾脏厚度(50.49±13.58mm)明显大于B组(38.45±8.14mm,P<0.01)和C组(32.25±3.73mm,P<0.01)。血小板数与脾脏大小呈负相关(r=-0.553,P<0.01)。血清TPO水平A组(88.05±17.09pg/mL)明显低于B组(100.20±17.63pg/mL,P<0.01)和C组(108.96±25.90pg/mL,P<0.01)。血小板数与血清TPO水平呈正相关(r=0.407,P<0.01)。结论病毒性肝炎血小板减少与脾脏肿大、血清TPO水平下降有关。     

Early onset of autoimmunity in MRL/++ mice following immunization with beta 2 glycoprotein I.

Antiphospholipid antibodies (aPL) are associated with thrombosis, thrombocytopenia and recurrent fetal loss in humans and in some animal models. Immunization with beta 2 glycoprotein I (beta 2GPI) induced aPL production in normal rabbits and mice. However, the association of these antibodies with disease manifestations remains controversial. To determine whether induction of aPL by beta 2GPI immunization in an autoimmune strain of mice (MRL/++) would result in acceleration of clinical and serological autoimmune disease manifestations, three groups of 8-week-old female mice were studied. One group was immunized with beta 2GPI, and one with ovalbumin (OVA); the third was not immunized. After two booster injections, sera were analysed for the presence of anticardiolipin (aCL) and anti-DNA by ELISA and anti-nuclear antibody (ANA) by immunofluorescence. Mice were studied for thrombocytopenia, proteinuria, fecundity rates, litter sizes and the development of central nervous system dysfunction. Elevated levels of aCL, anti-DNA and ANA were detected in all beta 2GPI-immunized, in three OVA-immunized, and in none of the unimmunized mice. The anti-DNA antibodies were inhibited by CL micelles, suggesting cross-reactivity between aCL and anti-DNA. Platelet counts, fecundity rates and litter size were reduced in beta 2GPI-immunized but not in OVA-immunized or unimmunized mice. None of the mice developed neurological dysfunction or significant proteinuria over a 10-week period post-immunization. These findings suggest that beta 2GPI immunization induces aPL in MRL/++ mice associated with accelerated autoimmune manifestations resembling the antiphospholipid syndrome.     

Diagnostic performance of aPS/PT antibodies in neuropsychiatric lupus and cardiovascular complications of systemic lupus erythematosus

Abstract

Background: Systemic lupus erythematosus (SLE) is associated with a constellation of complications affecting multiple organs, including neuropsychiatric manifestations (NPSLE) and ischaemic events, leading to increased long-term morbidity. Antiphospholipid antibodies (aPL) are a major determinant of vascular inflammation and thromboembolic risk. The diagnostic role of anti-phosphatidylserine/prothrombin (aPS/PT) antibodies in this setting is incompletely defined.

Aim: To verify whether aPS/PT add to diagnostics and disease stratification in patients with SLE with or without other aPL.

Methods: 131 consecutive patients were studied, including 20 patients with SLE and secondary antiphospholipid syndrome (APS). aPS/PT IgG and IgM were assessed through ELISA and patients were stratified based on the presence of other aPL, on their clinical and laboratory features at time of blood sampling and on their clinical history. Synthetic indices of disease activity, chronic damage and cardiovascular risk were calculated at time of venipuncture.

Results: Fifty-one (38.9%) patients with SLE had aPS/PT and 15 (11.5%) patients had aPS/PT as the only aPL (aPS/PT-only). aPS/PT-only patients had a significantly higher prevalence of NPSLE than quadruple aPL-negative patients (p?=?.007). Patients with aPS/PT were more likely to have a history of ischaemia, thrombocytopenia and Libman–Sacks’ endocarditis. The presence of aPS/PT also associated with previous accrual of at least one damage item (p?=?.043), but had limited predictive values for damage progression in the short term.

Conclusion: aPS/PT antibodies provide non-redundant information that could contribute to risk assessment and stratification of patients with SLE.     

Effect of Antiphospholipid Antibodies on β2Glycoprotein I-Phospholipid Interaction

PROBLEM: β₂ glycoprotein I (β₂GPI) physiologically binds to negatively charged phospholipids (PLs) and is a natural regulator of the coagulation cascade. Thrombotic clinical complications and recurrent fetal loss associated with autoimmune antiphospholipid (aPL) antibodies are thought to be related to their binding to β₂GPI-PL complex and interference with the physiological function of β₂GPI. METHOD OF STUDY: To investigate the effect of aPL on β₂GPI-PL interaction, we studied the binding of biotinylated β₂GPI to cardiolipin (CL) by enzyme-linked immunosorbent assay (ELISA) in the presence and absence of purified aPL immunoglobulin G (IgG) antibodies. RESULTS: Adding five different aPL IgG antibodies with different levels of aPL activity isolated from the sera of five patients with aPL-associated recurrent fetal death greatly increased the binding of biotinylated β₂GPI to CL-coated plates. The optical densities (ODs) were 0.635, 0.890, and 1.265 in the presence of three aPL IgG antibodies, compared to 0.425 in the absence of aPL IgG. In contrast, normal human IgG had no enhancing effect. The OD was 0.480 and 0.425, respectively. The enhancement of β₂GPI binding to CL by aPL IgG correlated with the titers of aPL antibodies. The use of phosphate-buffered saline with increasing salt concentrations as a washing buffer for the ELISA resulted in more stable binding of β₂GPI to PL in the presence of aPL IgG. CONCLUSIONS: These findings suggest that the binding of autoimmune aPL antibodies to β₂GPI-PL complex results in abnormally tighter interaction between β₂GPI and PLs, which may lead to physiological dysfunction of β₂GPI as a regulator of coagulation.     

Autoimmune thrombocytopenia (AITP) and thyroid autoimmune disease (TAD): overlapping syndromes?

The pathogenesis of thrombocytopenia associated with TAD and the occurrence of overlapping traits between TAD and AITP are still a matter of debate. For this reason, we investigated for the presence and specificity of platelet and thyroid autoantibodies in 18 TAD patients with thrombocytopenia, 19 TAD patients without thrombocytopenia and in 22 patients with primary AITP without clinical signs of TAD. Platelet-associated IgG and/or specific circulating platelet autoantibodies were detected in 83% of patients with TAD and thrombocytopenia, in 10% of patients with TAD without thrombocytopenia and in 86% of patients with primary AITP. The reactivity of serum autoantibodies, assayed by MoAb immobilization of platelet antigens (MAIPA), was directed against platelet glycoproteins Ib and/or IIb/IIIa in 50% of the patients with TAD and thrombocytopenia, as in 46% of the patients with primary AITP. Thyroid autoantibodies were found in 89% of patients with TAD and thrombocytopenia, in 95% of patients with TAD without thrombocytopenia, and in 18% of patients with primary AITP. Thyrotropin (TSH) levels determined in three of four AITP patients with thyroid autoantibodies revealed a subclinical hyperthyroidism in one patient. The present study supports the autoimmune aetiology of thrombocytopenia associated with TAD, since the prevalence and specificity of platelet autoantibodies are similar in TAD and primary AITP. The results indicate also that there exists an overlap between thyroid and platelet autoimmunity with or without clinical manifestations.     

山东省发热伴血小板减少综合征发病危险因素分析

目的 探讨影响山东省发热伴血小板减少综合征（SFTS）发病的危险因素,为科学防制该病提供依据。方法 应用1∶2匹配的病例对照研究方法,调查收集病例、对照的基本情况、可疑暴露因素等信息,采用单因素和多因素的配对条件logistic回归分析发病危险因素。结果 本研究共纳入374例SFTS确诊病例和748例对照。分析结果显示,有病例接触史（OR = 5.84,95%CI:1.11～30.88）、有家养动物（OR = 1.74,95%CI: 1.02～2.96）、近1个月见过蜱（OR = 5.85,95%CI: 2.73～12.53）、近2周有蜱叮咬史（OR = 29.58,95%CI: 6.70～130.60）、从事田间作业（OR = 2.63,95%CI:1.41～4.91）、住宅周围环境有杂草/农作物/菜地（OR = 3.24,95%CI:1.74～6.05）和住宅卫生条件差（OR = 2.20,95%CI:1.32～3.66）是SFTS发病的危险因素（P＜0.05）,近1个月有亲邻发病（OR = 0.01,95%CI:0～0.03）、采取防护措施（OR = 0.21,95%CI:0.10～0.46）是SFTS发病的保护因素（P＜0.05）。结论 接触病例、饲养家养动物、蜱叮咬、无防护措施的野外作业及住宅周围环境卫生较差等是影响山东省SFTS发病的危险因素。应加强重点人群SFTS健康教育和行为干预,减少危险因素暴露,以控制SFTS传播。     

发热伴血小板减少综合征流行病学研究进展

发热伴血小板减少综合征（SFTS）是21世纪初发现的一种新发蜱媒传染病。SFTS已在亚洲地区多个国家流行,包括中国、日本、韩国、越南、缅甸。截至2019年,我国已有25个省份报告SFTS病例,主要分布在山区和丘陵地带的农村,病例高度散发,但在地域分布上又相对集中,以河南、山东、安徽、湖北、辽宁、浙江和江苏7个省份为主。病例主要通过被携带病毒的蜱叮咬而感染,也可通过密切接触病例血液或体液感染。主要临床表现包括发热、胃肠道症状、血小板减少和白细胞减少,重症病例常因多器官功能衰竭而死亡。近年来,我国SFTS报告病例逐年上升,病死率始终维持较高水平,严重威胁人民身体健康。本文主要从SFTS的流行特征、传播流行的危险因素、临床特征等方面加以综述,旨在提升对SFTS疾病自然史的认知,加强传染病预防控制能力,降低疾病病死率。     

艾滋病合并重度血小板减少临床特征分析

目的　报告艾滋病合并重度血小板减少患者3例,并结合文献搜索讨论其有效治疗方法,为进一步提高临床诊治提供经验。方法　回顾分析3例艾滋病合并重度血小板减少患者的临床资料,讨论其有效治疗方法。结果　3例患者临床表现主要为全身皮肤瘀点、瘀斑,其中2例伴发黏膜出血。3例患者中2例在出现血小板减少时未启动抗病毒治疗,另1例患者已行抗病毒治疗2年,但CD4+ T淋巴细胞计数仍＜200个/μl。3例患者均使用甲泼尼松龙联合强效抗病毒治疗,后续贯泼尼松龙巩固治疗。1例患者激素治疗无效,行脾切除术。经过治疗3例患者血小板均逐渐恢复并出院。结论　HIV相关性血小板减少的发生可能与HIV在体内持续活跃复制有关,早期以强效抗病毒治疗联合激素冲击疗法为首选方案,可明显改善患者生活质量及结局。     

彩超对脾动脉栓塞术治疗血小板减少症的观察

目的　观察血小板减少症患者脾动脉栓塞术前后的脾动脉血流动力学的变化。方法　采用彩色多普勒超声仪观察栓塞术前后脾动脉内径、血流速度。结果　脾动脉内径缩小(P <0 .0 5 ) ,收缩期血流峰值、舒张期最小速度值降低 (P <0 .0 1) ,而阻力指数无明显改变 (P >0 .0 5 )。血小板、白细胞计数上升。结论　该项技术可用于检测脾动脉栓塞术前后脾动脉血流动力学的变化     

Immunobiology of T helper cells and antigen-presenting cells in autoimmune thrombocytopenic purpura (ITP)

Autoimmune thrombocytopenic purpura (AITP) is a bleeding disease in which autoantibodies are directed against the individual's own platelets, resulting in enhanced Fc-mediated platelet destruction by macrophages in the reticuloendothelial system. Most research in AITP has focused on characterization of the autoantibodies, while little has been devoted to the cellular immune mechanisms leading to autoantibody production. This report summarizes the current state of the literature and argues that enhanced T helper cell/antigen-presenting cell interactions in patients with AITP are the primary stimulus for the development of antiplatelet autoantibody production. Understanding these events is important for eventually identifying disease-initiating platelet autoantigens and ultimately developing specific immunotherapies for AITP.