A case report of tumor necrosis factor-alpha antibody-induced thrombocytopenia associated with emerging IgM anticardiolipin antibody in patients with scleroderma overlap/rheumatoid arthritis

It is commonly believed that infliximab-induced anticardiolipin antibody belongs to the IgM subclass but not the IgG subclass and that the IgM subclass could not produce clinical symptoms. However, we had a patient with scleroderma overlap/rheumatoid arthritis who developed thrombocytopenia associated with the appearance of IgM anticardiolipin antibody after treatment with infliximab. This is a report of a rare case that should make us aware of the possibility of the development of thrombocytopenia with the appearance of IgM anticardiolipin antibody induced by infliximab.     

Evaluation of the effect of partial splenic embolization on platelet values for liver cirrhosis patients with thrombocytopenia

AIM： TO investigate the effect of partial splenic embolization （PSE） on platelet values in liver cirrhosis patients with thrombocytopenia and to determine the effective embolization area for platelet values improvement.
METHODS： Blood parameters and liver function indicators were measured on 10 liver cirrhosis patients （6 in Child-Pugh grade A and 4 in grade B） with thrombocytopenia （platelet values 〈 80 × 10^3/μL） before embolization. Computed tomography scan was also needed in advance to acquire the splenic baseline. After 2 to 3 d, angiography and splenic embolization were performed. A second computed tomography scan was made to confirm the embolization area after 2 to 3 wk of embolization. The blood parameters of patients were also examined biweekly during the 1 year follow-up period. RESULTS： According to the computed tomography images after partial splenic embolization, we divided all paUents into two groups： low （〈 30%）, and high （≥ 30%） embolization area groups. The platelet values were increased by 3 times compared to baseline levels after 2 wk of embolization in high embolization area group. In addition, there were significant differences in platelet values between low and high embolization area groups. GPT values decreased significantly in all patients after 2 wk of embolization. The improvement in platelet and GPT values still persisted until 1 year after PSE. In addition, 3 of 4 （75%） Child-Pugh grade B patients progressed to grade A after 2 mo of PSE. The complication rate in 〈 30% and ≥30% embolization area groups was 50% and 100%, respectively. CONCLUSION： Partial splenic embolization is an effective method to improve platelet values and GPT values in liver cirrhosis patients with thrombocytopenia and the ≥ 30% embolization area is meaningful for platelet values improvement. The relationship between the complication rate and embolization area needs further studies.     

Antiplatelet drug induced isolated profound thrombocytopenia in interventional cardiology: a review based on individual case reports

A combination antithrombotic and antiplatelet therapy with clopidogrel, aspirin, glycoprotein IIb/IIIa receptor inhibitors and heparins is routinely used as adjunct therapy in patients undergoing percutaneous coronary intervention (PCI). As all substances inhibit platelet function, bleeding and thrombocytopenia may occur. We report on three patients who developed isolated profound thrombocytopenia (platelet count of < 20,000/mm³) within 24 h after initiation of combination antiplatelet and antithrombotic therapy during a 1 year observation period in 443 consecutive patients undergoing PCI and stent implantation. The data from our cardiology unit revealed an incidence of an isolated profound thrombocytopenia in 0.7% of all patients on combination antithrombotic therapy and in 1.5% of patients with GPIIb/IIIa-blockers. In all three cases with isolated profound thrombocytopenia GPIIb/IIIa-blockers were found to be the causative agents. Negative results of HIT-assays excluded heparin induced thrombocytopenia type II. Despite the extremely low platelet count no severe bleeding was observed and in all cases platelet counts normalized within 3–4 days without specific interventions except discontinuation of the responsible agent. These findings are discussed in conjunct with an overview of the recent literature.     

肝素诱导的血小板减少症的临床观察

目的 分析静脉血栓栓塞症肝素诱导的血小板减少症及其治疗.方法 对我院2006年5月至2008年5月临床确诊并以肝素抗凝治疗的静脉血栓栓塞症患者202例进行临床分析,定期监测血常规.结果 其中有6例患者发生肝素诱导的血小板减少症,在应用肝素第3～9天出现血小板数目下降,发生率为2.97%,其下降率为60.4%～82.2%.对需要继续抗凝的4例患者停用肝素后改为阿加曲班继续治疗,第3～7天血小板数目回升至入院时水平.结论 在使用肝素进行抗凝治疗期间,应常规监测血小板数目变化,如发现血小板数目进行性下降大于50%,应及时停用肝素,需继续抗凝的患者可改用阿加曲班治疗.     

HIT抗体检测对血小板减少症的临床诊断意义

目的探讨HIT抗体在肝素诱导的血小板减少症(HIT)中的诊断价值,使其作为1项有价值的指标,较早诊断HIT,减少HITTS的发生。方法选择2007-02~2007-12间,随机连续观察在哈尔滨医科大学第二临床医学院血管外科应用普通肝素治疗的46例住院患者。结果实验组中HIT抗体阳性例数为21例,对照组HIT抗体阳性例数为2例。实验组中有7例患者血小板减少(血小板下降范围25%~53.4%),且HIT抗体阳性,该7例患者后经功能性检查确诊为HIT患者。结论HIT抗体检测的实验敏感性较高,且不涉及放射性,操作简单。该方法可在实验室开展,与血小板计数检测结合可对应用肝素的患者进行初筛,防止HITTS的发生。     

主动脉内球囊反搏患者P-选择素与血小板减少症的相关性研究

通过观察主动脉内球囊反搏(IABP)置入前后血浆P-选择素的变化规律,探讨P-选择素与IABP相关血小板减少症发生与发展的关系。方法:选择安贞医院首次放置IABP辅助治疗患者40例。分别于其放置IABP前,放置IABP后12 h、24 h、48 h和72 h,抽取肘正中静脉血样,用酶联免疫吸附实验(ELISA)方法测定血浆P-选择素的浓度。分析IABP放置72 h内血浆P-选择素浓度的变化趋势。根据围手术期期间IABP放置时段的不同,将样本分为3组,分别为术前放置组、术中放置组及术后放置组,分析不同时点放置IABP对血小板活化的影响。结果:对40例患者进行的临床试验研究显示,IABP放置前后血浆P-选择素浓度的差异有统计学意义(P<0.05)。患者血浆中P-选择素的浓度在IABP放置后即开始升高,并于放置后48 h达到峰值,其后开始逐步下降。术前放置IABP、术中放置IABP和术后放置IABP,组间血浆P-选择素的浓度的差异无统计学意义(P>0.05)。结论:IABP置入后血浆P-选择素浓度表达升高,血小板活化程度增强,血小板破坏消耗增多,导致血小板计数减少。     

Fatal Thrombocytopaenia Temporally Related to the Administration of Alemtuzumab (MabCampath) for Refractory CLL Despite Early Discontinuation of Therapy

Alemtuzumab (Campath 1H -MabCampath), initially used for prophylaxis of graft versus host disease in allogenic transplantaion, is now increasingly used for refractory chronic lymphatic leukaemia (CLL). Its efficacy has been well documented in this--the commonest form of leukaemia. Alemtuzumab is associated with severe immunosuppression, allergic reactions and thrombocytopenia. Data sheet and information supplied by the manufacturer confirm the rare occurrence of serious immune thrombocytopenia, recommending discontinuation of therapy when platelet counts fall below 50×10 9 /l. We report a patient with refractory CLL in which relentless progressive cytopenia occurred despite the discontinuation of alemtuzumab therapy while the platelet count was over 97×10 9 /l. Marrow biopsy showed increased megakaryocytes, the patient bleed uncontrollably and died of cerebral haemorrhage with a platelet count <10×10 9 /l. Data on the predictive factors underlying this complication are few and deserve further study as this drug is increasingly used the treatment of CLL.     

Successful treatment of pure red cell aplasia and autoimmune cytopenia with cyclosporine and prednisolone in a patient with Sjögren’s syndrome

Abstract

A 68-year-old woman was admitted to our hospital with xerophthalmia, xerostomia, leukopenia, and thrombocytopenia. She was diagnosed to have Sjögren’s syndrome and autoimmune cytopenia. After 11 months, she was readmitted with severe anemia and reticulocytopenia. Mild hemolysis was seen, and bone marrow aspirate showed markedly decreased erythropoiesis. An association of pure red cell aplasia (PRCA) and autoimmune hemolytic anemia was diagnosed. After treatment with cyclosporine and prednisolone, her anemia dramatically improved. We discuss the mechanism of PRCA associated with Sjögren’s syndrome.     

Thrombotic thrombocytopenic purpura as an etiology of thrombocytopenia in systemic lupus erythematosus: case report

Abstract

Thrombotic thrombocytopenic purpura (TTP) is an unusual complication of systemic lupus erythematosus (SLE). Although the reported association between SLE and TTP is increasing, a few cases do improve without plasmatherapy. We report a case of TTP which was successfully treated without plasmatherapy, which might be underestimated as an etiology of thrombocytopenia in SLE. TTP should always be considered as a concomitant disease when Coombs' negative hemolytic anemia or thrombocytopenia is seen in SLE patients.     

Generation of platelet-derived microparticles and procoagulant activity by heparin-induced thrombocytopenia IgG/serum and other IgG platelet agonists: a comparison with standard platelet agonists

Heparin-induced thrombocytopenia (HIT) is a relatively common, immunoglobulin-mediated adverse drug reaction associated with in vivo thrombin generation and both venous and arterial thrombosis. Serum and purified IgG from patients with HIT induce normal platelets to generate procoagulant platelet-derived microparticles, but the magnitude of this response in comparison with other IgG and standard platelet agonists is unknown. We describe a comparison of IgG platelet agonists, including HIT-IgG/serum, heat-aggregated IgG, and platelet-activating murine monoclonal antibodies, with standard 'strong' and 'weak' platelet agonists, and have determined their relative ability to generate platelet procoagulant activity. Using washed normal platelets as targets, we observed that HIT sera as well as other IgG agonists produced similar or even greater numbers of microparticles and procoagulant activity than the standard strong platelet agonists (thrombin, collagen, and thrombin receptor agonist peptide). The only exception was the non-physiological platelet agonist, calcium ionophore, which consistently produced a platelet procoagulant response even greater than the IgG agonists. We conclude that the IgG class of platelet agonists (including pathogenic HIT antibodies) is an effective trigger of the platelet procoagulant response comparable at least to strong physiological platelet agonists. These results help to explain the association between HIT, in vivo thrombin generation, and thrombosis.