Use of Cangrelor as a Bridge to Left Ventricular Assist Device Implantation in a Patient with a Recent Drug-Eluting Stent Who Developed Acute Tirofiban-Related Thrombocytopenia

Current guidelines emphasize the need for at least 6–12 months of oral dual antiplatelet therapy consisting of aspirin and a P2Y12 inhibitor following drug-eluting coronary artery stent implantation. In patients with recently implanted coronary artery stents who require urgent cardiac or noncardiac surgery, the benefits of maintaining oral dual antiplatelet therapy must be carefully weighed against the risks of excessive bleeding, and current practice is largely guided by individual surgeon preferences. When the effects of a second oral antiplatelet agent are undesirable during the perioperative period, the use of a short-acting intravenous antiplatelet agent as “bridge” therapy that can be discontinued shortly before surgery is associated with a reduced occurrence of adverse clinical events in patients with recently implanted coronary stents requiring urgent coronary artery bypass graft surgery. Cangrelor is an intravenous adenosine triphosphate analog P2Y12 receptor antagonist with a short plasma half-life that has been used off label in patients with recent coronary stents as a bridge to invasive procedures with excessive bleeding risk. To our knowledge, this is the first case report to demonstrate the safe and effective use of cangrelor as a bridge to left ventricular assist device implantation in a patient with a recently implanted drug-eluting coronary artery stent who developed acute thrombocytopenia following reexposure to tirofiban, a glycoprotein IIb/IIIa inhibitor.     

DNA methylation plays an important role in immune thrombocytopenia

DNA methylation is the covalent addition of a methyl group to a DNA base, typically the cytosine of cytosine-phosphate-guanosine (CpG) dinucleotides. It is catalysed by methyltransferase enzymes using an S-adenosyl methionine donor, which is a heritable, stable and reversible DNA modification. Aberrant DNA methylation can influence gene expression without changing nucleotide sequences, inducing occurrence and development in autoimmune diseases, such as systemic lupus erythematosus and immune thrombocytopenia. Immune thrombocytopenia is an autoimmune disease characterised by bleeding and thrombocytopenia of peripheral blood, a normal or increased number of megakaryocytes and a maturation disorder. Recently, it was proven that aberrant DNA methylation is associated with the aetiology of immune thrombocytopenia. The defective methylation induces overexpression of methylation-related genes, such as CD70 and FOXP3, which can take part in autoreactive immune responses, and ultimately accelerated the progression of immune thrombocytopenia. Targeting the DNA methylation can be used as a new treatment for immune thrombocytopenia. As a demethylated drug, decitabine promotes megakaryocyte maturation and platelet release under the action of tumour necrosis factor-related apoptosis inducing ligand (TRAIL) promoter. This review highlights recent evidence on the role of DNA methylation in immune thrombocytopenia by describing the relationship between DNA methylation and immune thrombocytopenia, and the DNA methylation-related genes. Identifying and regulating abnormal DNA methylation provides new ideas for the diagnosis and treatment of immune thrombocytopenia.     

Inhibitory effects of cisplatin and its conjugate with glutathione on blood platelet activity

Cisplatin ( cis -diamminedichloroplatinum II, CDDP) is a widely used chemotherapeutic agent; however, its haematological toxicity may become an important dose-limiting factor. The aim of the present study was to evaluate the effects of cisplatin and its metabolite with glutathione (GS-Pt conjugate) on thrombin- induced platelet aggregation, the secretory process and the arachidonate pathway in vitro . Pre-treatment of platelets with GS-Pt conjugate (60min, 20 mu M) but not with cisplatin alone, caused inhibition of thrombin-induced platelet aggregation. GS-Pt conjugate had also a strong inhibitory effect on the release of proteins and adenine nucleotides from platelet granules. After pre-incubation of platelets with cisplatin and its conjugate, we observed in thrombin-activated platelets, a decreased amount of malonyldialdehyde (a marker of thromboxane A synthesis). We suggest that arachidonate metabolism playsan important role in determining the cytotoxicity 2 of cisplatin.     

Physiologic and pathologic changes of platelets in pregnancy

Platelets are key players in haemostasis and thrombus formation. Defects affecting platelets during pregnancy can lead to heterogeneous complications, such as thrombosis, first trimester miscarriage and postpartum haemorrhage. The incidence of complications is increased in women who have heritable platelet function disorders. Modifications of platelet count or platelet functions during normal pregnancy and preeclampsia will be summarized and the management of pregnant women with heritable platelet function disorders will be discussed.     

免疫性血小板减少症125例临床分析

本研究旨在探讨免疫性血小板减少症(ITP)患者的临床特点。回顾性分析125例于2005年1月-2010年5月在我院住院治疗的ITP患者的临床资料、实验室检查结果及治疗效果。结果表明,125例患者发病中位年龄41岁,男女比为1∶1.78;治疗前平均血小板计数(28.59±23.05)×109/L;69.1%(67/97)的患者有风湿免疫检查异常;肝炎病毒和细小病毒B19携带率分别为37.3%(22/59)和44.8%(26/58);慢性患者CD3+T细胞为(62.7%±14.11%),在急性患者为(55.44%±14.31%)。慢性患者CD19+B细胞为(12.83%±6.96%),在急性患者为(19.47%±6.93%);91例患者行骨髓细胞膜抗体检查显示,54.9%(50/91)的患者抗体阴性,45.1%(41/91)患者抗体阳性;急性患者阳性率63.0%(17/27),在慢性患者为37.5%(24/64);激素联合环孢素治疗有效率为81.7%(49/60),部分难治性患者对RCP化疗或硫唑嘌呤细胞毒药物治疗的有效率分别为57.14%(4/7)和40.0%(2/5)。结论:ITP患者常合并病毒感染或风湿免疫学异常,急性患者以体液免疫功能亢进为主,慢性患者则表现为细胞免疫功能亢进;骨髓细胞膜抗体阳性的患者多是急性患者,因此在治疗方案的选择上应根据不同的发病机制选择不同作用机制的药物或药物组合,以取得更好的疗效。     

７７例发热伴血小板减少综合征病例流行病学特征分析

摘要：目的　分析７７例发热伴血小板减少综合征病例的临床与流行病学特征，为预防与治疗该病提供科学
依据。方法　采用流行病学描述性分析与个案调查的方法，回顾性收集、分析２０１０－２０１３年湖北省广水市
发热伴血小板减少综合征７７例病例的临床表现、实验室检查、病原学检查、流行病学特征等情况资料。结
果　７７例病例中１４例危重型患者死亡，其他６３ 例患者痊愈。病例多为居住在丘陵地区３５ 岁以上的中老
年人；发病呈明显季节性，集中在４～１０月；病例呈现高度散发，以丘陵地区多见；病原体以新布尼亚病
毒为主。本辖区尚未发现人感染人的依据。结论　发热伴血小板减少综合征病例是一种可防可治的疾病，
只要提高对本病的认识，做到早诊断、早治疗，就能有效降低该病死亡率。
关键词：发热伴血小板减少综合征；流行病学特征；临床特征
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