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Drug-induced immune thrombocytopenia.

机译:药物诱导的免疫性血小板减少症。

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摘要

Thrombocytopenia can have several causes, including the use of certain drugs. The mechanism behind drug-induced thrombocytopenia is either a decrease in platelet production (bone marrow toxicity) or an increased destruction (immune-mediated thrombocytopenia). In addition, pseudothrombocytopenia, an in vitro effect, has to be distinguished from true drug-induced thrombocytopenia. This article reviews literature on drug-induced immune thrombocytopenia, with the exception of thrombo-haemorrhagic disorders such as thrombotic thrombocytopenic purpura and heparin-induced thrombocytopenia and thrombosis.A literature search in PubMed combined with a check of the reference lists of all the retrieved articles resulted in 108 articles relevant to the subject. The drug classes that are most often associated with drug-induced immune thrombocytopenia are cinchona alkaloid derivatives (quinine, quinidine), sulfonamides, NSAIDs, anticonvulsants, disease modifying antirheumatic drugs and diuretics. Several other drugs are occasionally described in case reports of thrombocytopenia; an updated review of these case reports can be found on the internet. A small number of epidemiological studies, differing largely in the methodology used, describe incidences in the magnitude of 10 cases per 1 000 000 inhabitants per year. No clear risk factors could be identified from these studies. The underlying mechanism of drug-induced immune thrombocytopenia is not completely clarified, but at least three different types of antibodies appear to play a role (hapten-dependent antibodies, drug-induced, platelet-reactive auto-antibodies and drug-dependent antibodies). Targets for drug-dependent antibodies are glycoproteins on the cell membrane of the platelets, such as glycoprotein (GP) Ib/IX and GPIIb/IIIa.Diagnosis of drug-induced immune thrombocytopenia may consist of identifying clinical symptoms (bruising, petechiae, bleeding), a careful evaluation of the causal relationship of the suspected causative drug, general laboratory investigation, such as total blood count and peripheral blood smear (to rule out pseudothrombocytopenia), and platelet serology tests. The sensitivity of these tests is dependent on factors such as the concentration of the drug in the test and the potential sensitisation of the patient by metabolites instead of the parent drug.Drug-induced immune thrombocytopenia can be treated by withholding the causative drug and, in severe cases associated with bleeding, by platelet transfusion.Although drug-induced thrombocytopenia is a relatively rare adverse drug reaction, its consequences may be severe. Therefore it is important to extend our knowledge on this subject. Future research should focus on the identification of potential risk factors, as well as the exact mechanism underlying drug-induced thrombocytopenia.
机译:血小板减少症可能有多种原因,包括使用某些药物。药物诱发的血小板减少的背后机制是血小板生成减少(骨髓毒性)或破坏增加(免疫介导的血小板减少)。另外,必须将伪性血小板减少症(一种体外作用)与真正的药物诱导的血小板减少症区分开来。本文回顾了有关药物诱发的免疫性血小板减少症的文献,但血栓性出血性疾病(如血栓性血小板减少性紫癜和肝素诱发的血小板减少症和血栓形成)除外。得出与该主题相关的108篇文章。与药物诱导的免疫性血小板减少症最常相关的药物类别是金鸡纳生物碱衍生物(奎宁,奎尼丁),磺胺类药物,非甾体抗炎药,抗惊厥药,抗风湿药和利尿药。血小板减少症的病例报告中偶尔会描述其他几种药物;这些案例报告的最新评论可以在互联网上找到。少数流行病学研究(所使用的方法差异很大)描述的发病率每年每10亿居民中有10例。从这些研究中没有明确的危险因素。药物诱导的免疫性血小板减少的潜在机制尚未完全阐明,但是至少三种不同类型的抗体似乎起作用(半抗原依赖性抗体,药物诱导的,血小板反应性自身抗体和药物依赖性抗体)。药物依赖性抗体的靶标是血小板细胞膜上的糖蛋白,例如糖蛋白(GP)Ib / IX和GPIIb / IIIa。诊断药物诱发的免疫性血小板减少症可能包括识别临床症状(瘀伤,瘀斑,出血) ,仔细评估可疑致病药物的因果关系,一般实验室检查,例如总血球计数和外周血涂片(以排除假性血小板减少症),以及血小板血清学检查。这些试验的敏感性取决于多种因素,例如试验中药物的浓度以及通过代谢产物(而非母体药物)对患者的潜在敏感性。药物引起的免疫性血小板减少症可以通过不使用引起原因的药物来治疗,并且药物引起的血小板减少症是一种相对罕见的药物不良反应,但其后果可能很严重。因此,重要的是扩展我们在该主题上的知识。未来的研究应侧重于确定潜在的危险因素,以及药物诱发的血小板减少的确切机制。

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