Drugs that Affect Platelet Function
Drugs that Affect Platelet Function
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DOI：
10.1055/s-0032-1328881
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发表时间：
2012-11-01
影响因子：
5.7
通讯作者：
Scharf, Ruediger E.
中科院分区：
文献类型：
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作者：
Scharf, Ruediger E.
在我们这个用药过度的社会里，药物是导致血小板功能障碍的最常见原因。虽然乙酰水杨酸(阿司匹林)、腺苷二磷酸受体拮抗剂(氯吡格雷和普拉格雷)和整合素αIIb-β3(GPIIb-IIIa)受体阻滞剂(阿昔单抗、依替菲替德和替罗非班)是众所周知的抗血小板药物的原型，但在某些临床情况下，其他广泛使用的药物如非类固醇抗炎药、抗生素、心血管和降脂药物、选择性5-羟色胺再摄取抑制剂和容量扩张剂也可以损害血小板功能，从而导致或加重出血。因此，出血素质的诱导仍然是一个重要的问题。这与先前存在的任何类型的止血缺陷的患者尤其相关，只要血小板功能(和/或凝血)不受药物抑制，这些缺陷就可能保持代偿状态。(1)预防意外出血并发症；(2)充分处理出血症状；(3)将侵入性手术的风险降至最低；(4)避免患者接触不必要的血液产品。本文综述了许多不是为抗血小板治疗而设计的药物，但它们干扰了血小板的反应性或导致了血小板抑制。特别是，药物的相互作用和这些药物可以触发或导致血小板功能障碍的机制被详细介绍。
Drugs represent the most common cause of platelet dysfunction in our overmedicated society. While acetylsalicylic acid (aspirin), adenosine diphosphate receptor antagonists (clopidogrel and prasugrel), and integrin alpha IIb beta 3 (GPIIb-IIIa) receptor blockers (abciximab, eptifibatide, and tirofiban) are well-known prototypes of antiplatelet drugs, other widely used agents such as nonsteroidal anti-inflammatory drugs, antibiotics, cardiovascular and lipid-lowering drugs, selective serotonin reuptake inhibitors, and volume expanders can also impair platelet function and thus cause or aggravate hemorrhages in certain clinical settings. Therefore, induction of a bleeding diathesis remains a significant concern. This is especially relevant in patients with preexisting hemostatic defects of any kind, which may remain compensated as long as platelet function (and/or coagulation) is not inhibited pharmacologically. Identification of individual patients with preexisting hemostatic defects remains crucial (1) to prevent otherwise unexpected bleeding complications, (2) to manage hemorrhagic symptoms adequately, (3) to minimize the risk from invasive procedures, and (4) to avoid unnecessary patient exposure to blood products. This article provides a review of the large variety of agents that have not been designed for antiplatelet therapy but nevertheless interfere with platelet reactivity or induce platelet inhibition. In particular, drug interactions and mechanisms by which these agents can trigger or cause platelet dysfunction are detailed.