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Unfractionated heparin compared with low-molecular-weight heparin as related to heparin-induced thrombocytopenia.

机译:普通肝素与低分子量肝素相比,与肝素诱导的血小板减少有关。

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PURPOSE OF REVIEW: Heparin-induced thrombocytopenia is a severe side effect of treatment with unfractionated heparin. The relation of low-molecular-weight heparin to heparin-induced thrombocytopenia is less well understood. This review will summarize what is known about the similarities and differences between thrombocytopenia induced by low-molecular-weight heparin and that induced by unfractionated heparin. RECENT FINDINGS: The pathophysiology of unfractionated heparin-induced thrombocytopenia, caused by the development of antibodies to heparin/platelet factor 4 complexes, holds true for low-molecular-weight heparin because the molecules of the latter are of the same saccharidic structure as those of unfractionated heparin. Owing to their smaller size, however, low-molecular-weight heparin does not interact with platelet factor 4 and platelets as efficiently as does unfractionated heparin. This translates to a two- to threefold lower risk of immune sensitization (antibody generation and occurrence ofclinical heparin-induced thrombocytopenia). Low-molecular-weight heparin-induced thrombocytopenia antibodies are more often immunoglobulin A and immunoglobulin M, in contrast to the immunoglobulin G antibodies generated with unfractionated heparin-induced thrombocytopenia, which tend to be more often associated with clinical heparin-induced thrombocytopenia. The clinical expression of low-molecular-weight heparin-induced thrombocytopenia is generally similar to that of unfractionated heparin-induced thrombocytopenia but can have a slower onset, more severe thrombocytopenia, and slower platelet count recovery. Given that low-molecular-weight heparin, of itself, is linked with heparin-induced thrombocytopenia pathophysiology and it can interact with most preexisting heparin-induced thrombocytopenia antibodies generated after exposure to unfractionated heparin, treatment of heparin-induced thrombocytopenia patients with low-molecular-weight heparin is contraindicated. SUMMARY: The risk of the development of heparin-induced thrombocytopenia with low-molecular-weight heparin treatment is reduced relative to the frequency of unfractionated heparin-induced thrombocytopenia, but it is not eliminated, and platelet counts should be monitored with treatment.
机译:审查目的:肝素诱导的血小板减少症是普通肝素治疗的严重副作用。低分子量肝素与肝素诱导的血小板减少症之间的关系还不太清楚。这篇综述将总结低分子量肝素诱导的血小板减少症与普通肝素诱导的血小板减少症之间的异同。最新发现:肝素/血小板因子4复合物抗体的发展引起的普通肝素诱导的血小板减少症的病理生理学对低分子量肝素仍然适用,因为后者的分子与糖基化的肝素相同。普通肝素。但是,由于分子量较小,低分子量肝素不像普通肝素那样有效地与血小板因子4和血小板相互作用。这意味着免疫致敏的风险降低了两倍到三倍(抗体生成和临床肝素诱导的血小板减少症的发生)。低分子量肝素诱导的血小板减少症抗体通常是免疫球蛋白A和免疫球蛋白M,与普通肝素诱导的血小板减少症产生的免疫球蛋白G抗体相反,后者通常与临床肝素诱导的血小板减少症有关。低分子量肝素诱导的血小板减少症的临床表达通常与普通肝素诱导的血小板减少症的临床表达相似,但起病速度较慢,血小板减少症更为严重,血小板计数恢复较慢。鉴于低分子量肝素本身与肝素诱导的血小板减少症的病理生理学相关,并且它可以与暴露于普通肝素后产生的大多数先前存在的肝素诱导的血小板减少症抗体相互作用,治疗肝素诱导的血小板减少症的低分子患者禁用肝素。总结:相对于普通肝素诱导的血小板减少症的发生频率,低分子量肝素治疗降低了肝素诱导的血小板减少症的风险,但并未消除,应通过治疗监测血小板计数。

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