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肝素诱导的血小板减少症:一种伴有皮肤坏死的罕见表现。

Heparin-induced thrombocytopenia: a rare presentation with skin necrosis.

作者信息

David Filipa, Trigo Ana Catarina, Ribeiro José, Cancela Joana

机构信息

Internal Medicine Service, Medical Department, Hospital Pedro Hispano, Matosinhos, Portugal.

出版信息

Dermatol Reports. 2023 Oct 16;16(3):9855. doi: 10.4081/dr.2023.9855. eCollection 2024 Sep 2.

Abstract

Heparin-induced thrombocytopenia is the most clinically relevant non-hemorrhagic complication of heparin and is characterized by the presence of anti-platelet factor 4 (PF4)/heparinimmunoglobulin G (IgG) antibodies. The circulating PF4/heparinIgG immune complex binds to platelets their FcyIIa receptors, activating them and promoting their aggregation, with consequent platelet consumption, thrombocytopenia, and thrombotic phenomena. Despite thrombocytopenia, this condition is not typically associated with bleeding complications. Instead, thrombosis is the most serious complication of heparin-induced thrombocytopenia, contributing to increased morbidity and mortality. Thrombotic events can be venous and arterial, such as deep vein thrombosis, pulmonary embolism, myocardial infarction, and thrombotic stroke. Skin necrosis at the site of heparin injections is a rare but well-described manifestation of heparin-induced thrombocytopenia. We report a case of heparin-induced thrombocytopenia presented as skin necrosis, highlighting the importance of recognizing this potentially fatal condition and the need for an immediate cessation of all sources of heparin and its replacement by other anticoagulants.

摘要

肝素诱导的血小板减少症是肝素最具临床相关性的非出血性并发症,其特征是存在抗血小板因子4(PF4)/肝素免疫球蛋白G(IgG)抗体。循环中的PF4/肝素IgG免疫复合物与血小板及其FcyIIa受体结合,激活血小板并促进其聚集,进而导致血小板消耗、血小板减少和血栓形成现象。尽管存在血小板减少症,但这种情况通常与出血并发症无关。相反,血栓形成是肝素诱导的血小板减少症最严重的并发症,会导致发病率和死亡率增加。血栓事件可以是静脉性和动脉性的,如深静脉血栓形成、肺栓塞、心肌梗死和血栓性中风。肝素注射部位的皮肤坏死是肝素诱导的血小板减少症一种罕见但已被充分描述的表现。我们报告了一例以皮肤坏死为表现的肝素诱导的血小板减少症病例,强调了认识这种潜在致命疾病的重要性以及立即停用所有肝素来源并改用其他抗凝剂的必要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/333d/11616585/52f40cb93672/dr-16-3-9855-g001.jpg

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