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自身免疫性肝素诱导的血小板减少症:经导管主动脉瓣置换术后的诊断与管理挑战

Autoimmune Heparin-Induced Thrombocytopenia: A Diagnostic and Management Challenge After Transcatheter Aortic Valve Replacement.

作者信息

Batool Aisha, Chaudhry Shahzad, Javaid Ayesha, Kenney Ashley

机构信息

Internal Medicine, Columbia St. Mary Hospital, Milwaukee, USA.

Family Medicine, Advocate Aurora Healthcare, Milwaukee, USA.

出版信息

Cureus. 2023 Sep 18;15(9):e45453. doi: 10.7759/cureus.45453. eCollection 2023 Sep.

DOI:10.7759/cureus.45453
PMID:37859883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10583616/
Abstract

Heparin-induced thrombocytopenia (HIT) is a commonly encountered condition, especially in inpatient settings, and is often attributed to high mortality and prolonged hospital stays. A rare entity, autoimmune heparin-induced thrombocytopenia (aHIT) refers to a condition in which antiplatelet factor-4 (PF4) antibodies activate platelets even in the absence of heparin. Our patient presented 12 days after transcatheter aortic valve replacement (TAVR) with altered mental status and severe thrombocytopenia. Further work-up revealed acute thromboembolic cerebrovascular accident (CVA),and the HIT antibody was positive. He was started on intravenous argatroban infusion with poor response. Platelet factor-4 antibodies were positive as well, and he was started on intravenous immunoglobulins (IVIG) therapy resulting in platelet recovery. This case is a reminder to consider autoimmune HIT, especially when platelet count fails to improve with conventional therapy.

摘要

肝素诱导的血小板减少症(HIT)是一种常见病症,尤其在住院患者中,常被认为与高死亡率和延长住院时间有关。一种罕见的自身免疫性肝素诱导的血小板减少症(aHIT)是指即使在没有肝素的情况下,抗血小板因子4(PF4)抗体也能激活血小板的病症。我们的患者在经导管主动脉瓣置换术(TAVR)后12天出现精神状态改变和严重血小板减少。进一步检查发现急性血栓栓塞性脑血管意外(CVA),且HIT抗体呈阳性。开始静脉输注阿加曲班,但反应不佳。血小板因子4抗体也呈阳性,于是开始静脉注射免疫球蛋白(IVIG)治疗,血小板得以恢复。该病例提醒我们要考虑自身免疫性HIT,尤其是在常规治疗后血小板计数未能改善的情况下。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/7fcaa970c98b/cureus-0015-00000045453-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/769ab7ab7899/cureus-0015-00000045453-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/59c26fa9c133/cureus-0015-00000045453-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/7fcaa970c98b/cureus-0015-00000045453-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/769ab7ab7899/cureus-0015-00000045453-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/59c26fa9c133/cureus-0015-00000045453-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e5/10583616/7fcaa970c98b/cureus-0015-00000045453-i03.jpg

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本文引用的文献

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Polyphosphate/platelet factor 4 complexes can mediate heparin-independent platelet activation in heparin-induced thrombocytopenia.多聚磷酸盐/血小板第4因子复合物可在肝素诱导的血小板减少症中介导不依赖肝素的血小板活化。
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Disruption of PF4/H multimolecular complex formation with a minimally anticoagulant heparin (ODSH).用一种具有最小抗凝血活性的肝素(ODSH)破坏 PF4/H 多分子复合物的形成。
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Experts' opinion or the serotonin release assay as a gold standard for the diagnosis of heparin-induced thrombocytopenia (HIT)?专家意见还是血清素释放试验作为肝素诱导的血小板减少症(HIT)诊断的金标准?
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