重症ITP合并EDTA、肝素钠、枸橼酸钠抗凝剂同时依赖性假性血小板减少一例及文献复习
A Case Report of Severe ITP Complicated with Pseudothrombocytopenia Due to Simultaneous Dependence on Anticoagulants Such as EDTA, Sodium Heparin, and Sodium Citrate and Literature Review

目的：本文报道一例罕见的重症原发免疫性血小板减少症(ITP)患者治疗过程中合并EDTA、肝素钠、枸橼酸钠抗凝剂同时依赖性假性血小板减少的病例，分析与探讨其病因，为临床工作提供处理预案及经验指导。方法：通过静脉采血同时送EDTA-K2抗凝管、肝素钠抗凝管和枸橼酸钠(1:9)抗凝管至血细胞分析仪进行PLT计数，手指末梢血采血立即手工稀释计数法作为对比。回顾性分析该例临床资料，结合文献复习探讨其发生可能的原因。结果：该例ITP患者使用EDTA-K2抗凝管、肝素钠抗凝管、枸橼酸钠(1:9)抗凝管的PLT计数分别为6.00 × 10⁹/L、9.00 × 10⁹/L、7.00 × 10⁹/L，手指末梢血校正手工稀释计数为PLT 32.00 × 10⁹/L。患者ITP出血评分5分，重症ITP合并EDTA、肝素钠、枸橼酸钠抗凝剂同时依赖性假性血小板减少诊断明确，其原因可能与自身免疫性疾病及EDTA螯合、诱导血小板活化等机制相关，临床发生率极低，很容易误诊、漏诊，影响后续治疗，需要予以关注。结论：对于重症ITP患者治疗后血小板仍低的情况，除考虑治疗效果不理想外同时需要考虑合并EDTA、肝素钠、枸橼酸钠抗凝剂依赖性假性血小板减少的可能，需结合临床表现及时手工计数校正，可以减少临床误诊、漏诊。
Objective: This article reports a rare case of severe primary immune thrombocytopenia (ITP) complicated with EDTA, sodium heparin, and sodium citrate anticoagulant-dependent pseudothrombocytopenia during treatment, shares and discusses its etiology, and provides treatment plans and experience guidance for clinical work. Methods: Venous blood was collected and sent to the blood cell analyzer for PLT counting in EDTA-K2 anticoagulant tubes, sodium heparin anticoagulant tubes, and sodium citrate (1:9) anticoagulant tubes. Finger-end blood sampling and immediate manual dilution counting were used as a comparison. The clinical data of this case were retrospectively analyzed, and the possible causes of its occurrence were discussed in combination with literature review. Results: The PLT counts of the ITP patient using EDTA-K2 anticoagulant tube, heparin sodium anticoagulant tube, and sodium citrate (1:9) anticoagulant tube were 6 × 10⁹/L, 9 × 10⁹/L, and 7 × 10⁹/L, respectively. The PLT count of fingertip blood corrected for manual dilution was 32 × 10⁹/L. The ITP bleeding score of the patient was 5 points, and the diagnosis of severe ITP combined with EDTA, heparin sodium, and sodium citrate anticoagulant-dependent pseudothrombocytopenia was clear. The cause may be related to autoimmune diseases and EDTA chelation, induction of platelet activation and other mechanisms. The clinical incidence is extremely low, and it is easy to misdiagnose and miss, which affects subsequent treatment and needs attention. Conclusion: For patients with severe ITP whose platelet count remains low after treatment, in addition to considering the unsatisfactory treatment effect, the possibility of EDTA, sodium heparin, and sodium citrate anticoagulant-dependent pseudothrombocytopenia should also