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Updated: Mar 25, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Evaluation of Amikacin Mediated Platelet Aggregate Dissociation in Multi-Anticoagulant-Dependent
Bo Wang1, Junwen Liu2, Wenying Yao1
1Department of Clinical Laboratory, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Abstract:
Anticoagulant-dependent pseudothrombocytopenia (PTCP) is an in vitro artifact that leads to falsely low platelet counts. To evaluate the efficacy of Amikacin in reversing platelet (PLT) clumping induced by various anticoagulants, including EDTA, heparin, and sodium citrate. we collected 26 blood samples demonstrating EDTA-dependent pseudothrombocytopenia. Amikacin solution (50 μL of 50 mg/L) was added to 500 μL of whole blood from each sample. Complete blood count (CBC) analysis was performed at 5, 30, 60, 240 min, and 24 h post-treatment. Additionally, five samples exhibiting PLT aggregation dependent on multiple anticoagulants (EDTA, heparin, and sodium citrate) were treated with Amikacin, and PLT counts were compared across the different anticoagulant tubes. For the Amikacin-treated EDTA tubes, differential leukocyte counts (DLC) were analyzed and compared with untreated controls, with validation by flow cytometry. Amikacin treatment significantly increased PLT counts in EDTA-dependent samples compared with untreated controls (p < 0.001), with the maximum effect observed at 240 min. In samples with multi-anticoagulant dependency, PLT counts in heparin- and sodium citrate-anticoagulated tubes remained significantly lower than those in EDTA tubes after Amikacin treatment (p < 0.01). Furthermore, in Amikacin-treated EDTA blood, the proportions of neutrophils and basophils were significantly increased (p < 0.0001), whereas the proportions of lymphocytes and monocytes decreased (p < 0.01). Amikacin effectively reverses EDTA-dependent PLT clumping within 240 min, but only partially resolves aggregation induced by heparin or sodium citrate. Moreover, the use of Amikacin in EDTA-anticoagulated blood compromises the accuracy of CBC differential counts, rendering such samples unsuitable for routine hematological analysis.
Insights
Amikacin effectively reverses EDTA-dependent platelet clumping, improving accuracy in pseudothrombocytopenia testing. However, it partially resolves heparin/citrate-induced clumping and impacts differential white blood cell counts.
Area of Science:
- Hematology
- Clinical Pathology
- Laboratory Medicine
Background:
- Anticoagulant-dependent pseudothrombocytopenia (PTCP) causes falsely low platelet counts.
- Platelet clumping is a common artifact in laboratory diagnostics.
Purpose of the Study:
- To assess Amikacin's efficacy in reversing platelet clumping induced by EDTA, heparin, and sodium citrate.
- To evaluate the impact of Amikacin on complete blood count differential analysis.
Main Methods:
- Collected blood samples with EDTA-dependent pseudothrombocytopenia.
- Treated samples with Amikacin and performed complete blood count analysis at various time points.
- Analyzed platelet counts in samples with multi-anticoagulant dependency and validated differential leukocyte counts via flow cytometry.
Main Results:
- Amikacin significantly increased platelet counts in EDTA-dependent samples within 240 minutes.
- Platelet counts remained lower in heparin- and sodium citrate-treated samples compared to EDTA.
- Amikacin use altered differential leukocyte proportions, compromising accuracy.
Conclusions:
- Amikacin effectively reverses EDTA-dependent platelet clumping but has limited effect on heparin or citrate-induced aggregation.
- Amikacin treatment in EDTA-anticoagulated blood interferes with accurate CBC differential counts, making samples unsuitable for routine analysis.
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