Clinical Analysis of Heparin-Induced Thrombocytopenia due to Therapeutic Plasmapheresis With Heparin Anticoagulation
Research article published in Seminars in dialysis (2025)
Abstract
OBJECTIVE: We investigated the clinical characteristics and treatment outcomes of heparin-induced thrombocytopenia (HIT) following therapeutic plasma exchange (TPE) with heparin anticoagulation in patients with neurological autoimmune diseases. METHODS: Clinical data were prospectively collected from 158 patients (79 males, 79 females; mean age 37.49 ± 16.95 years) with neurological autoimmune diseases who underwent TPE in the neuro-intensive care unit between January 2016 and June 2024. For patients with continuous platelet decline after TPE, the 4Ts score was determined, and platelet factor 4 (PF4) antibody tests were performed. Their platelet counts, clinical complications (thrombosis and bleeding), treatment plans, outcomes, and prognoses before and after TPE were analyzed. RESULTS: One hundred thirty-nine patients experienced at least one significant decrease in platelet count during TPE (average decrease 36.75 ± 19.63%), and the average 4Ts score was 3.55 ± 1.87 points. PF4 antibody testing was conducted on 23 patients with continuous platelet decline and 4Ts scores ≥ 4. Four PF4-positive patients were diagnosed with type II HIT and developed deep vein thrombosis. After heparin withdrawal, the platelet count gradually normalized after intravenous immunoglobulin (IVIG), nonheparin TPE, or argatroban/fondaparinux anticoagulant therapy (mean recovery time 8.17 ± 3.54 days). The platelet counts spontaneously recovered for the remaining 116 patients (mean recovery time 3.88 ± 2.66 days). CONCLUSION: Platelet counts should be dynamically monitored throughout TPE with heparin anticoagulation. Patients with continually decreasing platelet counts and an intermediate to high 4Ts score should be monitored for HIT. Heparin should be discontinued immediately for patients with type II HIT, and nonheparin anticoagulants, IVIG, or nonheparin TPE may be administered.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
We investigated the clinical characteristics and treatment outcomes of heparin-induced thrombocytopenia (HIT) following therapeutic plasma exchange (TPE) with heparin anticoagulation in patients with neurological autoimmune diseases.
Why This Matters for Hirudotherapy
This study prospectively collected clinical data from 158 patients with neurological autoimmune diseases who underwent therapeutic plasma exchange (TPE) with heparin anticoagulation in a neuro-intensive care unit, identifying four patients diagnosed with type II heparin-induced thrombocytopenia (HIT) who developed deep vein thrombosis. The findings highlight the ongoing clinical challenge of HIT and the critical need for effective non-heparin anticoagulant alternatives—a therapeutic area where direct thrombin inhibitors derived from or modeled on medicinal-leech hirudin, including lepirudin, desirudin, and bivalirudin, have historically contributed. The study documents HIT occurrence during heparin-anticoagulated TPE and clinical management with non-heparin agents, providing context relevant to understanding when hirudin-based anticoagulants may be clinically indicated. However, this study used argatroban or fondaparinux as alternative anticoagulants and did not specifically investigate hirudin-derived agents, so it provides no direct evidence of their efficacy in this setting.
Citation
Clinical Analysis of Heparin-Induced Thrombocytopenia due to Therapeutic Plasmapheresis With Heparin Anticoagulation.
Lv C et al. · Seminars in dialysis, 2025
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