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.
Resumen
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.
Por qué esto importa para la hirudoterapia
Este estudio prospectivo unicéntrico de 158 pacientes neurocríticos sometidos a recambio plasmático terapéutico anticoagulado con heparin encontró que cuatro desarrollaron trombocitopenia inducida por heparin tipo II (HIT) con trombosis venosa profunda, recuperándose solo después de la retirada de heparin y el cambio a agentes sin heparin como argatroban o fondaparinux. Para ASH, el valor es contextual: documenta una limitación real de heparin, la reacción de HIT inmunomediada, lo cual es parte de la razón por la que el campo continúa explorando mecanismos anticoagulantes alternativos, incluida la vía de inhibición directa de la trombina representada por la hirudin derivada de sanguijuelas que no depende del eje heparin–PF4. Salvedad honesta: esta es una serie observacional pequeña y unicéntrica sobre la seguridad de heparin y el manejo de HIT; no prueba ni menciona la hirudoterapia ni ningún agente derivado de sanguijuelas, por lo que cualquier vínculo con el secretoma de la sanguijuela es solo un trasfondo interpretativo.
Citación
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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Añadido a la biblioteca ASH: May 28, 2026 · Última actualización del sitio: June 18, 2026