Autoimmune heparin-induced thrombocytopenia and venous limb gangrene after aortic dissection repair: in vitro and in vivo effects of intravenous immunoglobulin
Research article published in Transfusion (2019)
Abstract
BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder characterized by heparin-dependent antibodies that activate platelets (PLTs) via PLT FcγIIa receptors. "Autoimmune" HIT (aHIT) indicates a HIT subset where thrombocytopenia progresses or persists despite stopping heparin; aHIT sera activate PLTs strongly even in the absence of heparin (heparin-independent PLT-activating properties). Affected patients are at risk of severe complications, including dual macro- and microvascular thrombosis leading to venous limb gangrene. High-dose intravenous immunoglobulin (IVIG) offers an approach to interrupt heparin-independent PLT-activating effects of aHIT antibodies. CASE REPORT: A 78-year-old male who underwent cardiopulmonary bypass for aortic dissection developed aHIT, disseminated intravascular coagulation, and deep vein thrombosis; progression to venous limb gangrene occurred during partial thromboplastin time (PTT)-adjusted bivalirudin infusion (underdosing from "PTT confounding"). Thrombocytopenia recovered with high-dose IVIG, although the PLT count increase began only after the third dose of a 5-day IVIG regimen (0.4 g/kg/day × 5 days). We reviewed case reports and case series of IVIG for treating HIT, focusing on various IVIG dosing regimens used. RESULTS: Patient serum-induced PLT activation was inhibited in vitro by IVIG in a dose-dependent fashion; inhibition of PLT activation by IVIG was much more marked in the absence of heparin versus the presence of heparin (0.2 U/mL). Our literature review indicated 1 g/kg × 2 IVIG dosing as most common for treating HIT, usually associated with rapid PLT count recovery. CONCLUSION: Our clinical and laboratory observations support dose-dependent efficacy of IVIG for decreasing PLT activation and thus correcting thrombocytopenia in aHIT. Our case experience and literature review suggests dosing of 1 g/kg IVIG × 2 for patients with severe aHIT.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
Peer-reviewed clinical and outcomes research relevant to anticoagulation, leech therapy, and microsurgical flap management. Indexed in PubMed and verified against the NCBI record.
Why This Matters for Hirudotherapy
This case report with accompanying literature review describes a 78-year-old man who developed autoimmune heparin-induced thrombocytopenia (aHIT) with DIC, deep vein thrombosis, and venous limb gangrene after aortic dissection repair; thrombocytopenia recovered with high-dose IVIG, in vitro testing showed IVIG inhibited platelet activation dose-dependently (more so without heparin), and the authors suggest 1 g/kg x 2 dosing for severe aHIT. It is pertinent to hirudotherapy because the patient's gangrene progressed during PTT-adjusted bivalirudin (a direct thrombin inhibitor in the same mechanistic class as the leech-derived anticoagulant hirudin), illustrating both the appeal and the dosing pitfalls of direct thrombin inhibition. As a single case plus narrative review, the findings are hypothesis-generating rather than definitive, the in vitro IVIG effect needs controlled confirmation, and nothing here bears on leech therapy itself.
Citation
Autoimmune heparin-induced thrombocytopenia and venous limb gangrene after aortic dissection repair: in vitro and in vivo effects of intravenous immunoglobulin.
Arcinas et al. · Transfusion, 2019
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