“Autoimmune HIT” antibodies in diagnostic samples are a potential artifact and not associated with more severe outcomes

Kanack, Adam J.; Athale, Janhavi; Leger, Rachel R.; Saadalla, Abdul; Heikal, Nahla M.; Chen, Dong; Garcia, David A.; Singh, Ravinder; Pruthi, Rajiv K.; Padmanabhan, Anand

doi:10.1182/bloodadvances.2023009811

Cited by 2 publications

(2 citation statements)

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“…An important technical issue raised by Kanack and colleagues [191] is to what extent false-positive diagnoses of aHIT may be made based on the presence of residual heparin in diagnostic samples. This is relevant because unaccounted for residual heparin could result in inadvertent detection of heparin-dependent antibodies.…”

Section: Technical Challengesmentioning

confidence: 99%

“…Further, one study [58] found residual heparin (at least 0.1 IU/mL) was present in 62% of samples referred for HIT testing. Approaches to minimize the false-positive detection of aHIT antibodies include either treatment of the sample with heparinase or to require a prolonged period (perhaps at least 12 h) from discontinuation of heparin to blood sampling [191]. Despite these reservations, Kanack and colleague did comment that some samples-including those of patients with SpHIT-do exhibit "true aHIT" with heparin-independent platelet activation.…”

Section: Technical Challengesmentioning

confidence: 99%

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Autoimmune Heparin-Induced Thrombocytopenia

Warkentin

2023

JCM

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Autoimmune thrombocytopenia (aHIT) is a severe subtype of heparin-induced thrombocytopenia (HIT) with atypical clinical features caused by highly pathological IgG antibodies (“aHIT antibodies”) that activate platelets even in the absence of heparin. The clinical features of aHIT include: the onset or worsening of thrombocytopenia despite stopping heparin (“delayed-onset HIT”), thrombocytopenia persistence despite stopping heparin (“persisting” or “refractory HIT”), or triggered by small amounts of heparin (heparin “flush” HIT), most cases of fondaparinux-induced HIT, and patients with unusually severe HIT (e.g., multi-site or microvascular thrombosis, overt disseminated intravascular coagulation [DIC]). Special treatment approaches are required. For example, unlike classic HIT, heparin cessation does not result in de-escalation of antibody-induced hemostasis activation, and thus high-dose intravenous immunoglobulin (IVIG) may be indicated to interrupt aHIT-induced platelet activation; therapeutic plasma exchange may be required if high-dose IVIG is ineffective. Also, aHIT patients are at risk for treatment failure with (activated partial thromboplastin time [APTT]-adjusted) direct thrombin inhibitor (DTI) therapy (argatroban, bivalirudin), either because of APTT confounding (where aHIT-associated DIC and resulting APTT prolongation lead to systematic underdosing/interruption of DTI therapy) or because DTI inhibits thrombin-induced protein C activation. Most HIT laboratories do not test for aHIT antibodies, contributing to aHIT under-recognition.

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Section: Technical Challengesmentioning

confidence: 99%

Section: Technical Challengesmentioning

confidence: 99%