Therapeutic plasma exchange in severe refractory autoimmune heparin‐induced thrombocytopenia with thrombosis

Bavli, Natalie; Christensen, Bradley; Sarode, Ravindra; Hofmann, Sandra L.; Ibrahim, Ibrahim

doi:10.1111/bjh.17917

Cited by 2 publications

(3 citation statements)

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“…These three patients also developed thrombotic complications: right coronary artery thrombotic occlusion resulting in STEMI [129], DVT complicated by transmetatarsal limb amputation [130], and DVT with saddle PE [131]; indirect support for heparin flush HIT being an aHIT disorder was seen in the case reported by McKenzie and colleagues [129], where prolonged thrombocytopenia eventually resulted in application of high-dose IVIG (discussed subsequently). It is notable that high-dose IVIG was not effective in the report by Bavli et al [130], with plasma exchange being required for platelet count recovery.…”

Section: Heparin Flushes During Stem Cell Transplantationmentioning

confidence: 93%

“…Overall, nine (64.3%) of the 14 patients identified in these reports [55,[127][128][129][130][131] of heparin flush HIT in the context of stem cell transplantation developed one or more thrombotic events.…”

Section: Heparin Flushes During Stem Cell Transplantationmentioning

confidence: 98%

“…In addition, three other single case reports [129][130][131] of HIT complicating heparin flush administration in the context of preparation for stem cell transplantation have been reported; these reports also noted the use of G-CSF (filgrastim), with two patients also receiving plerixafor (agent that mobilizes peripheral blood stem cells); together with the 4% frequency of HIT in the context of heparin flush exposure mentioned earlier, these observations suggest that the proinflammatory effects of these agents may dramatically increase the frequency of HIT for what otherwise would be a rare occurrence. These three patients also developed thrombotic complications: right coronary artery thrombotic occlusion resulting in STEMI [129], DVT complicated by transmetatarsal limb amputation [130], and DVT with saddle PE [131]; indirect support for heparin flush HIT being an aHIT disorder was seen in the case reported by McKenzie and colleagues [129], where prolonged thrombocytopenia eventually resulted in application of high-dose IVIG (discussed subsequently). It is notable that high-dose IVIG was not effective in the report by Bavli et al [130], with plasma exchange being required for platelet count recovery.…”

Section: Heparin Flushes During Stem Cell Transplantationmentioning

confidence: 98%

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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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