Management of heparin-induced thrombocytopenia with factor xa inhibitors: A systematic review

Heparin-induced thrombocytopenia (HIT) is a rare but severe prothrombotic disorder that develops in patients exposed to heparin products. Diagnosis is associated with significant morbidity and mortality. The mainstay of treatment for HIT involves discontinuing all heparin products and administering non-heparin anticoagulants. Since the publication of the American Society of Hematology (ASH) guidelines in 2018, factor Xa inhibitors have become an attractive alternative. We systematically reviewed the literature to determine the efficacy and safety of factor Xa inhibitors in managing HIT. We included any case series, retrospective, or prospective study that evaluated the efficacy of factor Xa inhibitors. We searched PubMed, Ovid, Embase, Cochrane Central Register of Controlled Trials, and Google Scholar from inception to September 2023. Three reviewers independently reviewed titles, abstracts, and full-text articles to determine eligibility using prespecified inclusion and exclusion criteria. Disagreements were resolved by discussion and consensus. Nine hundred sixty-four articles were screened against title and abstract, and 75 studies were selected for full-text review. Fifteen studies eventually met the inclusion criteria. Two hundred eighty-five patients across 15 studies were treated with factor Xa inhibitor. Across all study arms combined, HIT thrombosis-associated mortality was 0 % (n = 0), recurrent thrombosis was 4.56 % (n = 13), and major bleeding was 2.80 % (n = 8). Factor Xa inhibitors showed positive outcomes in HIT in terms of both safety and efficacy. Major limitation of this review is that the studies included are primarily retrospective and, thus, are subject to inherent limitations of observational study design. More randomized controlled trials (RCT) or prospective studies examining non-inferiority or superiority of transitioning to direct oral anticoagulant (DOAC) vs primary treatment with DOAC are needed.