Abstract
BackgroundHeparin-induced thrombocytopenia is caused by antibodies (Abs) specific to platelet factor 4 (PF4)/heparin complexes. In this study, we evaluated the rates of seroconversion of anti-PF4/heparin Ab between patients with rheumatoid arthritis (RA) and with osteoarthritis (OA) who underwent total knee arthroplasty.MethodsThe subjects of this randomized controlled trial were 124 patients who underwent total knee arthroplasty (TKA) and received edoxaban with or without a foot pump as thromboprophylaxis. We measured anti-PF4/heparin Abs before and 10 days after surgery, as well as preoperative PF4, using commercially available ELISAs. We also used the database of J-PSVT, a hospital-based, prospective cohort study designed to document the effectiveness of thromboprophylactic agents during arthroplasty.ResultsThe rates of seroconversion to anti-PF4/heparin Ab were lower in RA patients (4.0 %) than in OA patients (25.5 %). The anti-PF4/heparin IgG optical density (OD) values did not differ before and after surgery in RA patients. In contrast, there was a significant increase in anti-PF4/heparin IgG OD values in OA patients after TKA. In the J-PSVT data, the postoperative seroconversion rates of anti-PF4/heparin Ab were lower in RA patients (10.4 %) than in OA patients (21.8 %) who received fondaparinux. The titers of anti-CCP Ab were significantly lower in RA patients with postoperative ant-PF4/heparin Ab compared with those without postoperative ant-PF4/heparin Ab There was no significant difference in preoperative PF4 levels between RA patients and OA patients. The heparin-binding affinity of the circulating PF4 was similar between RA patients and OA patients; however, the IgG fractions isolated from the sera of RA patients contained PF4 more frequently (69.2 %) than those from OA patients (10.2 %).ConclusionsOur results showed a reduced likelihood of postoperative anti-PF/heparin Ab production in RA patients compared with OA patients. This suggests that the mechanisms underlying the anti-PF4 immune response in RA patients differ from the mechanisms of the anti-PF4/heparin immune response seen in OA patients after joint replacement.Trial registrationISRCTN 18090286. Registered 8 July 2016
Highlights
Heparin-induced thrombocytopenia is caused by antibodies (Abs) specific to platelet factor 4 (PF4)/ heparin complexes
The primary aim of the J-PSVT was to determine the rates of Venous thromboembolism (VTE) and seroconversion rates of anti-PF4/heparin Ab in patients undergoing total knee arthroplasty (TKA) and total hip arthroplasty (THA), with all patients evaluated for the presence of all Deep vein thrombosis (DVT) on postoperative day (POD) 10
In rheumatoid arthritis (RA) patients, the use of prednisolone or methotrexate did not associate with the Discussion In this study we examined the differences in the rates of seroconversion to anti-PF4/heparin Ab positive status between patients with OA and with RA who underwent TKA
Summary
Heparin-induced thrombocytopenia is caused by antibodies (Abs) specific to platelet factor 4 (PF4)/ heparin complexes. Heparin-induced thrombocytopenia (HIT) is an immunemediated disorder that can develop during anticoagulant therapy with heparin [1]. HIT is associated with antibodies (Abs) that recognize the complexes formed between platelet factor 4 (PF4) and heparin [2]. Anti-PF4/heparin Abs can be induced in patients who have undergone major surgery, even without any exposure of unfractionated heparin [6]. The development of HIT has been associated with postoperative thromboprophylaxis with fondaparinux, a factor Xa inhibitor [7]. Anti-PF4/heparin IgG Abs are generated in approximately 20 % of patients undergoing total knee arthroplasty (TKA) [10]. In addition to the administration of heparin for anticoagulation during thromboprophylaxis, TKA poses a substantial challenge to the immune system because of mechanical damage to articular connective tissue [11]
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