Key result
Infliximab treatment for 6 months in patients with refractory rheumatoid arthritis was associated with a statistically significant increase in B2GP-I IgM antibodies (p<0.05).
Why the study?
Does infliximab treatment induce antiphospholipid antibodies in patients with refractory rheumatoid arthritis?
Cohort
Does infliximab treatment induce antiphospholipid antibodies in patients with refractory rheumatoid arthritis?
p-value: p=<0.05
Infliximab treatment in refractory rheumatoid arthritis is associated with a significant increase in B2GP-I IgM antibodies over 6 months, highlighting the need to monitor for signs of thromboembolism.
May prompt antiphospholipid antibody monitoring with infliximab in RA; leaves open thromboembolic risk and needs prospective confirmation.
BACKGROUND: The introduction of tumor necrosis factor (TNF) antagonists (adalimumab, infliximab, and etanercept) was a major advance and was highly important and beneficial in most rheumatoid arthritis (RA) patients. The adverse effects of this treatment are infrequent, but include opportunistic intracellular infection (especially the reactivation of latent Mycobacterium tuberculosis); exacerbation of demyelinating disorders; and the production of various types of antibodies such as antinuclear antibodies (ANA) or double-stranded DNA autoantibodies (dsDNA) and antiphospholipid antibodies (aPL) such as anti-cardiolipin antibodies (aCL) and anti-B2GP-I antibodies (B2GP-I). The aim of the study was to determine the prevalence of aCL and B2GP-I in IgM and IgG classes, using ELISA tests, during 6 months of follow-up in patients with refractory RA successfully treated with infliximab. MATERIAL/METHODS: We determined the prevalence of aCL and B2GP-I in IgM and IgG classes, using ELISA tests, during 6 months of follow-up in patients with refractory RA successfully treated with infliximab. RESULTS: We observed a statistically important increase only in the group of B2GP-I IgM (p<0.05). There are contradictory results concerning the ability of infliximab to induce aPL, but most authors confirm this phenomenon. CONCLUSIONS: Further investigations are needed to determine if the new aPL appears in patients with β2-GPI gene polymorphisms such as leucine-to-valine substitution at position 247, which can lead to a conformational changes in β2-GPI protein, leading to aPL synthesis. The role of aPL in pathogenesis of APS is still unclear, but we should remember the immunogenic aspect of TNF antagonist treatment. Therefore, we recommend early detection of aPL and observation of the patient, paying special attention to signs and symptoms of thromboembolism.
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A 2014 study conducted a cohort in Refractory rheumatoid arthritis (RA). Infliximab was evaluated on Prevalence of aCL and B2GP-I in IgM and IgG classes (p=<0.05). Infliximab treatment for 6 months in patients with refractory rheumatoid arthritis was associated with a statistically significant increase in B2GP-I IgM antibodies (p<0.05).
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