title: Antiphospholipid antibodies during 6-month treatment with infliximab: a preliminary report.
abstract: 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.
  
  
  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.
authors.affiliation: Department of Clinical Immunology, Medical University of Lublin, Lublin, Poland.
authors.forename: Bogdan
authors.initials: B
authors.lastname: Kolarz
authors.affiliation: Department of Rheumatology and Connective Tissue Diseases, Medical University of Lublin, Lublin, Poland.
authors.forename: Maria
authors.initials: M
authors.lastname: Majdan
authors.affiliation: Department of Obstetrics and Gynecology, Medical University of Lublin, Lublin, Poland.
authors.forename: Dorota A
authors.initials: DA
authors.lastname: Darmochwal-Kolarz
authors.affiliation: Department of Rheummatology and Connective Tissue Diseases, Medical University of Lublin, Lublin, Poland.
authors.forename: Magdalena
authors.initials: M
authors.lastname: Dryglewska
mesh_terms: D000328:Adult; D017152:Antibodies, Antiphospholipid / Q000097:blood*; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000494:pharmacology; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D002308:Cardiolipins / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D000069285:Infliximab; D008297:Male; D008727:Methotrexate / Q000494:pharmacology; D008875:Middle Aged; D018709:Statistics, Nonparametric; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D053482:beta 2-Glycoprotein I / Q000276:immunology
chemical_list: D017152:Antibodies, Antiphospholipid; D000911:Antibodies, Monoclonal; D002308:Cardiolipins; D014409:Tumor Necrosis Factor-alpha; D053482:beta 2-Glycoprotein I; D000069285:Infliximab; D008727:Methotrexate