Patients with rheumatoid arthritis (RA), Crohn's disease (CD) and spondyloarthritis (SpA) treated with selective tumor necrosis factor-alpha (TNFα) inhibitors may develop autoantibodies such as antinuclear antibodies (ANAs) and anti-double-stranded DNA (anti-dsDNA) antibodies. According to the available safety data, 63.8% of CD patients and 49.1% of RA patients develop newly positive ANAs during infliximab treatment, and respectively 13 and 21.5% develop newly positive anti-dsDNA antibodies; the percentages are lower in patients treated with etanercept. We have recently reported that ANA and anti-dsDNA, but not anti-phospholipid (anti-aPL), antibodies can be induced by adalimumab, but to a lesser extent than other TNFα blocking agents. Interestingly, these autoantibodies have been only anecdotally associated with clinical manifestations suggesting drug-induced systemic lupus erythematosus (SLE). It was thought that the absence of such an association was related to the IgM or IgA isotypes of anti-dsDNA antibodies, as well as to low antibody affinity. Anti-phospholipid antibodies, which are mainly detectable by means of an anti-cardiolipin assay (aCL), have also been found in RA patients receiving TNF-blockers. In some cases, their appearance has been related to concomitant infectious processes but one paper suggests that they may predict a poor clinical outcome, no clear correlation has been found with the specific clinical manifestations of anti-aPL syndrome. There have also been reports on the development of anti-drug antibodies.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)