Rheumatoid arthritis (RA) is frequently associated with organ or non-organ-specific autoantibodies or overt autoimmune disorders. Aim of our study was to assess the prevalence and concentration of a panel of organ-specific autoantibodies in patients with RA and to evaluate their relationship with clinical manifestations and treatment efficacy.
Clinical and serological data from 20 patients with active RA (3M/17F), aged from 28 to 80 years and 50 healthy controls were analyzed. All patients fulfilled the 1987 American College of Rheumatology (ACR) classification criteria for RA and were treated with adalimumab and methotrexate. At baseline and after 6 months of therapy we tested anti-thyroid antibodies for thyroperoxidase (TPOAb) and thyroglobulin (TgAb) using an automated immunochemiluminescence assay (Immulite 2000, DPC, Los Angeles, CA), and anti-tissue transglutaminase (anti-tTG) using the ELISA assay (Phadia, Freiburg, Germany). Anti-smooth muscle (SMA), anti-liver kidney microsome (LKM), anti-parietal cells (APCA), anti-mitochondrial (AMA) and anti-liver cytosolic protein type 1 (LC1), anti-adrenal gland (ACA), anti-pancreatic islet (ICA) and anti-steroid-producing cell (stCA) antibodies were analyzed using a commercially available indirect immunofluorescence methods. Statistics were performed by the SPSS statistical software for Windows, using non parametric tests.
At baseline 6 out of 20 (30%) patients were positive for TPOAb and 8 (40%) for TgAb. After 6 months of treatment 5 (25%) patients had TPOAb and 8 (40%) TgAb. At baseline and after 6 months of treatment only 1 (5%) patient tested positive for IgA anti-tTG (celiac disease was confirmed by intestinal biopsy), and no patients had IgG anti-tTG. However, in RA patients IgG anti-tTG levels significantly increased during treatment (p = 0.017) and were higher than in healthy individuals both at baseline (p = 0.028) and after 6 months of treatment (p = 0.001). Only 1 (5%) patient was positive for APCA and no patient was positive for the other anti-organ-specific antibodies either at baseline or after 6 months of treatment.
The prevalence of organ-specific antibodies does not seem to change during anti-TNF treatment in RA patients. However, a slight and probably irrelevant increase of IgG anti-tTG antibody levels was observed.