OBJECTIVE: [corrected] Systemic lupus erythematosus has been associated with false positive autoantibodies for primary biliary cirrhosis, chronic active hepatitis, Sjogren's syndrome, rheumatoid arthritis, thyroid disorders, syphilis, and scleroderma. An increased prevalence of autoantibodies are found in celiac disease and systemic lupus erythematosus, which share the human lymphocyte HLA-B8 and HLA-DR3 histocompatibility antigens. This study examines the prevalence of celiac disease autoantibodies in systemic lupus erythematosus patients. METHODS: Patients observed in the Department of Rheumatology at our institutions in San Antonio, Texas with known systemic lupus erythematosus were offered participation in the study. One hundred three of the 130 patients contacted agreed to participate. Patients were excluded if they were pregnant or medically unable to undergo endoscopy. All volunteers were tested for the serological presence of IgA and IgM antigliadin and IgA antiendomysial antibodies. Those with positive serology underwent esophagogastroduodenoscopy with duodenal mucosal biopsy. RESULTS: Twenty-four of 103 (23.3%) systemic lupus erythematosus patients tested positive for either antigliadin antibody, whereas none of the 103 patients tested positive for antiendomysial antibody. None of the 24 antigliadin positive patients were found to have endoscopic or histological evidence of celiac disease, making the false positive rate of antigliadin antibody 23%. CONCLUSION: The presence of false positive antigliadin antibodies in patients with systemic lupus erythematosus is common. Despite shared human lymphocyte antigen loci there does not seem to be an association between celiac disease and systemic lupus erythematosus.
OBJECTIVE: [corrected] Systemic lupus erythematosus has been associated with false positive autoantibodies for primary biliary cirrhosis, chronic active hepatitis, Sjogren's syndrome, rheumatoid arthritis, thyroid disorders, syphilis, and scleroderma. An increased prevalence of autoantibodies are found in celiac disease and systemic lupus erythematosus, which share the human lymphocyte HLA-B8 and HLA-DR3 histocompatibility antigens. This study examines the prevalence of celiac disease autoantibodies in systemic lupus erythematosuspatients. METHODS:Patients observed in the Department of Rheumatology at our institutions in San Antonio, Texas with known systemic lupus erythematosus were offered participation in the study. One hundred three of the 130 patients contacted agreed to participate. Patients were excluded if they were pregnant or medically unable to undergo endoscopy. All volunteers were tested for the serological presence of IgA and IgM antigliadin and IgA antiendomysial antibodies. Those with positive serology underwent esophagogastroduodenoscopy with duodenal mucosal biopsy. RESULTS: Twenty-four of 103 (23.3%) systemic lupus erythematosuspatients tested positive for either antigliadin antibody, whereas none of the 103 patients tested positive for antiendomysial antibody. None of the 24 antigliadin positive patients were found to have endoscopic or histological evidence of celiac disease, making the false positive rate of antigliadin antibody 23%. CONCLUSION: The presence of false positive antigliadin antibodies in patients with systemic lupus erythematosus is common. Despite shared human lymphocyte antigen loci there does not seem to be an association between celiac disease and systemic lupus erythematosus.