ABSTRACT
<p><b>OBJECTIVES</b>The aim of this study was to detect anti-topoisomerase I (anti-topo I) autoantibodies, which are known to be limited in systemic sclerosis patients, in silicosis patients with no clinical symptoms of autoimmune disease.</p><p><b>METHODS</b>Serum anti-topo I autoantibodies were detected using ELISA. Differences in clinical parameters between patients with and without anti-topo I autoantibodies were analyzed.</p><p><b>RESULTS</b>Seven of 69 patients had anti-topo I autoantibodies. These 7 patients showed elevated PaCO(2) values (P=0.0212), and inverse correlations between serum soluble Fas levels and PaCO(2) values were found.</p><p><b>CONCLUSION</b>Anti-topo I autoantibodies were detected in 10.1% of silicosis patients without any clinical symptoms of autoimmune disease. The findings here suggest that the genesis of anti-topo I autoantibodies might be related to pulmonary involvement or lung fibrosis associated with progression of silicosis.</p>
ABSTRACT
Objectives: The aim of this study was to detect anti-topoisomerase l (anti-topo I) autoantibodies, which are known to be limited in systemic sclerosis patients, in silicosis patients with no clinical symptoms of autoimmune disease. Methods: Serum anti-topo I autoantibodies were detected using ELISA. Differences in clinical parameters between patients with and without anti-topo I autoantibodies were analyzed. Results: Seven of 69 patients had anti-topo I autoantibodies. These 7 patients showed elevated PaCO2 values (P=0.0212), and inverse correlations between serum soluble Fas levels and PaCO2 values were found. Conclusion: Anti-topo I autoantibodies were detected in 10.1% of silicosis patients without any clinical symptoms of autoimmune disease. The findings here suggest that the genesis of anti-topo l autoantibodies might be related to pulmonary involvement or lung fibrosis associated with progression of silicosis.