Hsin-Hua Chen1,2,3,4,5, Ching-Heng Lin1,4,6,7, Tsu-Yi Hsieh2,8,9, Der-Yuan Chen5,10,11, Jia-Ching Ying12, Wen-Cheng Chao13,14. 1. Department of Medical Research. 2. Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital. 3. Institute of Biomedical Science and Rong Hsing Research Centre for Translational Medicine, Chung Hsing University. 4. Department of Industrial Engineering and Enterprise Information, Tunghai University. 5. School of Medicine, China Medical University, Taichung. 6. Department of Healthcare Management, National Taipei University of Nursing and Health Sciences, Taipei. 7. Department of Public Health, College of Medicine, Fu Jen Catholic University, New Taipei City. 8. Department of Medical Education, Taichung Veterans General Hospital. 9. PhD Programme of Business, Feng Chia University. 10. Rheumatology and Immunology Centre, China Medical University Hospital. 11. Translational Medicine Laboratory, Rheumatic Diseases Research Centre, China Medical University Hospital. 12. Department of Management Information Systems, National Chung Hsing University. 13. Department of Critical Care Medicine, Taichung Veterans General Hospital. 14. Department of Computer Science, Tunghai University, Taichung, Taiwan.
Abstract
OBJECTIVE: To assess the association of severe pulmonary arterial hypertension (PAH) with particulate matter <2.5 μm (p.m.2.5) and clinical data in patients with systemic autoimmune rheumatic diseases (SARDs). METHODS: We used the 2003-2017 nationwide data in Taiwan to identify patients with SARDs, including systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, dermatomyositis/polymyositis and primary Sjögren's syndrome. We identified 479 cases with severe PAH and selected controls matched (1:4) for age, sex, and index year. We used conditional logistic regression analysis to determine factors associated with risks for severe PAH shown as odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: We found that severe PAH was highly associated with interstitial lung disease (OR, 8.57; 95% CI: 5.52, 13.32), congestive heart failure (OR, 7.62; 95% CI: 5.02, 11.55), valvular heart disease (OR, 3.34; 95% CI: 2.03, 5.50) and slightly associated with thyroid diseases (OR, 1.88; 95% CI: 1.18, 3.00), but not the level of exposure to p.m.2.5. Increased risk for PAH was found in patients receiving corticosteroid (prednisolone equivalent dosage, mg/day, OR, 1.03; 95% CI: 1.01, 1.05), biologics (OR, 2.18; 95% CI: 1.15, 4.12) as well as immunosuppressants, including ciclosporin (OR, 2.17; 95% CI: 1.31, 3.59), azathioprine (OR, 1.96; 95% CI: 1.48, 2.61), cyclophosphamide (OR, 2.01; 95% CI: 1.30, 3.11) and mycophenolate mofetil/mycophenolic acid (OR, 2.42; 95% CI: 1.37, 4.27), and those with the highest level of insured amount (reference, lowest level; OR, 0.53; 95% CI: 0.34, 0.83). CONCLUSION: The population-based study identified risks for severe PAH in patients with SARDs, and these findings provide evidence for PAH risk stratification in patients with SARDs.
OBJECTIVE: To assess the association of severe pulmonary arterial hypertension (PAH) with particulate matter <2.5 μm (p.m.2.5) and clinical data in patients with systemic autoimmune rheumatic diseases (SARDs). METHODS: We used the 2003-2017 nationwide data in Taiwan to identify patients with SARDs, including systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, dermatomyositis/polymyositis and primary Sjögren's syndrome. We identified 479 cases with severe PAH and selected controls matched (1:4) for age, sex, and index year. We used conditional logistic regression analysis to determine factors associated with risks for severe PAH shown as odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: We found that severe PAH was highly associated with interstitial lung disease (OR, 8.57; 95% CI: 5.52, 13.32), congestive heart failure (OR, 7.62; 95% CI: 5.02, 11.55), valvular heart disease (OR, 3.34; 95% CI: 2.03, 5.50) and slightly associated with thyroid diseases (OR, 1.88; 95% CI: 1.18, 3.00), but not the level of exposure to p.m.2.5. Increased risk for PAH was found in patients receiving corticosteroid (prednisolone equivalent dosage, mg/day, OR, 1.03; 95% CI: 1.01, 1.05), biologics (OR, 2.18; 95% CI: 1.15, 4.12) as well as immunosuppressants, including ciclosporin (OR, 2.17; 95% CI: 1.31, 3.59), azathioprine (OR, 1.96; 95% CI: 1.48, 2.61), cyclophosphamide (OR, 2.01; 95% CI: 1.30, 3.11) and mycophenolate mofetil/mycophenolic acid (OR, 2.42; 95% CI: 1.37, 4.27), and those with the highest level of insured amount (reference, lowest level; OR, 0.53; 95% CI: 0.34, 0.83). CONCLUSION: The population-based study identified risks for severe PAH in patients with SARDs, and these findings provide evidence for PAH risk stratification in patients with SARDs.