Arthritis & rheumatology (Hoboken, N.J.) 2017-03
Progressive Decline of Lung Function in Rheumatoid Arthritis-Associated Interstitial Lung Disease.
Abstract
Objective
Interstitial lung disease (ILD) is associated with substantial morbidity in rheumatoid arthritis (RA), but very little is known about its long-term progression. This study was undertaken to investigate the progression of pulmonary disease using a large single-center cohort of patients with RA-associated ILD.
Methods
Records of all patients with RA-associated ILD seen at Mayo Clinic between 1998 and 2014, with at least 4 weeks follow-up and at least 1 pulmonary function test, were identified and manually screened for study inclusion. Progression was defined as a diffusing capacity for carbon monoxide (DLco) <40% predicted (or patients whose illness was too advanced to undergo screening) or a forced vital capacity (FVC) <50% predicted. Time to progression was analyzed using the Kaplan-Meier method.
Results
Of the 167 patients included in the study, 81 (49%) were female, with a mean ± SD age of 67 ± 10 years at diagnosis of ILD. Median follow-up time from diagnosis of ILD was 3.3 years (range 0.01-14.8). One-third of the patients required supplemental oxygen, 40% developed DLco <40% predicted, and 22% developed FVC <50% predicted within 5 years after ILD diagnosis. Usual interstitial pneumonia (UIP) versus nonspecific interstitial pneumonia (NSIP) was a risk factor for DLco progression (hazard ratio 3.29 [95% confidence interval 1.28-8.41]). Lower DLco and FVC at baseline increased the risk for progression to DLco <40% predicted and FVC <50% predicted, and higher rates of change in the first 6 months also increased the risk of progression.
Conclusion
Progressive loss of pulmonary function is common in RA-associated ILD and is worse in patients with UIP than in those with NSIP. Predictors of progression in patients with RA-associated ILD may aid clinicians in identifying patients at highest risk for progression of ILD.
Related Questions
What is your approach to using nintedanib in patients on baseline immunosuppression?
Typically I start antifibrotic therapy in a few situations: The most common reason is ILD progression despite adequate immune suppression, defined as no extra-pulmonary disease activity (usually joint disease, but can tailor according to the patient's disease/situation, such as by presence of rash, ...
When do you begin antifibrotic therapy for a patient with newly diagnosed ILD that is not IPF?
The evidence behind starting anti-fibrotic therapy for non-IPF ILD is largely based on the results of the INBUILD trial where patients who have non-IPF ILD who demonstrate progression (based on at least a 10% decline in FVC or a 5% decline in FVC with worsening symptoms or radiologic progression) ha...