Kluanwan, Yanisa

Abstract RATIONALE: Pulmonary fibrosis is recognized as the end result of multiple and recurrent pathways of lung injury. However, the role of chronic inflammation in non-idiopathic pulmonary fibrosis fibrotic interstitial lung disease (non-IPF f-ILD) remains inconclusive, as acute responses to anti-inflammatory treatment may vary. A reliable predictor for identifying patients who stand to benefit from treatment may be helpful for improving or sustaining lung function and avoiding adverse treatment effects. Our study aims to assess whether initial serum inflammatory markers, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), in the absence of clinically suspected infection or other causes of inflammation, are predictive of therapeutic response to anti-inflammatory medications in non-IPF f-ILD. METHODS: We performed a retrospective study comparing treatment response to anti-inflammatory therapy in non-IPF f-ILD stratified by initial CRP or ESR levels. Treatment was defined as corticosteroid or steroid-sparing agent for three months or more with lung function response defined as: 1) relative increase in percent predicted forced vital capacity (FVC%) > 5% in 6 months or > 10% or greater in 12 months; or 2) no change or any increase in FVC% if FVC% was declining prior to treatment initiation (relative decline in FVC% > 5% in the prior 6 months or > 10% in the prior 12 months). Logistic regression was used to predict treatment response as stratified by high vs low-to-normal inflammatory markers, with a mixed model for repeated measures for comparing FVC% change while treated. RESULTS: One hundred sixty-seven non-IPF f-ILD pts received anti-inflammatory therapy with baseline inflammatory markers stratified by high (N = 104) vs low-to-normal (N = 63) prior to treatment. Median age was 64 years with systemic rheumatic disease diagnosed in 58%. Treatment response was higher in patients with elevated inflammatory markers (55.77% vs. 34.92%, P = 0.011), even after adjustment for age, sex, baseline FVC%, and treatment duration (OR 2.45 [1.243-4.828], P = 0.010). FVC% slope from treatment initiation to discontinuation appeared to be increasing in patients with higher baseline inflammatory markers compared to those with low to normal marker levels (P = 0.003) (Figure1). CONCLUSION: Patients with non-IPF f-ILD and high initial inflammatory markers appear to be more acutely responsive to anti-inflammatory therapy with slower FVC decline or improvement over time while on treatment. These findings suggest baseline serum CRP and ESR may be reliable predictors of treatment response and direct treatment duration and intensity for efficacy or reducing adverse effects.