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...

I appreciate and agree with Dr. @Ria Gripaldo's excellent answer and treatment approach. It is important to recognize the INBUILD study had several restrictions which impact how its findings translate into routine clinical care, even though the study has provided notable information on the use of N...

When I consider treatment for a patient with ILD, I am considering whether the patient has a predominantly inflammatory phenotype, fibrotic phenotype or both. In the absence of other reliable biomarkers, I use findings on the HRCT (consolidation, ground glass, organizing pneumonia), surgical lung bi...

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,...

I use the same principles in my approach to autoimmune disease-related ILD, namely, identifying and treating patients with progressive disease. The INBUILD study inclusion criteria provided this useful guidance in patients meeting one of these three parameters within two years prior to receiving nin...

This has been a very interesting and informative discussion on the use of antifibrotic therapy (essentially the FDA-approved Nintedanib) in patients with non-IPF ILD by rheumatologists and pulmonologists. I will restrict my comments to scleroderma patients with ILD (although I suspect there is to a ...