Is it still significant to denote the etiology of ILD in a patient with PPF?

Yes, absolutely! Infact, the most effective treatment in patients without IPF (PPF) is treatment of the cause. So if there is underlying autoimmune disease or exposure, primary treatment should be directed against that trigger and this has potential to stop progression and even improve lung function. Antifibrotics are only an adjunct in PPF and only slow the decline.

I agree with @Dr. First Last: We rheumatologists need to understand (and teach others) that systemic autoimmune diseases can present with manifestations other than those that we most identify with that of SARD.

For example, this is particularly true with Sjogren's disease. If we only measure ANA/SSA/RF/centromere on patients who have sicca, sclerodactyly, etc, we will cause an extended amount of delay in diagnosis. Delayed diagnoses are one of the main causes of morbidity, poor quality of life, and organ damage in our patients.

Especially today, when autoantibodies are much cheaper in the past. One can make a cost-benefit argument, I'm sure.

ILD related to Sjogren's disease can present prior to the onset of sicca symptoms (Manfredi et al., PMI...

I don’t have a great answer for this. I screen nearly every new ILD patient with ENA screen, myositis panel, RA, scleroderma, and Sjogren’s. But I’ve got to say this feels like a “thing we/I do for no reason.”

Honest question: what is the hit rate for indiscriminate screening for CTD in this population?

I’m not talking about getting a few markers back as positive and then calling it IPAF; rather, how often does sending this stuff lead to a CTD diagnosis in a patient who otherwise doesn’t have signs/symptoms of one? The only examples I can think of in my career are a couple of RA patients I should have taken a better history of and a few amyopathic antisynthetase patients.

Curious if anyone is aware of data!

ILD caused by an autoimmune process may precede other clinical manifestations of autoimmune disease. Knowing if or which serologies are positive can guide the most appropriate and earliest interventions and monitoring.

The longer amount of time I have spent in this space in collaboration with pulmonolgists in CTD-ILD clinics at two institutions now, I am firmly in the camps of Drs. @Dr. First Last and @Dr. First Last. Not sure pan-serologic profiling is productive for the patient coming in with pulmonary fibrosis with known occupational/environmental exposures and/or the absence of radiographic alveolitis, but knowing the underlying serology in circumstances otherwise can inform use and intensity of IS therapy, specific expectant observation for extra-pulmonary manifestations, and prognosis.