Abstract Rheumatoid arthritis induced interstitial lung disease (RA-ILD) is a serious extra-articular complication of rheumatoid arthritis (RA). There are currently no evidence-based guidelines for treating RA-ILD, however RA management with immunomodulatory therapy, including methotrexate, is frequently used for disease control. Methotrexate, a folate metabolism inhibitor, has an array of side effects, however it rarely affects the pulmonary system with an incidence of 1-7%. Here we present the case of methotrexate induced pneumonitis (MTX-P) in a patient with RA. A 76-year-old male with a history of interstitial lung disease and seropositive rheumatoid arthritis presented to the emergency department with an ongoing and worsening cough and dyspnea in the last two weeks. 5 months prior, he was initiated on methotrexate for his RA and reports that since then his symptoms had worsened. The patient was afebrile, normotensive, and O2 saturation was 90% on 3L nasal cannula. Initial labs showed no leukocytosis, and procalcitonin, blood cultures, legionella, COVID, Influenza and MRSA were all negative. Respiratory cultures revealed normal respiratory flora. Initial chest x-ray showed congestive changes and further imaging with a CT was obtained which showed fibrotic changes in the lung bases and ground class opacities. Given the negative infectious workup and no indication of worsening ILD on imaging, methotrexate was promptly discontinued and the patient was started on steroids with improvement in symptoms. Methotrexate-induced pneumonitis is rare, however, should be suspected in patients who develop new or worsening respiratory symptoms within the first year of methotrexate therapy. It remains a diagnostic challenge because its clinical and radiologic features may overlap with RA-ILD or infectious pneumonia. As methotrexate induced pneumonitis is a diagnosis of exclusion, the diagnosis is often delayed while other causes are being ruled-out. Prompt recognition and discontinuation of the drug is essential to prevent progression to respiratory failure and to avoid unnecessary antimicrobial or immunosuppressive escalation. This abstract is funded by: None
Erb et al. (Fri,) studied this question.