Diffuse Lung Disease: Student/Resident Case Report Poster - Diffuse Lung Disease |

A Rare Case of Methotrexate Pneumonitis Progressing to Respiratory Failure FREE TO VIEW

Michelle Spiegel, MD; Neeti Kanodra, MBBS; Lee Tormos, MD; Rahul Argula, MD; Lynn Schnapp, MD
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Medical University of South Carolina, Charleston, SC

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):519A. doi:10.1016/j.chest.2016.08.533
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SESSION TITLE: Student/Resident Case Report Poster - Diffuse Lung Disease

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM

INTRODUCTION: Drug-induced pulmonary disease is a challenging diagnosis, as it is typically one of exclusion. Patients with Rheumatoid Arthritis (RA) are at increased risk, as disease modifying therapies used in its treatment are implicated in development of pulmonary disease.

CASE PRESENTATION: A 79 yo Caucasian man with history of prostate cancer treated with curative radiation therapy and RA with only articular involvement presented with progressive dyspnea 2 weeks after initiation of methotrexate therapy. Exam was notable for dry crackles, and chest computed tomography (CT) demonstrated bilateral, diffuse, ground glass opacities (Fig 1). His rheumatoid factor and anti-citrullinated peptide antibody titers were elevated. Bronchoalveolar lavage (BAL) revealed lymphocytic predominance and work-up for infection, pulmonary embolism and heart failure was negative. He was treated with IV methylprednisolone for probable methotrexate-induced lung injury (based on clinical and radiological criteria) and broad-spectrum antibiotics. His condition deteriorated, necessitating intubation. Despite low tidal volume ventilation, his condition worsened, requiring inhaled epoprostenol for hypoxemia and vasopressors for shock. Based on his known wishes, he was transitioned to comfort care. Autopsy showed bilateral, diffuse alveolar damage (DAD) with bronchiolar metaplasia and hyperplasia including squamous changes with mild cellular atypia. (Fig 2)

DISCUSSION: This case illustrates progressive respiratory failure shortly after initiation of methotrexate. Previous case series have demonstrated a spectrum of pathology in patients with methotrexate lung toxicity--features ranging from hypersensitivity pneumonitis to DAD1. Eosinophilia is not always present and is not necessary for diagnosis. Timely cessation of the drug and use of glucocorticoids are typically associated with recovery; unfortunately this was not the case for our patient. His severe degree of metaplasia and DAD may have indicated advanced disease not amenable to glucocorticoid rescue. Case series have reported a mortality rate up to 13% from methotrexate associated respiratory failure.1

CONCLUSIONS: Nearly half of all documented cases of methotrexate lung toxicity have occured in RA patients. Drug cessation and glucocorticoids may aid recovery, but progression to irreversible injury and death is possible. Often, DAD is not amenable to glucocorticoid rescue in patients with methotrexate pneumonitis.Treating clinicians should be mindful of the risk of methotrexate lung injury, especially in patients with RA.2

Reference #1: Imokawa S, Colby TV, Leslie KO, Helmers RA. Methotrexate pneumonitis: review of the literature and histopathological findings in nine patients. Eur Respir J. 2000;15(2):373-81.

Reference #2: Alarcón GS, Kremer JM, Macaluso M, et al. Risk factors for methotrexate-induced lung injury in patients with rheumatoid arthritis. A multicenter, case-control study. Methotrexate-Lung Study Group. Ann Intern Med. 1997;127(5):356-64.

DISCLOSURE: The following authors have nothing to disclose: Michelle Spiegel, Neeti Kanodra, Lee Tormos, Rahul Argula, Lynn Schnapp

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