Cyclosporine Induced Organizing Pneumonia: When the Immunosuppressant Causes Inflammation
Recommended Citation
Singh H, Patel P, Mawari SK, Menon P. Cyclosporine Induced Organizing Pneumonia: When the Immunosuppressant Causes Inflammation. American Journal of Respiratory and Critical Care Medicine 2023; 207(1).
Document Type
Conference Proceeding
Publication Date
5-21-2023
Publication Title
American Journal of Respiratory and Critical Care Medicine
Abstract
Introduction: Cryptogenic organizing pneumonia (COP) is a form of idiopathic interstitial pneumonia caused by injury to the alveolar wall. If the cause is known, it is labeled as secondary organizing pneumonia (OP) which can happen in association with connective tissue diseases, malignancy, infections, and drugs. Here, we report a case in which respiratory failure with OP pattern was observed in a patient receiving cyclosporine which resolved after its discontinuation. Case presentation: A 30-year-old female with a history of autoimmune hepatitis on chronic prednisone and cyclosporine presented with fever, dyspnea, and cough. On examination, she had stable vital signs and was saturating 100% on room air. She appeared to be in respiratory distress and had scattered inspiratory crackles. She was admitted to the hospital one month ago, was found to have scattered ground glass infiltrates, and was started on Trimethoprim/Sulfamethoxazole for possible Pneumocystis pneumonia. CT (Computed Tomography) of the chest showed non-resolution of previous ground-glass opacities seen at that time. The patient was started on Cefepime and Azithromycin due to the concern for bacterial pneumonia. Due to previous reports of cyclosporine associated lung injury, it was discontinued after consultation with the patient's hepatologist, and her home prednisone (40 mg once daily) was continued. In the next four days, her oxygen requirements went up from room air to 12 liters/minute via nasal cannula. She also became febrile with persistent temperatures around 103 degrees Fahrenheit. CT-chest was repeated which showed extensive ground glass patchy opacities, particularly on the right side and lower lung lobes (figure). Bronchoalveolar lavage with culture and transbronchial biopsy was unremarkable with negative bacterial and fungal cultures. She underwent video-assisted thoracoscopy with surgical lung biopsy which showed acute fibrinous and organizing pneumonia. On day 12 of discontinuation of Cyclosporine, her oxygen requirements started decreasing and went on to saturating 96% on room air on day 16 of hospitalization. Repeat chest imaging showed interval resolution of ground glass opacities. She was then discharged home and continues to hold cyclosporine while continuing prednisone. Discussion: Cyclosporine is an immunosuppressant reported to cause lung injury. In this patient, due to rapid improvement in the clinical picture and infiltrates after stopping cyclosporine, the cause of OP as deemed to be due to it. In COP, extensive medication reconciliation should be done to evaluate drug-induced liver injury. If there is high suspicion, discontinuation of culprit medications can achieve favorable response as described in this case. (Figure Presented).
Volume
207
Issue
1
