Case presentation reveals atypical unilateral interstitial pneumonitis in a patient undergoing infliximab treatment, suggesting the need for careful monitoring.
Introduction Tumor necrosis factor-alpha (TNF-α) inhibitors, such as infliximab, can cause adverse effects including infections, hepatitis, anemia, and infusion reactions. Infliximab-induced interstitial pneumonitis generally has a bilateral presentation. We present an atypical case of infliximab-induced unilateral interstitial pneumonitis. Case Presentation 65-year-old male presented with one week shortness of breath and productive cough. He completed a seven-day course of levofloxacin for possible pneumonia with no improvement. Past medical history significant for Crohn’s disease refractory to initial therapy, small bowel resection, and on infliximab. Infliximab scheduled every eight weeks; last dose one month before this presentation with no flares in the last four months. On presentation, patient hypoxemic on room air (91%) which improved with supplemental oxygen and had bilateral rales on auscultation. Labs unremarkable with negative white count. Chest X-ray (CXR) revealed patchy multilobar opacities in the left upper and lower lobes (Figure A). He was started on azithromycin and ceftriaxone for suspected pneumonia with no improvement, and still dependent on supplemental oxygen despite antibiotics and nebulization for 5 days. Infectious and autoimmune workup negative. Computed tomography of the chest showed patchy ground glass opacities in left upper and lower lobe with scattered interstitial thickening (Figure B). Due to minimal improvement with two-week antibiotics, infliximab-induced interstitial pneumonitis was suspected. He received pulse steroids of 1 gram daily for three days followed by month-long steroid taper concurrent with trimethoprim-sulfamethoxazole for Pneumocystis jirovecii prophylaxis. Symptoms improved and did not require supplemental oxygen. Bronchoscopy deferred due to rapid symptom resolution. Repeat CXR showed improvement in lung opacities (Figure C). On outpatient follow-up after steroid course, he had no pulmonary symptoms with a significant reduction in the CXR opacities (Figure D). Discussion Infliximab-induced interstitial pneumonitis is a rare complication. Likely mechanism involves TNF-α in pulmonary inflammation/fibrosis. Imaging usually shows bilateral interstitial infiltrates. However, our case showed unilateral findings. Differentials include secondary organizing pneumonia, which presents similarly but with insidious onset. Definitive diagnosis requires lung biopsy. Infliximab pneumonitis does not exhibit a pathognomonic appearance on pathology. Instead, manifests with various patterns including organizing pneumonia, diffuse alveolar damage, non-specific interstitial pneumonia and hypersensitivity pneumonitis. Although no confirmatory diagnostic biopsy was performed, the rapid resolution of symptoms and imaging with steroids favored this diagnosis. It is imperative to rule out infectious etiologies before initiating steroid therapy. Conclusion This case highlights an atypical unilateral presentation of infliximab-induced interstitial pneumonitis and its resolution with systemic steroids.*Equal Primary Contributor This abstract is funded by: None
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Behzadi et al. (2026) studied this question.
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