A42-20 Suspected Stimulant-induced Interstitial Lung Disease: A Case Report With Diagnostic Challenges

Abstract Introduction Interstitial lung diseases (ILDs) encompass a diverse group of disorders caused by autoimmune, infectious, occupational, and drug-related exposures. Among drug-induced causes, stimulant-related ILD secondary to inhalational cocaine and amphetamine use has emerged as an increasingly recognized but diagnostically challenging entity. We present a case of a 36-year-old man with recurrent, steroid-responsive ILD associated with chronic cocaine and MDMA (ecstasy) use. This case underscores the overlap between stimulant-induced ILD, Hypersensitivity pneumonitis, sarcoidosis and other inflammatory ILDs. Case Presentation A 36-year-old male with a 10-year history of polysubstance abuse (intranasal cocaine, MDMA, tobacco, alcohol) presented with progressive dyspnea, fatigue, and productive cough for one year. He reported 20-pound weight loss, night sweats, and subjective fevers. Occupational history included wood exposure with no bird or metal exposure. CT chest showed bilateral, upper-lobe predominant reticular and ground-glass opacities with peribronchovascular distribution, traction bronchiectasis, and micronodules. Given the broad differential, an in-depth workup was pursued which revealed ANCA positivity, elevated IgG (1800 mg/dL), negative ANA, MPO, and PR3. Transbronchial biopsy showed necrotizing and non-necrotizing granulomatous inflammation with focal organizing pneumonia; stains and cultures for bacteria, mycobacteria, and fungi were negative. Eosinophilia (11%, 1100/µL) normalized after corticosteroid initiation. He showed marked improvement with prednisone but relapsed repeatedly after resuming intranasal cocaine use. Each relapse correlated with positive cocaine and negative amphetamine urine screens. PFTs showed a mixed obstructive-restrictive pattern with severely reduced diffusion capacity. Sustained abstinence led to near-complete clinical remission for almost 6 months but then symptoms recurred upon cocaine reuse, requiring repeated steroid courses. Discussion This case underscores the overlap between stimulant-induced ILD, HP, and sarcoidosis. Necrotizing granulomas, steroid responsiveness, and temporal association of symptoms with drug abuse favored a substance-induced etiology. HP-like features could be related to occupational exposure and inhalational stimulant use. Sarcoidosis typically presents with non-necrotizing granulomas; however necrotizing variants are reported. Stimulant-induced ILD is thought to result from direct alveolar toxicity, oxidative stress, and immune dysregulation. Urine assays for cocaine are highly specific, whereas MDMA detection is variable, explaining the negative amphetamine screens. Conclusion Stimulant-induced ILD is an underrecognized cause of granulomatous and organizing pneumonia patterns. A strong temporal relationship between substance uses and relapse, steroid responsiveness, and exclusion of infection and autoimmune disease support a drug-induced mechanism. Clinicians should maintain a high index of suspicion for substance-induced ILD in young patients with unexplained granulomatous lung disease, as early exposure cessation remains the most effective intervention. This abstract is funded by: None