Anabolic-androgenic steroid–induced pneumonitis and myocardial injury in a young bodybuilder

Introduction: Anabolic-androgenic steroids (AAS) are frequently misused by athletes to increase muscle mass and performance, and their toxicity affects multiple organ systems. This case describes cardiopulmonary complications. Case description: We report a 29-year-old competitive bodybuilder who presented with cough, haemoptysis, exertional dyspnoea, and fatigue after escalating AAS use before a competition. Investigations revealed systemic inflammation, bilateral pulmonary ground-glass opacities, pleural effusions, and myocardial oedema with pericardial involvement. Anti-glomerular basement membrane antibodies were tested to exclude Goodpasture’s syndrome, tuberculosis was excluded (GeneXpert and multiplex biomarker test negative), and polymerase chain reaction testing for coronavirus disease-19 was negative. Lab results showed mildly elevated troponin T (0.08 ng/ml, normal <0.014), supporting myocardial injury. Cultures of blood and sputum showed no pathogenic growth, and antinuclear antibodies (ANA) were negative. The patient received empirical antibiotics, corticosteroids, and diuretics, with marked clinical improvement within 72 hours. Oral corticosteroid therapy was tapered over 7 days. Follow-up computed tomography scan of the chest 7 days later showed complete resolution of pleural effusions and ground-glass opacities. Echocardiography revealed resolution of pericardial effusion and normalization of myocardial appearance coinciding with sustained cessation of AAS. At 6-month follow-up, the patient had discontinued anabolic steroid use, remained clinically well, and resumed recreational sports. Conclusion: This case demonstrates that AAS misuse may cause combined pulmonary and cardiac complications. Although infection cannot be fully excluded due to concurrent antibiotics, negative cultures, ANA, and Anti-GBM results support the interpretation that AAS was the primary cause of pneumonitis and myocardial injury. Improvement after cessation of AAS strengthens the causal link, supported by existing literature.