Abstract Introduction Anti-synthetase syndrome (ASyS) is an uncommon autoimmune condition within the spectrum of idiopathic inflammatory myopathies. It is defined by antibodies against aminoacyl-tRNA synthetases and presents with varying combinations of myositis, arthritis, and interstitial lung disease (ILD). ILD is the leading cause of morbidity and mortality in this group. Because its pulmonary manifestations often resemble infection, patients may undergo repeated antibiotic treatments before the correct diagnosis is recognized. Case Presentation A 55-year-old Gulf War veteran and lifelong non-smoker presented with two months of worsening shortness of breath, intermittent low-grade fevers, and functional decline. Over the prior year, he had multiple admissions for presumed bacterial pneumonia, including one complicated by ARDS requiring intubation. Chest CTs repeatedly showed diffuse bilateral ground-glass opacities, and pulmonary function testing demonstrated a restrictive pattern (FVC 48%, DLCO 40%). Further evaluation revealed ANA (1:320 nucleolar), anti-Jo-1 (328 U), and SSA positivity. Electromyography showed myopathic potential, and muscle biopsy demonstrated rare necrotic fibers. The overall picture was consistent with anti-synthetase syndrome manifesting as ILD, necrotizing myositis, and arthritis. Despite outpatient prednisone and mycophenolate mofetil (MMF), he was readmitted with acute hypoxic respiratory failure. Infectious studies, including cultures, procalcitonin, and bronchoalveolar lavage, were negative. High-resolution CT revealed patchy ground-glass opacities with mild fibrosis and moderate pulmonary hypertension. He was treated with IV methylprednisolone (500 mg daily for three days), followed by a prednisone taper and MMF escalation to 1 g twice daily. His oxygen requirements gradually improved, and he was discharged on 2 L nasal oxygen with plans for close follow-up. Discussion This case illustrates how anti-synthetase-related ILD can masquerade as infection, leading to diagnostic delay and prolonged antibiotic exposure. His clinical course, marked by recurrent “pneumonias” unresponsive to antimicrobials, underscores the need to recognize noninfectious inflammatory lung disease early. The patient’s Gulf War exposures—burn pits and sandstorms—may have served as environmental triggers, a connection that remains incompletely understood but increasingly reported.Recognizing the combination of progressive dyspnea, ground-glass opacities, and systemic features such as myositis or arthritis should prompt autoimmune evaluation. Early identification and aggressive immunosuppressive therapy are critical to preserving lung function and preventing irreversible fibrosis. Conclusion Not every pneumonia is infectious. Anti-synthetase syndrome-associated ILD should be considered in patients with recurrent respiratory failure and inconclusive infectious workups. Early recognition and treatment can dramatically alter prognosis and quality of life. This abstract is funded by: None
Noureldin et al. (Fri,) studied this question.