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Internal Medicine

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Abstract

Introduction: Community-acquired pneumonia (CAP) is a prevalent and often treatable cause of respiratory failure. However, in cases where patients fail to demonstrate clinical improvement, clinicians must reevaluate the initial diagnosis. A key diagnostic pitfall is the failure to identify noninfectious mimics such as granulomatosis with polyangiitis (GPA), which presents with diffuse alveolar hemorrhage (DAH), which also manifests in other etiologies such as microscopic polyangiitis, systemic lupus erythematosus, or anti-glomerular basement membrane disease. Prompt recognition and initiation of immunosuppressive therapy is critical for improving clinical outcomes and ultimately decreasing mortality or long-term pulmonary sequelae.

Case Presentation: A previously healthy 35-year-old male of Latin American descent presented with two months of progressive exertional dyspnea, intermittent low-grade fevers, nonproductive cough evolving into hemoptysis, night sweats, anorexia, and unintentional weight loss. Despite previous outpatient management for presumed CAP, his condition worsened, requiring hospitalization. Upon presentation, he was febrile (39.3°C), tachycardic (121 bpm), and hypoxemic (SpO2 91% requiring 5 L/min oxygen via nasal cannula). High-resolution computed tomography revealed bilateral ground-glass opacities, interlobular septal thickening, and peribronchial distribution. An extensive infectious etiology workup did not reveal an appreciable response, and bronchoscopy confirmed diffuse alveolar hemorrhage, prompting the initiation of high-dose methylprednisolone and an autoimmune workup. GPA became the working diagnosis upon positive c-ANCA testing, and the patient was discharged following the initiation of rituximab infusion and oral prednisone, which resulted in remarkable clinical improvement.

Conclusion: Granulomatosis with polyangiitis is a rare small- and medium-sized autoimmune vasculitis that must be distinguished from common etiologies, such as CAP, particularly when standard therapies fail. Early workup, including autoimmune testing and bronchoscopy, is crucial for diagnosis, and the early initiation of immunosuppression may significantly improve clinical outcomes. This case highlights the necessity of considering noninfectious etiologies in the differential diagnosis of pneumonia-like syndromes, especially in the presence of anemia, hemoptysis, or worsening bilateral infiltrates. Furthermore, clinicians must remain vigilant against their cognitive pitfalls, such as anchoring bias. A multidisciplinary and methodical approach is paramount for accurate diagnosis and timely treatment.

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Granulomatosis with Polyangiitis Masquerading as Refractory Community-Acquired Pneumonia in an Immunocompetent Adult: A Diagnostic Imperative

Introduction: Community-acquired pneumonia (CAP) is a prevalent and often treatable cause of respiratory failure. However, in cases where patients fail to demonstrate clinical improvement, clinicians must reevaluate the initial diagnosis. A key diagnostic pitfall is the failure to identify noninfectious mimics such as granulomatosis with polyangiitis (GPA), which presents with diffuse alveolar hemorrhage (DAH), which also manifests in other etiologies such as microscopic polyangiitis, systemic lupus erythematosus, or anti-glomerular basement membrane disease. Prompt recognition and initiation of immunosuppressive therapy is critical for improving clinical outcomes and ultimately decreasing mortality or long-term pulmonary sequelae.

Case Presentation: A previously healthy 35-year-old male of Latin American descent presented with two months of progressive exertional dyspnea, intermittent low-grade fevers, nonproductive cough evolving into hemoptysis, night sweats, anorexia, and unintentional weight loss. Despite previous outpatient management for presumed CAP, his condition worsened, requiring hospitalization. Upon presentation, he was febrile (39.3°C), tachycardic (121 bpm), and hypoxemic (SpO2 91% requiring 5 L/min oxygen via nasal cannula). High-resolution computed tomography revealed bilateral ground-glass opacities, interlobular septal thickening, and peribronchial distribution. An extensive infectious etiology workup did not reveal an appreciable response, and bronchoscopy confirmed diffuse alveolar hemorrhage, prompting the initiation of high-dose methylprednisolone and an autoimmune workup. GPA became the working diagnosis upon positive c-ANCA testing, and the patient was discharged following the initiation of rituximab infusion and oral prednisone, which resulted in remarkable clinical improvement.

Conclusion: Granulomatosis with polyangiitis is a rare small- and medium-sized autoimmune vasculitis that must be distinguished from common etiologies, such as CAP, particularly when standard therapies fail. Early workup, including autoimmune testing and bronchoscopy, is crucial for diagnosis, and the early initiation of immunosuppression may significantly improve clinical outcomes. This case highlights the necessity of considering noninfectious etiologies in the differential diagnosis of pneumonia-like syndromes, especially in the presence of anemia, hemoptysis, or worsening bilateral infiltrates. Furthermore, clinicians must remain vigilant against their cognitive pitfalls, such as anchoring bias. A multidisciplinary and methodical approach is paramount for accurate diagnosis and timely treatment.

 

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