Abstract Diagnostic errors remain a critical challenge in modern medicine, often stemming from cognitive shortcuts and premature diagnostic closure. Chronic lymphocytic leukemia (CLL) often presents with lymphocytosis or lymphadenopathy, but may present with B symptoms like fever, weight loss, and night sweats. Pulmonary involvement is rare and usually occurs later. In contrast, sarcoidosis is a systemic granulomatous disease that often affects lungs and mediastinal lymph nodes, with image findings like perihilar infiltrates, fibrosis, and lymphadenopathy. In atypical presentations, however, distinguishing these entities can be challenging. We present a case of a 64-year-old woman with progressive exertional dyspnea and dry cough, initially presumed to have advanced pulmonary sarcoidosis based on imaging and clinical history. Despite treatment with corticosteroids and supplemental oxygen, her condition showed modest improvement. Pulmonary function testing revealed a severely reduced diffusion capacity and restrictive physiology, consistent with interstitial lung disease (ILD). High-resolution computed tomography (HRCT) of the chest demonstrated moderate diffuse interstitial thickening, subpleural reticulation with bronchiectasis throughout all lung zones with extensive hilar, mediastinal, and axillary lymphadenopathy, leading to a presumptive diagnosis of stage IV sarcoidosis. She was empirically started on prednisone. Three weeks after, she underwent bronchoscopy with endobronchial ultrasound-guided lymph node biopsy, which showed CD5-positive B-cell lymphoma consistent with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL). No granulomas or infectious organisms were identified. Flow cytometry confirmed a monoclonal B-cell population expressing CD5, CD19, CD20, CD23, CD200, CD45, and kappa light chains. Her respiratory symptoms were ultimately attributed to pulmonary involvement by CLL, a rare manifestation often mistaken for granulomatous or fibrotic lung disease. Pulmonary manifestations of CLL are rare and can closely mimic granulomatous diseases like sarcoidosis. In this case, the patient’s initial chest CT showing bilateral hilar lymphadenopathy and interstitial changes led to a working diagnosis of sarcoidosis. The initial response to corticosteroids reinforced this impression, a classic example of anchoring bias and premature diagnostic closure. When the patient’s condition failed to improve, a diagnostic re-evaluation prompted a biopsy revealing CLL/SLL infiltration. This underscores how recognition of diagnostic momentum and deliberate diagnostic timeout allowed clinicians to step back, reassess, and arrive at the correct diagnosis. Incorporating metacognitive strategies, actively questioning initial assumptions, seeking disconfirming evidence, and engaging in reflective practice, can mitigate cognitive errors. Clinicians should maintain diagnostic openness when faced with incongruent disease courses. By doing so, we not only enhance diagnostic accuracy but also uphold the principles of patient safety and thoughtful clinical reasoning. This abstract is funded by: None
Rezek et al. (Fri,) studied this question.
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