Eosinophils in the lungs: Not always straightforward

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INTRODUCTION: Chronic eosinophilic pneumonia (CEP) is a rare cause of respiratory failure and its diagnosis relies on the exclusion of other, more frequent pathologies. It must be considered whenever eosinophilia accompanies dyspnea, as treatment is simple and effective. CASE PRESENTATION: A 79-year-old man, with significant smoking history, was admitted with acute worsening of longstanding unexplained hypoxemic respiratory failure. CBC showed eosinophilia (4.3 x 109/L), which had been persistent since his first presentation 16 months prior. Imaging revealed a left-sided pleural effusion and right basilar nodules. Past studies showed nodules, ground glass opacities, lymphadenopathy and bilateral effusions that improved spontaneously and alternatively implicated the right and left hemithoraces (Figure). Work-up to rule out malignancy (transbronchial and CT-guided biopsies, as well as lymph node biopsy obtained by mediastinoscopy), infection (parasitic, fungal) and rheumatologic disease (ANA, anti-double stranded DNA, ANCA antibodies) had been negative. A primary eosinophilic lung disease was suspected and bronchoscopy with bronchoalveolar lavage yielded fluid with a high percentage of eosinophils (42%). CEP was diagnosed using clinical and laboratory criteria, despite atypical radiographic features. Systemic glucocorticoids resulted in dramatic improvement. DISCUSSION: CEP has an insidious onset over several months with respiratory (dyspnea, productive cough, wheezing) and constitutional symptoms (fever, night sweat, weight loss). In contrast to acute eosinophilic pneumonia, most patients have significant peripheral eosinophilia at diagnosis. Proposed criteria include a combination of chronic (>2 weeks) respiratory symptoms, either peripheral blood ($109/L) or alveolar eosinophilia (>25%) and pulmonary infiltrates with a peripheral predominance; diagnosis requires exclusion of other eosinophilic lung diseases (1). CEP usually presents with peripheral lung opacities (alveolar infiltrates with air bronchograms or ground glass opacities) involving the upper lobes, which can be migratory. Nodules and mediastinal lymphadenopathy are infrequent, whereas very rare findings (cavitation, pleural effusions) should prompt reconsideration of the diagnosis. Interestingly, our case presented with alternating bilateral pleural effusions and migratory opacities that spontaneously improved over time. When radiographic features are atypical, surgical lung biopsy may be necessary. CONCLUSIONS: CEP has no absolute diagnostic criteria and, given its rarity and protean manifestations, high clinical suspicion is warranted. Ensuring an accurate diagnosis is crucial, as the mistaken administration of glucocorticoids for infectious eosinophilic pneumonias may prove harmful.




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