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Chronic eosinophilic pneumonia: causes, symptoms, diagnosis, treatment
Last reviewed: 04.07.2025
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Chronic pulmonary eosinophilia (long-term pulmonary eosinophilia, Lehr-Kindberg syndrome) is a variant of simple pulmonary eosinophilia with the existence and recurrence of eosinophilic infiltrates in the lungs for more than 4 weeks. Chronic eosinophilic pneumonia is characterized by chronic pathological accumulation of eosinophils in the lung.
The prevalence and incidence of chronic eosinophilic pneumonia (CEP) are unknown. Chronic eosinophilic pneumonia is thought to be an allergic diathesis. Most patients are nonsmokers.
[ What causes chronic eosinophilic pneumonia?
The causes of this form of pulmonary eosinophilia are the same as those of Löffler syndrome, however, in addition, the disease can be caused by tumors (stomach cancer, thyroid cancer, lung cancer), hemoblastoses, systemic vasculitis and systemic connective tissue diseases.
The main pathogenetic factors are the same as in simple pulmonary eosinophilia.
Symptoms of Chronic Eosinophilic Pneumonia
Chronic eosinophilic pneumonia often develops rapidly: cough, fever, progressive shortness of breath, weight loss, wheezing, and night sweats appear. Bronchial asthma accompanies or precedes the disease in more than 50% of cases.
Where does it hurt?
What's bothering you?
Diagnosis of chronic eosinophilic pneumonia
Diagnosis requires exclusion of infectious causes and is based on clinical presentation, blood tests, and chest radiography. Peripheral blood eosinophilia, a very high ESR, iron deficiency anemia, and thrombocytosis are common. Chest radiographs show bilateral lateral or subpleural infiltrates (in about 60% of cases), usually in the middle and upper lungs, described as pulmonary edema negative; this finding is pathognomonic (although it occurs in <25% of patients). CT scans show similar findings in virtually all cases. Bronchoalveolar lavage eosinophilia (>40%) is a reliable finding in chronic eosinophilic pneumonia; serial bronchoalveolar lavage studies may help monitor the course of the disease. Histologic examination of lung biopsy reveals interstitial and alveolar eosinophils and histiocytes, including multinucleated giant cells, and obliterative bronchiolitis with organizing pneumonia. Fibrosis is minimal.
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Treatment of chronic eosinophilic pneumonia
Chronic eosinophilic pneumonia responds well to intravenous or oral glucocorticoids; lack of response suggests another diagnosis. Initial treatment of chronic eosinophilic pneumonia consists of prednisolone (40 to 60 mg once daily). Clinical recovery is often remarkably rapid, possibly within 48 hours. Complete resolution of clinical manifestations and radiographic changes occurs within 14 days in most patients and within 1 month in almost all patients. Therefore, assessment of the dynamics of these parameters is a reliable and effective means of monitoring the effectiveness of therapy. Although CT is more sensitive in detecting radiographic changes, its advantages in assessing the dynamics of the process have not been shown. The number of eosinophils in peripheral blood, ESR, andIgE concentrations can also be used to monitor the clinical course of the disease during treatment. However, not all patients have pathological changes in laboratory test results.
Clinical or radiographic relapse occurs in 50% to 80% of cases after discontinuation of therapy or, less commonly, when the glucocorticoid dose is reduced. Relapse may occur months to years after the initial episode. Thus, glucocorticoid treatment of chronic eosinophilic pneumonia is sometimes continued indefinitely. Inhaled glucocorticoids (eg, fluticasone or beclomethasone 500 to 750 mcg twice daily) are probably effective, particularly when the maintenance dose of the oral glucocorticoid is reduced.
Chronic eosinophilic pneumonia occasionally results in physiologically significant and irreversible pulmonary fibrosis, although mortality is extremely rare. Relapse probably does not indicate treatment failure, a worse prognosis, or a more severe course. Patients continue to respond to glucocorticoids as in previous episodes. Fixed airflow limitation may be noted in some recovered patients, but these abnormalities are usually of limited clinical significance.