bubble_chart Overview

Chronic eosinophilic pneumonia, also known as prolonged pulmonary eosinophilic infiltration, was first described by Carrington in 1969. The disease course and radiographic findings are often prolonged, typically exceeding one month, and the symptoms are more severe than those of simple pulmonary eosinophilic infiltration (PIE).

bubble_chart Etiology

The causes of the disease are generally similar to those of simple pulmonary eosinophilic infiltration, and some consider it a type of Löffler syndrome. Among parasitic infections, hookworms and roundworms are the most common causes. In terms of medications, nitrofurantoin is frequently implicated. Other disease causes include coccidioidomycosis and brucellosis. Many patients have an allergic constitution, but the exact trigger remains unknown.

bubble_chart Pathological Changes

There is dense infiltration of eosinophils and macrophages in the interstitium and alveoli, accompanied by a small number of lymphocytes and plasma cells. Additionally, hyperplasia of type II epithelial cells, protein exudation in the alveoli, fibroblast proliferation, and collagen deposition in the septa can be observed. Eosinophils can also produce pyrogens, leading to frequent fever symptoms in such patients.

bubble_chart Clinical Manifestations

The male-to-female ratio among patients is 1:2, with most aged between 20 and 50. Half of the patients have an allergic constitution, and the severity of symptoms varies widely, ranging from only abnormal chest X-ray findings to severe respiratory failure. The disease course lasts approximately 1 to 8 months. Common symptoms include cough, fever, shortness of breath, weight loss, night sweating, and lack of strength, with a few patients experiencing hemoptysis. Over half of the patients exhibit wheezing on physical examination, and fine moist rales may also be heard.

The typical X-ray findings often have diagnostic value and include three types of changes: ① Exudative shadows unrelated to pulmonary lobes or segments, mainly distributed in the outer regions of both lungs and showing progression; ② Rapid absorption of exudative lesions after the use of adrenal corticosteroids; ③ Recurrent exudative changes corresponding to the recurrence of clinical symptoms.

Pulmonary function tests often reveal restrictive ventilatory dysfunction accompanied by diffusion impairment and hypoxemia. The proportion of eosinophils in peripheral blood ranges from 10% to 40%, and the erythrocyte sedimentation rate (ESR) may increase significantly, reaching up to 100 mm/h. The proportion of eosinophils in bronchoalveolar lavage fluid can be as high as 40% or more, whereas it is normally less than 1%. All the above changes may resolve after treatment.

bubble_chart Diagnosis

The diagnosis often relies on typical medical history and X-ray findings. This condition should be differentiated from pulmonary subcutaneous nodules, Hodgkin's disease, etc. If there is doubt about the diagnosis, a lung biopsy or bronchoalveolar lavage should be pursued. Sometimes, adrenal corticosteroids may also be used for diagnostic treatment.

bubble_chart Treatment Measures

Less than 10% of patients can achieve spontaneous remission. Adrenocortical hormones are the first-line treatment, with prednisone 30-40mg/d commonly used. Within hours of administration, symptoms such as fever and general malaise begin to improve. Within one to two days, symptoms like dyspnea, wheezing, and cough start to alleviate. Radiographic abnormalities typically show improvement after 2 days of treatment and return to normal within approximately 2 weeks. All clinical manifestations can completely disappear after one month of treatment. Considering the high likelihood of relapse after discontinuation, it is generally recommended to maintain adrenocortical hormone therapy for 6-12 months, with some patients requiring treatment for several years. Maintenance therapy usually involves prednisone 10mg/d. If wheezing is significant, theophylline or β₂

receptor agonists may be added.