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A 42-year-old man was admitted to our hospital, complaining of dyspnea and cough for six months. Chest CT demonstrated thickening of the bronchial walls and some centrilobular nodules. From the laboratory data and the clinical course, he was first suspected to have bronchial asthma. However, it was necessary to rule out bronchiolitis due to other causes, because he had no previous asthma history and also because of the CT findings. We performed surgical lung biopsy to make a definite diagnosis. The pathological findings revealed eosinophilic bronchiolitis. While dyspnea and the eosinophilic nasal polyp improved by treatment with oral steroid therapy, the eosionophilic sinusitis and bronchiolitis relapsed after steroid tapering. Improvement and relapse of nasal and lower airway symptoms were synchronously observed. Eosinophilic bronchiolitis and eosionophilic sinusitis in this case may be considered to be a category of airway eosinophilic inflammation.

A 62 year-old woman presented with diffuse, centriacinar nodular densities on chest radiography and CT, and an increase of peripheral blood eosinophils, four years after diagnosis of bronchial asthma. Diffuse panbronchiolitis was diagnosed, and was treated with erythromycin for a long period. One year later, she noticed exertional dyspnea, and her chest radiograph showed increased nodular densities. Lung biopsy under video-assisted thoracoscopy was performed, and revealed chronic bronchiolitis with eosinophilic infiltration, and focal, peribronchiolar eosinophilic infiltration in the alveolar septa and alveoli. She was treated with prednisolone, and her symptoms and nodular densities on chest radiography and CT were improved. We consider that the clinico-pathological findings of this case are consistent with those of chronic eosinophilic bronchiolitis, which has recently been reported in Japan. This case is different from previously reported ones in that eosinophilic bronchiolitis appeared in the course of bronchial asthma, suggesting the possibility that eosinophilic bronchiolitis may be accompanied with bronchial asthma or eosinophilic pneumonia.

This case, in a 23-year-old man presenting with cough, sputum, dyspnea on effort and wheezing, had been diagnosed as bronchial asthma at another hospital. Because inhaled steroid and theophylline were far from effective, he was admitted to our hospital for further evaluation. A blood test revealed marked eosinophilia. Chest radiography showed diffuse, small nodular shadows in both lung fields, and a chest CT scan demonstrated diffuse centrilobular nodules and thickening of the bronchi and bronchioles. A spirometric test showed obstructive and restrictive ventilatory impairment, but the depressed forced vital capacity failed to show improvement in response to bronchodilator inhalation, discouraging a diagnosis of asthma. Eosinophilic lung disease with prominent eosinophilic bronchiolitis was diagnosed on the basis of BAL eosinophilia and thoracoscopic lung biopsy findings. The symptoms and blood eosinophilia were responsive to administration of oral prednisolone (30 mg daily); radiographic and CT findings also showed improvement. This case showed a marked similarity to the recently reported "eosinophilic bronchiolitis", and was probably not a type of bronchial asthma.

A 35 year-old man was admitted to our hospital because of cough, wheezing, and paresthesia of the right upper extremity. He demonstrated marked eosinophilia, bronchial asthma, and mononeuritis multiplex. We diagnosed Churg-Strauss syndrome. Serum MPO-ANCA was elevated to 189 U/ml. Chest high-resolution computed tomography showed panlobular ground-glass attenuation in both lungs. BALF showed bloody fluid, and TBLB revealed findings consistent with eosinophilic pneumonia. Lung biopsy by VATS revealed eosinophilic pneumonia, pulmonary vasculitis, capillaritis, and hemosiderosis. The patient recovered after treatment with prednisolone and cyclophosphamide. We concluded that alveolar hemorrhage due to pulmonary capillaritis could be a complication in cases of Churg-Strauss syndrome.

A 47-year-old man was admitted to our hospital with complaints of cough and shortness of breath. Chest radiography showed infiltration of the right lung and left pleural effusion, the eosinophil count increased notably in the peripheral blood, sputum, and pleural effusion. Transbronchial lung biopsy revealed the invasion of eosinophils like eosinophilic pneumonia. Heart failure easily developed in this patient after the intravenous infusion. Myocardial involvement was suspected, and hypereosinophilic syndrome was diagnosed. After prednisolone was administered, the peripheral blood eosinophil count normalized rapidly, and subsequently, the pleural effusion and infiltration shadows in the lung disappeared.

A 54-year-old woman complained of dyspnea, cough, and productive sputum. Auscultation detected a wheeze in the left and right lung fields. Chest x-ray and computed tomographic films showed non-segmental infiltration in the left upper lung field. Laboratory data revealed eosinophilia in peripheral blood and sputum, elevated levels of serum interleukin-5 (IL-5), airflow limitation, hypoxemia, and heightened airway sensitivity to methacholine (D min : 0.42 units). Bronchoalveolar lavage disclosed an increase in the total number of cells, a 32% increase in eosinophils, and a decreased CD 4/CD 8 ratio of 0.7. Transbronchial lung biopsy specimens revealed infiltrations of eosinophils in the alveolar and interstitial compartments. The histologic features of bronchial biopsy specimens included increased eosinophils in the submucosa and squamous metaplasia. In addition, blood glucose and HbA 1 c levels were elevated. Chronic eosinophilic pneumonia complicated by bronchial asthma and diabetes mellitus was diagnosed. Because the patient was diabetic, she was given suplatast tosilate to reduce the production of IL-5, and high-dose inhaled corticosteroid (beclometasone dipropionate, 1,600 mcg/day) instead of oral corticosteroid therapy. Her symptoms were relieved, peak expiratory flow rates increased, serum IL-5 levels became undetectable, airway sensitivity to methacholine decreased (D min : 4.64 units), and the radiographic abnormalities disappeared. Furthermore, treatment with beclomethasone dipropionate was progressively reduced to 1,200 mcg/day over the subsequent year without relapse. It was concluded that suplatast tosilate and high-dose inhaled corticosteroid therapy may be an effective alternative therapeutic approach to chronic eosinophilic pneumonia in some cases.

We report a case of a 55-year-old man who had been treated for bronchial asthma diagnosed at the age of 51. One year following diagnosis, chest X-ray films disclosed nodular shadows. Biopsy specimens obtained by video-assisted thoracoscopic surgery were histopathologically identified as intrapulmonary lymph nodes. Three years after the initial diagnosis, the patient experienced sensory disturbance of the lower extremities, low-grade fever, and weight loss. At this point he was admitted to our hospital. On admission, physical examination and clinical investigations showed peripheral eosinophilia and signs of vasculitis. Specimens obtained by transbronchial lung biopsy and bronchoalveolar lavage showed strong evidence of tissue damage with infiltration of eosinophils but no evidence of necrotizing vasculitis or extra-vascular granuloma. Churg-Strauss syndrome (CSS) was diagnosed, and treatment was initiated with prednisolone at a dose of 60 mg/day. Except for the sensory disturbances in the lower extremities, after a few days of treatment the patient's symptoms subsided and his clinical data improved. This case was clinically important because pulmonary eosinophilic infiltration into vessel walls was confirmed a year after the diagnosis of bronchial asthma, and 2 years before the patient demonstrated signs of vasculitis. Further, it was a very rare case of CSS in which intrapulmonary lymph nodes had developed beneath the visceral pleura despite the absence of a history of heavy smoking, thus suggesting continuous stimulation by some as yet unknown antigen.

We encountered a 23-year-old woman with allergic granulomatous angiitis (AGA) associated with cerebral infarction, myo-pericarditis, and acute respiratory failure due to extended eosinophilic pneumonia. She underwent emergency treatment at our hospital because of right hemiparesis and impaired consciousness. AGA was suspected because the patient had a history of bronchial asthma accompanied by pulmonary infiltrations with eosinophilia, and presented with diffuse pulmonary infiltrates, pericardial effusion, diffuse hypokinesis of myocardium, cerebral infarction and marked peripheral eosinophlia. Pulmonary eosinophilia was confirmed by examination of broncho-alveolar lavage fluid. Myocardial tissue biopsy specimens revealed fibrous granulation indicative of myocarditis. The patient responded well to corticosteroid therapy.