Abstract: A 37‐year‐old woman was admitted to our hospital because of acute respiratory distress. Two weeks previously, amoxapine (75 mg/day) had been administered for the first time. Ten days later she developed a high fever, severe hypoxaemia and pulmonary infiltrates on chest CT, including patchy areas of ground‐glass opacity, thickening of the interlobular septae and bronchial walls and pleural effusions. BAL showed a predominance of neutrophils, lymphocytes and erythrocytes but not eosinophils. Amoxapine was stopped, resulting in complete resolution of the pulmonary infiltrates. When the patient was re‐exposed to amoxapine (52.5 mg total dose), high fever, reduced SaO 2 and pulmonary infiltrates reappeared. We concluded that acute respiratory distress may be associated with amoxapine treatment.
A 32-year-old man was incidentally found to have abnormal shadows on a chest X-ray film and was admitted on May 2004. His chest images showed mediastinal and bilateral hilar lymphadenopathy. The serum level of angiotensin-converting enzyme was elevated. We also found non-caseating epithelioid cell granulomas in transbronchial lung biopsy specimens, and confirmed the diagnosis of sarcoidosis. We carried out bronchoalveolar lavage (BAL) for evaluation of disease activity of sarcoidosis. After BAL, he suffered high fever and polyarthralgia. Both ankles were extremely inflamed. We suspected infectious arthropathy caused by atypical pathogens and thus administered antibiotics, but they had no effect at all. Also, no findings suggesting collagen-vascular disorders, including rheumatoid arthritis, were detected. His symptoms improved after three-weeks of treatment with non-steroidal anti-inflammatory drugs. Thus, this case was diagnosed as having acute sarcoid polyarthritis. BAL may have influenced the onset of febrile arthritis in this patient This case indicates that sarcoidosis should be considered as a possible cause of acute febrile polyarthritis.
Objective : Interleukin‐4 stimulates collagen synthesis in fibroblasts in vitro . The purpose of this study was to clarify the role of interleukin‐4 in the pathogenesis of idiopathic pulmonary fibrosis. Methodology : We compared interleukin‐4 expressing cells in tissues from 11 patients with pathologically confirmed idiopathic pulmonary fibrosis with early stage inflammatory lesions versus advanced lesions. We also performed double staining in order to elucidate which inflammatory cells produce interleukin‐4 in idiopathic pulmonary fibrosis. Results : Greater numbers of interleukin‐4 positive cells were observed in the advanced lesions than in the early lesions. We also found that early stage lesions showed a predominance of CD3/interleukin‐4 double positive cells whereas, the advanced stage lesions had higher percentages of the EG2/interleukin‐4 double positive cells and the tryptase/interleukin‐4 double positive cells. Conclusions : Our results suggest that interleukin‐4 may be involved in progression of interstitial fibrosis in idiopathic pulmonary fibrosis, in which we confirmed a significant contribution of eosinophils and mast cells to interleukin‐4 production.
A 68-year-old woman presenting dyspnea on exertion was admitted. Hypoxemia and a considerably elevated level of serum KL-6 were noted. Chest high-resolution computed tomography (HRCT) scans demonstrated panlobular ground-glass opacities with a mosaic distribution and hilar and mediastinal lymphadenopathy. Bronchoalveolar lavage revealed an increased percentage of lymphocytes and an elevated CD4/CD8 ratio, implicating a diagnosis of sarcoidosis. However, as we could not exclude other diffuse lung diseases because of unusual HRCT pattern in sarcoidosis, video-assisted thoracoscopic lung biopsy was performed. The histology of epithelioid cell granulomas in the specimens of the lung and the lymph nodes confirmed a diagnosis of sarcoidosis. The lung specimens corresponding to areas of increased opacity demonstrated diffuse alveolitis with minimal fibrosis between individual granulomas. Immunohistochemistry for KL-6 provided positive results on alveolar lining cells in areas of alveolitis but not on granulomas. After steroid treatment, the ground-glass opacities disappeared and the serum KL-6 level normalized. We discuss this rare case of pulmonary sarcoidosis presenting panlobular ground-glass opacities with mosaic distribution.
<i>Background:</i> Sinusitis occurs frequently in asthmatic patients. Epidemiologic data on sinusitis and lower airway disease must be evaluated with caution because they are based mostly on symptoms and do not include nasal endoscopic or computed tomography (CT) findings. Clinical support and evidence for this association are lacking. We evaluated the impact of sinusitis on lower airway disease in patients with well-characterized asthma. <i>Methods:</i> Subjects (n = 188) completed a questionnaire designed to provide information about their signs and symptoms related to asthma, allergic rhinitis (AR) and sinus disease. Patients (n = 104) were divided into four groups based on the presence or absence of sinusitis and/or AR. Clinical findings were compared in asthma patients with and without diagnosed sinusitis, by an otorhinolaryngologist or based on sinus CT findings. <i>Results:</i> The prevalence of sinusitis in patients with asthma was 36.7%. Sinus CT scan abnormalities were detected in 66.3% of patients with asthma. The scans revealed abnormal opacity in 17.9% of asthmatic patients without a history of sinusitis. There was a significant correlation between the rate of asthma severity and sinus morphologic abnormalities in patients with and without sinusitis. In adult-onset asthma (≧16 years old), sinusitis frequently preceded asthma, whereas in non-adult-onset asthma (<16 years old) it preceded sinusitis. The complication rate of sinusitis in asthmatic patients was significantly higher in adult-onset asthma than in non-adult-onset asthma. <i>Conclusions:</i> Our findings suggest that bronchial asthma is closely related to sinusitis and the onset age of asthma is important when considering allergic disease frequency. Whether sinus disease directly affects the intensity of bronchial inflammation remains to be elucidated.
