• Tuberculosis and Respiratory Diseases
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• v.40 no.6
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• pp.677-682
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• 1993

Background: Massive hemoptysis is a major clinical problem with high mortality. Bronchial artery embolization is well accepted and widely used for treatment of massive and recurrent hemoptysis, especially in patients with chronic diffuse pulmonary disease who are poor candidates for surgery. We evaluated the therapeutic effect of transcatheter arterial embolization for immediate control and prevention of recurrent hemoptysis. Method: We reviewed 20 cases(M:F=13:7) of bronchial artery embolization for the management of massive hemoptysis from Jun 1989 to Aug 1992 retrospectively. Results: Underlying causes of hemoptysis were pulmonary tuberculosis(n=14), bronchiectasis(n=3), aspergilloma(n=2) and paragonimiasis(n=1). Embolization material was choosed randomly gelfoam(n=7) or Ivalon(n=11) and in 2 cases both were used simultaneously. Target arteries of embolization were bronchial artery only in 15 cases, non-bronchial systemic arteries with or without bronchial artery in 5 cases. After the arterial embolization, immediate cessation of hemoptysis was achieved in 17 cases(85%) and total recurrence rate including 3 cases of immediate treatment failure was 50%. Among recurrences 3 cases were achieved lobectomy, 1 case was expired by asphyxia due to massive hemoptysis and remained 6 were managed by medical conservative treatment with no further recurrence of hemoptysis during follow up periods. Conclusion: Bronchial artery embolization for treatment of massive or recurrent hemoptysis was effective in immediate bleeding control. Despite high recurrence rate the rebleeding after embolization was less severe and controllable by conservative management. Bronchial artery embolization is valuable as primary trial to massive hemoptysis.

• Tuberculosis and Respiratory Diseases
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• v.65 no.6
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• pp.457-463
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• 2008

Background: The attenuation of the lung parenchyma increases on expiration as a consequence of decreased air in the lung. Expiratory CT scans have been used to show air trapping in patients with chronic airway disease and diffuse parenchymal disease and also in asymptomatic smokers. Although there have been several reports investigating the regional air trapping on a expiratory CT scan, there have been only a few reports evaluating the changes of whole lung attenuation with considering its clinical significance, and especially in healthy subjects. The purpose of this study was to evaluate the correlation of an expiratory increase of lung attenuation with age and smoking in healthy subjects. Methods: Asymptomatic subjects who underwent a low dose chest CT scan as part of a routine check-up and who showed normal spirometry and a normal inspiratory CT scan were recruited for this study. We excluded the subjects with significant regional air trapping seen on their expiratory CT scan. Lung attenuation was measured at 24 points of both the inspiratory and expiratory CT scans, respectively, for 100 subjects. The correlations between an expiratory increase of the lung attenuation and the amount of smoking, the patient's age and the results of spirometric test were assessed. Results: There were 87 men and 13 women included in this study. Their median age was 49.0 years old (range:25~71). Sixty current smokers, 24 ex-smokers and 16 non-smokers were included. As age increased, the expiratory increase of lung attenuation was reduced at every measuring points (r=-0.297~-0.487, Pearson correlation). The statistical significance was maintained after controlling for the effect of smoking. Smoking was associated with a reduction of the expiratory increase of lung attenuation. But the significance was reduced after controlling for the patient's age. The $FEV_1$, FVC, $FEV_1/FVC$ and $FEF_{25{\sim}75%}$ were not associated with an expiratory increase of lung attenuation. Conclusion: The expiratory increase of lung attenuation in subjects with a normal inspiratory CT scan was negatively correlated with age. It was also reduced in heavy smokers. It may reflect aging and the smoking related changes.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.965-975
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• 1996

Background : Exogenous lipoid pneumonia is caused by inhalation or aspiration of animal, vegetable or mineral oil. Most cases are ascribed to aspiration of oil in laxatives or nose drops Petroleum, another pure hydrocarbon used as a base in various medications, is occasionally involved. Especially animal oil produces severe tissue inflammatory reaction, but most patients present with only abnormal chest X-ray and no specific clinical symptoms or signs. Method: Seven patients, 3 males and 4 females, with exogenous lipoid pneumonia, who was hospitalized or referred to pulmonary division at Samsung Medical Center from December 1994 10 July 1996, were included. They hadn a history of laking shark liver oil(so-called "squalene") for varying period of time. We reviewed clinical, radioloic and pathologic findings. Result: Patients look 7 to 30 capsules of "squalene" a day for at least one month to 5 years. Six cases had chronic disease such as diabetes, hypertension, or cerebrovascular accident. Respiratory symptoms of mild fever, cough and sputum were present in 3 cases and in 3 cases there was no clinical symptoms and signs but abnormal findings by chest X - ray. The major radiologic findings by simple chest X - ray and computed tomography consisted of consolidation, infiltration involving mainly right middle and both lower lobes, and ground-glass opacity. Five of six bronchoscopic examinations demonstrated both lipid droplets floating on the surface of bronchoalveolar lavage fluid and Lipid-laden macrophages in bronchoalveolar lavage fluid or lung tissue. Follow-up chest X -ray showed improvement in 4 cases but no marked interval change in 3 cases after removal of exposure to "squalene". Conclusion: Shark liver oil can induce lipoid pneumonia in adults. In case of high clinical suspicion, confirmation of "squalene" use by careful history taking is required and bronchoscopy is helpful in diagnosis.

• Clinical and Experimental Pediatrics
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• v.51 no.5
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• pp.487-491
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• 2008

Purpose : Although Mycoplasma pneumoniae (M. pneumoniae) infection can cause wheezing in non-asthmatic children, the mechanisms of this symptom remain unclear. Vascular endothelial growth factor (VEGF) is a major mediator of angiogenesis and vascular permeability, and is also known to be elevated in cases of chronic pulmonary disease such as asthma. We hypothesized that VEGF may increase in children with acute M. pneumoniae pneumonia and wheezing. Methods : Nine patients with clinical and laboratory evidence of acute M. pneumoniae pneumonia were enlisted from children admitted to Korea University Hospital. They had had more than one episode of wheezing during the illness, which was confirmed by a physician; they comprised the wheezer group. The individuals with M. pneumoniae pneumonia without wheezing were 63 in number, and they comprised the non-wheezer group. Patients with a history of asthma or who had received asthma medications were excluded. Serum concentrations of VEGF, total IgE, eosinophil cationic protein (ECP), and peripheral blood eosinophil counts were measured. Results : The serum VEGF concentrations were higher in the wheezer group ($mean{\pm}SD$; $650.2{\pm}417.9pg/mL$) than in the non-wheezer group ($376.5{\pm}356.2pg/mL$, P=0.049). M. pneumoniae antibody (1:1,380 vs. 1:596, P=0.048) and serum total IgE (591.8 IU/mL vs. 162.2 IU/mL, P=0.032) were higher in the wheezer group than in the non-wheezer group. There were no differences between the two groups in terms of serum ECP concentration or blood eosinophil count. Conclusion : In the presence of wheezing, serum VEGF concentrations were higher in the children with M. pneumoniae pneumonia. This finding suggests that VEGF may associate with wheeze-related symptoms in children with acute M. pneumoniae pneumonia.