• Tuberculosis and Respiratory Diseases
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• v.49 no.3
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• pp.353-364
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• 2000

Background : Bronchoscopy is a useful diagnostic tool, for accurate localization of the bleeding site and the management of hemoptysis. However, there is some controversy about the optimal timing of bronchoscopy. Method : To determine the optimal timing of bronchoscopy in hemoptysis, we reviewed the medical records of 118 patients and analyzed the following relationships amongst simple chest PA findings, namely, the duration and amount of hemoptysis, and the timing of bronchoscopy retrospectively. Results : The major causes of hemoptysis were active tuberculosis(28.8%), inactive tuberculosis(10.2%), bronchiectasis(17.0%), lung cancer(7.6%), and aspergilloma(7.6%). Localization of the bleeding focus by bronchoscopy was possible in 87.5% (21/24 cases) during active bleeding, and it was possible in 40.4% after bleeding had stopped(p<0.05). The localization rate of bleeding focus was 59.8% when the chest PA showed certain abnormalities, but it decreased to 27.8% when the chest PA finding was normal(p<0.05). When chest PA showed diffuse abnormalities or its finding was normal, the localization rate of bleeding focus significantly increased if bronchoscopy was performed during bleeding or within 48 hours of the cessation of active bleeding. The localization rate was higher as the amount of hemoptysis became larger(p<0.05). The localization rate of early bronchoscopy(during bleeding or within 48 hours of the cessation of active bleeding) was significantly higher when the duration of hemoptysis was less than 1 week, but there was no advantage if the duration was 1 week or longer. Early bronchoscopy was also necessary to localize the bleeding focus for surgical resection in 4 patients, and the bronchoscopy itself was therapeutic in 1 patient whose bleeding was successfully managed with thrombin-application via bronchoscope. Conclusion : It is concluded that flexible bronchoscopy is useful at not only localizing the bleeding focus but also in preparing a therapeutic plan, and early bronchoscopy is more favorable in hemoptysis.

• Tuberculosis and Respiratory Diseases
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• v.44 no.6
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• pp.1332-1342
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• 1997

Background : Acute pulmonary injury by paraquat are caused by multiple mechanisms including direct injury with oxygen free radicals and several mediators released from inflammatory cells. In order to clarify whether vitamin E could reduce tissue damages induced by intraperitoneal administration of paraquat and to investigate the pathogenetic mechanisms of paraquat-induced pulmonary injury, vitamin E as a free radical scavenger was administered. Method : Rats were divided into three groups (group 1 : control, group 2 : paraquat treated group, group 3 : paraquat and vitamin E treated group). Animals were sacrificed on day 1, day 2, day 3, and day 8 after the administration of saline, paraquat, or paraquat/vitamin E. Results : Treatment with vitamin E decreased the death rate of rats treated with paraquat. Comparing with control group ($1.37{\times}10^6/ml$), mean total cell counts recovered from the lavage fluid from animals treated with paraquat($1.65{\times}10^6/ml$) were increased(p=0.06). Magnitudes of increment of the total cell counts on the Day 8 in the vitamin E treated group were smaller than those of the animals treated with paraquat alone. The neutrophils began to appear in significant amounts in the lavage fluid on Day 8 after the administration of paraquat(37.0+12.7%). A significant decreasing neutrophil concentration at Day 8 was observed in the paraquat/vitamin E treated group(20.6+13.4%). Histologically the degree of pulmonary fibrosis was most prominent in the paraquat treated group while diffuse alveolar damage was continuously observed in the paraquat/vitamin E treated group and extensive interstitial lymphocytic infiltration was seen in the paraquat/vitamin E treated group. The paraquat/vitamin E treated group showed the less histologic changes. Conclusion : In this study vitamin E acting as a scavenger of neutrophil-derived free radicals and suppressant of lipid peroxidation, seemed to be the effective antioxidant in the inhibition of paraquat-induced pulmonary injury.

• The Korean Journal of Nuclear Medicine Technology
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• v.14 no.2
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• pp.145-149
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• 2010

Purpose: Recently, $^{18}F$-FDG Fusion PET which has a high sensitivity for diagnosing cancer is being used for purpose of health examination. This study is to demonstrate that $^{18}F$-FDG fusion PET study is useful for diagnosing an early stage cancer. Materials and Methods: This research has been conducted with 2790 patients visited Seoul National University Hospital Healthcare System (SNUHHS) for $^{18}F$-FDG fusion PET study for a health examination from February, 2004 to December 2008. PET/CT images were acquired from skull base to femur after 1 hour from injecting $^{18}F$-FDG 0.14 mCi/kg to the patients. GEMINI GS (Philips, Netherlands) was used for scanning. Results: From February 2004 to December 2008, $^{18}F$-FDG Fusion PET study was performed for 99,009 patients among all patients who visited SNUHHS and 2,790 patients was performed. Diagnostic rate for malignant cancer was 0.95% for the patients who were not examined by $^{18}F$-FDG Fusion PET study. 1.94% was for the patients who were. The rate of malignant tumor was showed 10% and benign tumor was 90% among 542 patients who showed abnormality in the PET/CT images. Types and rates of malignant tumor showed thyroid cancer: 31.5%, lung cancer: 14.8%, stomach cancer: 9.3%, rectum cancer: 3.7%, breast cancer: 3.7%, metastasis cancer: 16.7%. Nonspecific lymph node in the mediastinum, physiologic uptake in the colon, diffuse mild hypermetabolism in bilateral thyroid gland were shown as a benign tumor. Conclusion: The diagnostic rate of malignant tumor with $^{18}F$-FDG Fusion PET for a purpose of health examination was relatively higher than general medical examination. Consequently, it is superior and useful for applying $^{18}F$-FDG Fusion PET study for health examination.

• Tuberculosis and Respiratory Diseases
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• v.67 no.3
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• pp.205-211
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• 2009

Background: Serum procalcitonin level has been considered prognostic during sepsis and septic shock. We investigated the significance of procalcitonin in critically ill patients with respiratory infections. Methods: The patients who had radiographically diagnosed diffuse lung infiltrations were enrolled on a prospective basis. Bronchoalveolar lavage (BAL) fluid for the purpose of quantitative cultures (${\geq}10^4$ cfu/mL) was obtained from all patients. Serum procalcitonin levels determined by PCT-Q kit were measured on BAL day and classified as follows; <0.5 ng/mL, 0.5~2.0 ng/mL, 2.0~10.0 ng/mL and >10.0 ng/mL. We analyzed the patient's characteristics according to outcome; favorable or unfavorable, defined as death. Results: Patients from the following categories were included: medical 17 (47.2%), surgical 9 (25%), and burned 10 (27.8%). APACHE II scores on admission to intensive care unit were 11.5${\pm}$6.89 and 11 (30.6%) had unfavorable outcomes. A procalcitonin level ${\geq}$0.5 ng/mL was in 17 (47.2%) of all. On univariate analysis, the frequencies of burn injury, mechanical ventilation, multiple organ failure, and a procalcitonin level ${\geq}$0.5 ng/mL were more often increased in patients with unfavorable outcomes than in those with favorable outcomes (p<.05). Also, a higher procalcitonin range and ventilator-associated pneumonia (VAP) were more closely associated with an unfavorable outcome (p<.05). However in multivariate analysis, a strong predictor of unfavorable outcome was burn injury (p<.05). A procalcitonin level ${\geq}$0.5 ng/mL was more sensitive in predicting VAP than unfavorable outcome. Conclusion: A higher procalcitonin level seems to be associated with VAP, but further study is required to know that procalcitonin would be a prognostic marker in critically ill patients with respiratory infections.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.861-869
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• 1998

Backgrounds: The injury of a tissue results in the infalmmation, and the imflammed tissue is replaced by the normal parenchymal cells during the process of repair. But, constitutional or repetitive damage of a tissue causes the deposition of collagen resulting in the loss of its function. These lesions are found in the lung of patients with idiopathic pulmonary fibrosis, complicated fibrosis after diffuse alveolar damage (DAD) and inorganic dust-induced lung fibrosis. The tissue from lungs of patients undergoing episodes of active and/or end-stage pulmonary fibrosis shows the accumulation of inflammatory cells, such as mononuclear cells, neutrophils, mast cells and eosinophils, and fibroblast hyperplasia. In this regard, it appears that the inflammation triggers fibroblast activation and proliferation with enhanced matrix synthesis, stimulated by inflammatory mediators such as interleukin-1 (IL-1) and/or tumor necrosis factor (TNF). It has been well known that TGF-$\beta$ enhance the proliferation of fibroblasts and the production of collagen and fibronectin, and inhibit the degradation of collagen. In this regard, It is likely that TGF-$\beta$ undergoes important roles in the pathogenesis of pulmonary fibrosis. Nevertheless, this single cytokine is not the sole regulator of the pulmonary fibrotic response. It is likely that the balance of many cytokines including TGF-$\beta$, IL-1, IL-6 and TNF-$\alpha$ regulates the pathogenesis of pulmonary fibrosis. In this study, we investigate the interaction of TGF-$\beta$, IL-1$\beta$, IL-6 and TNF-$\alpha$ and their effect on the proliferation of fibroblasts. Methods: We used a human fibroblast cell line, MRC-5 (ATCC). The culture of MRC-5 was confirmed by immunofluorecent staining. First, we determined the concentration of serum in cuture medium, in which the proliferation of MRC-5 is supressed but the survival of MRC-5 is retained. Second, we measured optical density after staining the cytokine-stimulated cells with 0.5% naphthol blue black in order to detect the effect of cytokines on the proliferation of MRC-5. Result: In the medium containing 0.5% fetal calf serum, the proliferation of MRC-5 increased by 50%, and it was maintained for 6 days. IL-1$\beta$, TNF-$\alpha$ and IL-6 induced the proliferation of MRC-5 by 45%, 160% and 120%, respectively. IL-1$\beta$ and TNF-$\alpha$ enhanced TGF-$\beta$-induced proliferation of MRC-5 by 64% and 159%, but IL-6 did not affect the TGF-$\beta$-induced proliferation. And lNF-$\alpha$-induced proliferation of MRC-5 was reduced by IL-1$\beta$ in 50%. TGF-$\beta$, TNF-$\alpha$ and both induced the proliferation of MRC-5 to 89%, 135% and 222%, respectively. Conclusions: TNF-$\alpha$, TGF-$\beta$ and IL-1$\beta$, in the order of the effectiveness, showed the induction of MRC-5 proliferation of MRC-5. TNF-$\alpha$ and IL-1$\beta$ enhance the TGF-$\beta$-induced proliferation of MRC-5, but IL-6 did not have any effect TNF-$\alpha$-induced proliferation of MRC-5 is diminished by IL-1, and TNF-$\alpha$ and TGF-$\beta$ showed a additive effect.