• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.231-238
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• 1999

Background: Nocturnal hypoxemia occurs in patients with chronic obstructive pulmonary disease(COPD) and the detection and treatment of nocturnal hypoxemia should be part of the management of COPD patients. We performed this study to evaluate the factors influencing to sleep related arterial oxygen desaturation($SaO_2$) in patients with COPD. Methods: Resting and exercise cardiopulmonary function test, polysomnography, and $SaO_2$ during resting, exercise and sleep were measured in 12 patients with COPD. Results: The $SaO_2$ fell twice as much during sleep as during maximal exercise($13.1{\pm}9.3%$ fall in nocturnal $SaO_2$ vs. $6.4{\pm}3.3%$, p<0.05). Fall in nocturnal $SaO_2$ was well correlated with mean exercise $SaO_2$(r=-0.78, p<0.05), minimum exercise $SaO_2$(r=-0.90, p<0.01), and resting $SaO_2$(Cr=-0.82, p<0.05). Lowest sleep $SaO_2$ was well correlated with mean exercise $SaO_2$(r=0.80, p<0.05), lowest exercise $SaO_2$(r=0.90, p<0.01), and resting $SaO_2$(r=0.84, p<0.05). Conclusion: Resting and exercise $SaO_2$ was well correlated with nocturnal $SaO_2$, but exercise study add no additional information to predicting the nocturnal oxygen desaturation in patients with COPD.

• Tuberculosis and Respiratory Diseases
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• v.56 no.6
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• pp.600-610
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• 2004

Background : The plasma B-type natriuretic peptide(BNP) concentration increases with the degree of pulmonary hypertension in patients with chronic respiratory disease. The aim of this study was to examine the prognostic role of BNP in the acute exacerbation of chronic obstructive lung disease (COPD). Method : We selected 67 patients who were admitted our hospital because of an acute exacerbation of COPD. Their BNP levels were checked on admission at the Emergency Department. Their medical records were analyzed retrospectively. The patients were divided into two groups according to their in-hospital mortality. The patients' medical history, comobidity, exacerbation type, blood gas analysis, pulmonary function, APACHE II severity score and plasma BNP level were compared. Results : Multiple logistic regression analysis identified three independent predictors of mortality: $FEV_1$, APACHE II score and plasma BNP level. The decedents group showed a lower $FEV_1$($28{\pm}7$ vs. $37{\pm}15%$, p=0.005), a higher APACHE II score($22.4{\pm}6.1$ vs. $15.8{\pm}4.7$, p=0.000) and a higher BNP level ($201{\pm}116$ vs. $77{\pm}80pg/mL$, p=0.000) than the sSurvivors group. When the BNP cut-off level was set to 88pg/mL using the receiver operating characteristic curve, the sensitivity was 90% and the specificity was 75% in differentiating between the survivors and decedents. On Fisher's exact test, the odds ratio for mortality was 21.2 (95% CI 2.49 to 180.4) in the patients with a BNP level > 88pg/mL. Conclusion : The plasma BNP level might be a predictor of mortality in an acute exacerbation of COPD as well as the $FEV_1$ and APACHE II score.

• Laboraroty Animal Research
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• v.33 no.1
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• pp.40-47
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• 2017

HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-${\alpha}$, interleukin (IL)-6 and IL-$1{\beta}$ in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

• Tuberculosis and Respiratory Diseases
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• v.54 no.4
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• pp.395-402
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• 2003

Background : Patients with chronic obstructive pulmonary disease (COPD) are at increased risk for osteoporosis, which has implications for mobility and even mortality. The goal of this pilot study was to evaluate bone mineral density (BMD) and risk factors for osteoporosis in a limited number of men with COPD. Methods : We checked BMD, $FEV_1$(% of predicted) and investigated risk factors for osteoporosis in 44 male patients with COPD who visited our hospital from January to August 2002. Results : Mean(${\pm}$) age was $69{\pm}9$ yrs, body mass index(BMI) $21{\pm}3kg/m^2$, $FEV_1$ $50{\pm}18%$ of predicted, lumbar spine T-score $-3.0{\pm}1.2$, lumbar spine Z-score $-2.0{\pm}1.2$, and lumbar spine BMD $0.76{\pm}0.13g/cm^2$. Osteoporosis(T-score below -2.5) was present in 27 patients(61.4%) and osteopenia(T-score between -1 and -2.5) in 17(38.6%). None of the patients had normal BMD. There was no relationship between BMD and $FEV_1$(% of predicted). There were significant differences in smoking, alcohol consumption, exercise, cumulative steroid dose, BMI and BMD among the three groups according to $FEV_1$(% of predicted) (group1 : ${\geq}65%$, group2 : 50-64%, group3 : ${\leq}49%$), except age. However, there were no significant differences in these variables between the osteopenia and osteoporosis groups, except BMI. Linear Regression(Stepwise) analysis showed that lumbar BMD was correlated with BMI & exercise. Conclusion : BMD is significantly reduced in men with COPD. There was no relationship between BMD and pulmonary function.

• Tuberculosis and Respiratory Diseases
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• v.48 no.6
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• pp.944-955
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• 2000

Background : In patients with chronic obstructive pulmonary disease(COPD), several factors have been associated with a poor prognosis. These include old age, low $FEV_1$ low diffusing capacity, high alveolar-arterial oxygen pressure difference, and finally cor pulmonale. This study was done to investigate if the ECG signs suggesting cor pulmonale were independent prognostic factors in patients with COPD. Method : We analyzed ECG, pulmonary function data and arterial blood gas values in 61 patients who were admitted through the emergency department with an acute exacerbation of COPD. The ECG signs reflecting cor pulmonale were right strial overloading(RAO), right bundle branch block, right ventricular hypertrophy and low-voltage QRS. The 61 patients were divided into 2 groups ; group I with no ECG signs(n=36) and group II with one or more ECG signs(n=25) suggesting cor, pulmonale. Results : Poor, prognostic factors by univariate analysis were low $FEV_1$, $FEV_1$ % pred., VC % pred., DLco, DLco % pred., $PaO_2$ and $SaO_2$ high $PaCO_2$ presence of ECG signs reflecting cor pulmonale, presence of mental status change, use of mechanical ventilator, and long term use of glucocorticoid. A multivariate analysis indicated that age(risk ratio=1.13, 95% confidence interval 1.05-1.23), DLco % pred. (risk ratio=0,97. 95% confidence interval 0.94-0.99), $PaO_2$ (risk ratio=0.95, 95% confidence interval 0.90-0.99) and RAO(risk ratio=5.27, 95% confidence interval 1.40-19.85) were independent prognostic factors of survival. There was a significant difference in survival between the patients with and without RAO(p=0.038). The survival rates at 1, 2, and 5 years were 94.5%. 81.4%, and 50.0% in patients without RAO and 82.4%, 70.6%, and 27.5% in patients with RAO, respectively. Conclusion : These results suggest that the presence of ECG signs reflecting cor pulmonale is a predictor of survival and that RAO of these ECG signs is a significant independent predictor of survival in patients with COPD.

• Tuberculosis and Respiratory Diseases
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• v.55 no.1
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• pp.88-97
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• 2003

Background : Although smoking is a major cause of chronic obstructive pulmonary disease (COPD), only 10-20% of cigarette smokers develop symptomatic COPD, which suggests the presence of genetic susceptibility. This genetic susceptibility to COPD might depend on variations in the activities of the enzyme that detoxify hazardous chemical products, such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase M1 subunit (GSTM1) genes. Methods : The genotypes of 58 patients with COPD, and 79 age matched control subjects, were determined by a polymerase chain reaction, followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX, and multiplex PCR for the GSTM1. Results : GSTM1 was deleted in 53.3% of the subjects. There was no difference in GSTM1 deletion rates between the COPD patients (32/58, 55.2%) and the control subjects (41/79, 51.9%). The combination patterns of two polymorphisms of mEPHX showed slow enzyme activity in 29(21.2%), normal in 73(53.3%) and fast in 32(23.4%). The COPD group (7/57, 12.3%) showed a significantly lower incidence of slow enzyme activity compared to the control subjects (22/77, 28.6%, p<0.05). However, when the COPD and control groups were compared with smokers only, there were no significant differences in the genotypes of GSTM1 and mEPHX. Conclusion : The genotypes of GSTM1 and mEPHX were not significant risk factors of COPD in this cohort of study.

• Tuberculosis and Respiratory Diseases
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• v.74 no.1
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• pp.7-14
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• 2013

Background: Fractional exhaled nitric oxide (FeNO) can be measured easily, rapidly, and noninvasively for the assessment of airway inflammation, particularly mediated by eosinophil, such as asthma. In bronchiectasis (BE), the pathogenesis has been known as chronic airway inflammation and infection with abnormal airway dilatation; however, there are little studies to evaluate the role of FeNO in BE. Methods: From March 2010 to February 2012, 47 patients with BE, diagnosed by high resolution computed tomography (HRCT), performed FeNO, compared with asthma and chronic obstructive pulmonary disease (COPD). All patients carried out a complete blood count including eosinophil count, chemistry, sputum examination, and spirometry, if indicated. A retrospective analysis was performed to elucidate the clinical role of FeNO in BE patients. Results: The mean FeNO levels in patients with BE was $18.8{\pm}1.5$ part per billion (ppb), compared to $48.0{\pm}6.4$ and $31.0{\pm}4.3$ in those with asthma and COPD, respectively (p<0.001). The FeNO levels tended to increase along with the disease severity scores by HRCT; however, it was statistically not significant. FeNO in BE with a co-infection of nontuberculous mycobacteria was the lowest at $17.0{\pm}3.5$ ppb among the study population. Conclusion: FeNO in BE was lower than other chronic inflammatory airway diseases, particularly compared with asthma. For clinical application of FeNO in BE, more large-scaled, prospective studies should be considered.

• Biomolecules & Therapeutics
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• v.28 no.3
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• pp.250-258
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• 2020

Emphysema, a major component of chronic obstructive pulmonary disease (COPD), is a leading cause of human death worldwide. The progressive deterioration of lung function that occurs in the disease is caused by chronic inflammation of the airway and destruction of the lung parenchyma. Despite the main impact of inflammation on the pathogenesis of emphysema, current therapeutic regimens mainly offer symptomatic relief and preservation of lung function with little therapeutic impact. In the present study, we aimed to discover novel therapeutics that suppress the pathogenesis of emphysema. Here, we show that LJ-2698, a novel and highly selective antagonist of the adenosine A₃ receptor, a G protein-coupled receptor involved in various inflammatory diseases, significantly reversed the elastase-induced destructive changes in murine lungs. We found that LJ-2698 significantly prevented elastase-induced airspace enlargement, resulting in restoration of pulmonary function without causing any obvious changes in body weight in mice. LJ-2698 was found to inhibit matrix metalloproteinase activity and pulmonary cell apoptosis in the murine lung. LJ-2698 treatment induced increases in anti-inflammatory cytokines in macrophages at doses that displayed no significant cytotoxicity in normal cell lines derived from various organs. Treatment with LJ-2698 significantly increased the number of anti-inflammatory M2 macrophages in the lungs. These results implicate the adenosine A₃ receptor in the pathogenesis of emphysema. Our findings also demonstrate the potential of LJ-2698 as a novel therapeutic/preventive agent in suppressing disease development with limited toxicity.

• Biomedical Science Letters
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• v.15 no.4
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• pp.309-317
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• 2009

Occupational exposure to inorganic dusts such as coal and silica has been identified as a chronic obstructive pulmonary disease (COPD) risk factor. This risk factor causes lung inflammation and protease-antiprotease imbalance. This abnormal inflammatory response of the lung induces parenchymal tissue destruction and leads to progressive airflow limitation that is characteristics of COPD. The aim of this study was to determine the relationship of proteases such as neutrophil elastase (NE) and matrix metalloproteinase (MMP)-9 and antiproteases such as alpha-1 antitrypsin (AAT) and tissue inhibitors of metalloproteinase (TIMP)-1 with lung function. The study population contained 223 retired workers exposed to inorganic dusts. We performed lung function test, including percent of forced expiratory volume in one second ($%FEV_1$) predicted and $%FEV_1$/forced vital capacity (FVC). We analyzed serum MMP-9, AAT, TIMP-1 and plasma NE concentrations by sandwich enzyme immunoassay. NE, AAT, and TIMP-1 concentrations in workers, who had $%FEV_1$<80% predicted, were higher than those of workers who had $%FEV_1{\geq}80%$ (P<0.05). Both AAT and TIMP-1 concentrations in workers with airflow limitation were higher than those of workers with normal airflow (P<0.05). $%FEV_1$ predicted showed significant negative correlation with AAT (r=-0.255, P<0.0l), TIMP-1 (r=-0.232, P<0.01), and NE (r=-0.196, P<0.01). $%FEV_1$/FVC predicted showed significant negative correlation with NE (r=-0.172, P<0.05). From the results of stepwise multiple regression analysis about $%FEV_1$ and $%FEV_1$/FVC, significant independents were NE (r=-0.135, P=0.001) and AAT (r=-0.100, P=0.013) in $%FEV_1$, and NE (r=-0.160, P=0.014) in $%FEV_1$/FVC. In the present study, there were significant correlations between airflow limitation and protease concentration and between airflow limitation and antiprotease concentration. Serum protease and antiprotease concentrations, however, may be affected by the biological and inflammatory responses. It is necessary to evaluate specimens more reflected the effects of proteases and antiproteases in the lung such as lung tissue, bronchoalveolar lavage fluid, and exhaled breath condensate (EBC).

• Tuberculosis and Respiratory Diseases
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• v.58 no.1
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• pp.25-30
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• 2005

Background : An insertion-deletion polymorphism of angiotensin converting enzyme (ACE) gene has been shown to be associated with enzyme activity levels of ACE. Reported results that have been mutually contradictory about asthmatic hypersensitiveness and occurrence according to ACE gene insertion (I)/deletion (D) polymorphism. Also, the involvement of the ACE genes as the genetic basis of bronchial asthma is currently controversy. We investigated whether there was any association between polymorphisms of the ACE genes and airway hyper-responsiveness in chronic obstructive pulmonary disease (COPD). Methods : A total of 100 patients with COPD were enrolled in this study. The ACE genotypes were determined in all subjects by polymerase chain reaction. Pulmonary function test including bronchodilator response (BDR), methacholine bronchial provocation test (MBPT) were done in those patients. Airway hyper-responsiveness include any findings of positive BDR or MBPT. Results : In COPD patients, the ACE genotype distribution did not differ significantly among groups of patients with severities of COPD, and with or without airway hyper-responsiveness. Conclusions : These results suggest that polymorphisms of the ACE gene may not be associated with airway hyper-responsiveness, development and severity of COPD.