Kim, So Ri;Choe, Yeong Hun;Lee, Ka Young;Min, Kyung Hoon;Park, Seoung Ju;Lee, Heung Bum;Lee, Yong Chul;Rhee, Yang Keun
Tuberculosis and Respiratory Diseases
/
v.64
no.2
/
pp.125-132
/
2008
Background: In chronic obstructive pulmonary disease (COPD) patients, the serum levels of C-reactive protein (CRP) are elevated and an increase of CRP is more exaggerated in the acute exacerbation form of COPD (AECOPD) than in stable COPD. Pulmonary arterial hypertension is a common complication of COPD. An increased level of CRP is known to be associated with the risk of systemic cardio-vascular disorders. However, few findings are available on the potential role of CRP in pulmonary arterial hypertension due to COPD. Methods: This study was performed prospectively and the study population was composed of 72 patients that were hospitalized due to AECOPD. After receiving acute management for AECOPD, serum CRP levels were evaluated, arterial oxygen pressure ($PaO_2$), was measured, and the existence of pulmonary arterial hypertension under room air inhalation was determined in the patients. Results: The number of patients with pulmonary arterial hypertension was 47 (65.3%)., There was an increased prevalence of pulmonary arterial hypertension and an increase of serum CRP levels in patients with the higher stages of COPD (e.g., patients with stage 3 and stage 4 disease; P<0.05). The mean serum CRP levels of patients with pulmonary arterial hypertension and without pulmonary arterial hypertension were $37.6{\pm}7.4mg/L$ and $19.9{\pm}6.6mg/L$, respectively (P<0.05). However, there was no significant difference of the mean values of $PaO_2$ between patients with pulmonary arterial hypertension and without pulmonary arterial hypertension statistically ($77.8{\pm}3.6mmHg$ versus $87.2{\pm}6.0mmHg). Conclusion: We conclude that higher serum levels of CRP can be a sign for pulmonary arterial hypertension in AECOPD patients.
Quitting smoking helps smokers maintain their health and extend their lifespan by 10 or more years. Treatment strategies for smoking cessation should be tailored to individual smokers with special needs based on their specific circumstances. It is recommended that pregnant women adopt smoking cessation through counseling and behavioral interventions because the safety of medications has yet to be established. Counseling is the main strategy for smoking cessation in adolescents and nicotine replacement therapy can be used with caution in individuals with serious nicotine dependence. It is important for smokers with psychiatric diseases to quit smoking following accurate assessment of their depression status. Nicotine replacement therapy, varenicline, and bupropion can be used for smoking cessation in smokers with psychiatric disorders. The incidence of cardiovascular disease decreased according to the smoking status and the duration of smoking cessation. In smokers with chronic obstructive pulmonary disease (COPD) who used a combination of counseling and pharmacotherapy the quitting rate was more than twice as high as subjects who used behavioral interventions alone. Varenicline can be used as the most effective anti-smoking drug by most smokers including those with psychiatric disorders, cardiovascular disease, and COPD.
Uh, Soo-Taek;Koo, So-My;Kim, Yang Ki;Kim, Ki Up;Park, Sung Woo;Jang, An Soo;Kim, Do Jin;Kim, Yong Hoon;Park, Choon Sik
Tuberculosis and Respiratory Diseases
/
v.73
no.5
/
pp.258-265
/
2012
Background: Vitamin D can translocate a vitamin D receptor (VDR) from the nucleus to the cell membranes. The meaning of this translocation is not elucidated in terms of a role in pathogenesis of chronic obstructive pulmonary disease (COPD) till now. VDR deficient mice are prone to develop emphysema, suggesting that abnormal function of VDR might influence a generation of COPD. The blood levels of vitamin D have known to be well correlated with that of lung function in patients with COPD, and smoking is the most important risk factor in development of COPD. This study was performed to investigate whether cigarette smoke extracts (CSE) can inhibit the translocation of VDR and whether mitogen activated protein kinases (MAPKs) are involved in this inhibition. Methods: Human alveolar basal epithelial cell line (A549) was used in this study. 1,25-$(OH_2)D_3$ and/or MAPKs inhibitors and antioxidants were pre-incubated before stimulation with 10% CSE, and then nucleus and microsomal proteins were extracted for a Western blot of VDR. Results: Five minutes treatment of 1,25-(OH2)D3 induced translocation of VDR from nucleus to microsomes by a dose-dependent manner. CSE inhibited 1,25-$(OH_2)D_3$-induced translocation of VDR in both concentrations of 10% and 20%. All MAPKs inhibitors did not suppress the inhibitory effects of CSE on the 1,25-$(OH_2)D_3$-induced translocation of VDR. Quercetin suppressed the inhibitory effects of CSE on the 1,25-$(OH_2)D_3$-induced translocation of VDR, but not in n-acetylcysteine. Conclusion: CSE has an ability to inhibit vitamin D-induced VDR translocation, but MAPKs are not involved in this inhibition.
Objective: This study aimed to use a mouse model to evaluate the effects of Gwaruhaengryeon-hwan (GHH) on chronic obstructive pulmonary disease (COPD) and particulate matter induced lung injury. Materials and Methods: The study was carried out in two ways (in vitro, in vivo). In vitro RAW 264.7 cells (mouse macrophage) were used and analyzed by flow cytometry, ELISA. In vivo lipopolysaccharide (LPS) and cigarette smoke solution (CSS), or coal, fly ash, diesel exhaust particle (CFD) challenged mice were used and its BALF was analyzed by ELISA, lung tissue by real-time PCR. Results: In vitro, GHH maintained an 80-100% rate of viability. So cytotoxicity was not shown. In the ELISA analysis with RAW 264.7 cells, GHH significantly decreased NO over $30{\mu}g/ml$. In the ELISA analysis, GHH significantly decreased $TNF-{\alpha}$, IL-6 over $300{\mu}g/ml$. In the COPD model, the GHH 200 mg/kg dosage group, the application of GHH significantly decreased the increasing of neutrophils, $TNF-{\alpha}$, IL-17A, MIP2, CXCL-1 in BALF, $TNF-{\alpha}$, $IL-1{\beta}$ mRNA expression in lung tissue and histological lung injury. In the CFD induced lung injury model, the GHH 200 mg/kg dosage group, the application of GHH significantly decreased the increase of neutrophils, $TNF-{\alpha}$, IL-17A, MIP2, CXCL-1 in BALF, MUC5AC, $TGF-{\beta}$ mRNA expression in lung tissue and histological lung injury. Conclusion: This study suggests the usability of GHH for COPD patients by controlling lung tissue injury.
Park, Jinkyeong;Lim, Myoung Nam;Hong, Yoonki;Kim, Woo Jin
Tuberculosis and Respiratory Diseases
/
v.78
no.4
/
pp.326-335
/
2015
Background: Asian dust is known to have harmful effects on the respiratory system. Respiratory conditions are also influenced by environmental conditions regardless of the presence of pollutants. The same pollutant can have different effects on the airway when the air is dry compared with when it is humid. We investigated hospital visits for chronic obstructive pulmonary disease (COPD) and asthma in relation to the environmental conditions. Methods: We conducted a retrospective study using the Korean National Health Insurance Service claims database of patients who visited hospitals in Chuncheon between January 2006 and April 2012. Asian dust, haze, mist, and fog days were determined using reports from the Korea Meteorological Administration. Hospital visits for asthma or COPD on the index days were compared with the comparison days. We used two-way case-crossover techniques with one to two matching. Results: The mean hospital visits for asthma and COPD were $59.37{\pm}34.01$ and $10.04{\pm}6.18$ per day, respectively. Hospital visits for asthma significantly increased at lag0 and lag1 for Asian dust (relative risk [RR], 1.10; 95% confidence interval [CI], 1.01-1.19; p<0.05) and haze (RR, 1.13; 95% CI, 1.06-1.22; p<0.05), but were significantly lower on misty (RR, 0.89; 95% CI, 0.80-0.99; p<0.05) and foggy (RR, 0.89; 95% CI, 0.84-0.93; p<0.05) days than on control days. The hospital visits for COPD also significantly increased on days with Asian dust (RR, 1.29; 95% CI, 1.05-1.59; p<0.05), and were significantly lower at lag4 for foggy days, compared with days without fog (RR, 0.85; 95% CI, 0.75-0.97; p<0.05). Conclusion: Asian dust showed an association with airway diseases and had effects for several days after the exposure. In contrast to Asian dust, mist and fog, which occur in humid air conditions, showed the opposite effects on airway diseases, after adjusting to the pollutants. It would require more research to investigate the effects of various air conditions on airway diseases.
Jae Eun Song;So Hyeon Bak;Myoung-Nam Lim;Eun Ju Lee;Yoon Ki Cha;Hyun Jung Yoon;Woo Jin Kim
Journal of the Korean Society of Radiology
/
v.84
no.5
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pp.1123-1133
/
2023
Purpose Our study aimed to evaluate the association between automated quantified body composition on CT and pulmonary function or quantitative lung features in patients with chronic obstructive pulmonary disease (COPD). Materials and Methods A total of 290 patients with COPD were enrolled in this study. The volume of muscle and subcutaneous fat, area of muscle and subcutaneous fat at T12, and bone attenuation at T12 were obtained from chest CT using a deep learning-based body segmentation algorithm. Parametric response mapping-derived emphysema (PRMemph), PRM-derived functional small airway disease (PRMfSAD), and airway wall thickness (AWT)-Pi10 were quantitatively assessed. The association between body composition and outcomes was evaluated using Pearson's correlation analysis. Results The volume and area of muscle and subcutaneous fat were negatively associated with PRMemph and PRMfSAD (p < 0.05). Bone density at T12 was negatively associated with PRMemph (r = -0.1828, p = 0.002). The volume and area of subcutaneous fat and bone density at T12 were positively correlated with AWT-Pi10 (r = 0.1287, p = 0.030; r = 0.1668, p = 0.005; r = 0.1279, p = 0.031). However, muscle volume was negatively correlated with the AWT-Pi10 (r = -0.1966, p = 0.001). Muscle volume was significantly associated with pulmonary function (p < 0.001). Conclusion Body composition, automatically assessed using chest CT, is associated with the phenotype and severity of COPD.
Recently, Machine Learning Methods are widely used with high prediction performance. But if the limit of the data is solved by the statistical technique, It can, lead to higher prediction performance than the existing one. In this study, the SMOTE method is used to solve the imbalance problem in the longitudinal and imbalanced data. As a result, It, was confirmed that the prediction performance increases. Additionally, Although, studies on COPD have been actively conducted, only studies that are related to acute exacerbation have been conducted. So there are no studies on the prediction of acute exacerbation through multiple perspectives and predictive models for various factors. In this study, We examined the factors related to acute exacerbation of COPD and constructed a personalized specific disease prediction model.
Moon, Ji Yong;Bae, Joong Ho;Kim, Tae Hyung;Sohn, Jang Won;Yoon, Ho Joo;Shin, Dong Ho;Park, Sung Soo
Tuberculosis and Respiratory Diseases
/
v.59
no.6
/
pp.656-663
/
2005
Background : The B-type natriuretic peptide (BNP) is a cardiac neurohormone that is specifically secreted from the ventricles in response to volume expansion and a pressure overload. Differentiating congestive heart failure from the pulmonary causes of dyspnea is very important for patients presenting with acute dyspnea. Methods : A retrospective study was carried out on 261 patients who were admitted to the emergency department of Hanyang University Hospital due to acute dyspnea from March to July 2004. The serum BNP levels of the patients were measured using the ELISA method. Results : The BNP levels were 382, 111-1140 pg/ml (median, interquartile range) in the heart failure group (n=119) and 29, 7-81 pg/ml in the non-heart failure group (n=142). The BNP levels according to the subgroups of heart failure were 820, 354-1620 pg/ml, 1650, 239-1990 pg/ml, and 378, 106-1120 pg/ml for the chronic obstructive pulmonary disease (COPD) with combined left heart failure (n=5), cor pulmonale (n=3), and left heart failure groups (n=111), respectively. The BNP levels according to the subgroups of non-heart failure were 39, 21-101 pg/ml, 59, 10-129 pg/ml, and 15, 6-47 pg/ml for the COPD (n=20), other pulmonary diseases (n=56), and other causes groups (n=66), respectively. The BNP levels were significantly different according to the underlying etiology (p<0.001), and were significantly higher in the COPD patients with left heart failure than in those without (p=0.002). When the patients with no cardiovascular risk factor such as diabetes mellitus, hypertension, smoking or renal failure were analyzed, the BNP levels were also significantly higher in the patients with heart failure than in those without(p<0.001). When 133 pg/ml was designated as the BNP cut-off level the sensitivity for predicting heart failure was 73 percent and the specificity was 87 percent. Conclusion : BNP measurements are useful for determining the presence of heart failure in the patients presenting with acute dyspnea. The possibility of heart failure must be seriously considered in patients with high BNP levels even when they have a pre-existing pulmonary disease such as COPD or no risk factors for heart failure.
Park, Hyeon-Kwan;Yu, Young-Kwon;Kim, Kyu-Sik;Lim, Sung-Chul;Kim, Young-Chul;Park, Kyung-Ok
Tuberculosis and Respiratory Diseases
/
v.50
no.2
/
pp.158-170
/
2001
Background : Although an oxidants and antioxidants imbalance has been considered in the pathogenesis of chronic obstructive pulmonary disease (COPD), there is a paucity of reports focussing on the smoking-induced changes of oxidants and antioxidants in COPD. Method : The concentration of antioxidants (ascorbic acid, uric acid, retinol, and $\alpha$- & $\gamma$-tocopherol) was measured in the serum and induced sputum of 30 healthy controls and 34 stable COPD patients using high performance liquid chromatography (HPLC). The inhibition of lipid peroxidation as an index of antioxidant capacity was measured in the serum by a TBA assay. Results : The serum concentration of ascorbic acid, $\alpha$-tocopherol, and retinol were significantly lower in the patients with COPD than in healthy controls ($484.8{\pm}473.3$ vs $1497.8{\pm}819.2\;pmol/L$, $48.38{\pm}17.34$ vs $73.96{\pm}26.29\;pmol/L$, p<0.001, and $9.51{\pm}8.33$ vs $15.01{\pm}5.88\;pmol/L$, p<0.05, respectively, mean$\pm$SD). However, there were little differences in the ascorbic acid and uric acid concentrations in the induced sputum between the COPD patients and the controls. The induced sputum to serum ratio of ascorbic acid was significantly higher in COPD patients compared with healthy control (0.375 vs 0.085, p<0.05). In the normal controls, the serum ascorbic acid concentration was lower in smokers than in nonsmokers ($1073{\pm}536$ vs $1757{\pm}845\;pmol/L$, p<0.05), but the level was still higher than that of the COPD patients (p<0.05). The serum retinol levels were correlated with $FEV_1$ in COPD patients (r=0.58, p<0.05). The products of lipid peroxidation were increased in normal smokers and COPD compared with norma1 nonsmokers ($115.56{\pm}19.93$ vs $120.02{\pm}24.56$ vs $91.87{\pm}20.71\;{\mu}mol/{\mu}mol$ Pi of liposome, p<0.05). Conclusion : Cigarette smoking may induce the dep1etion of serum antioxidants and this depletion of antioxidants is suggested to play a role in the pathogenesis of COPD.
Backgrounds: This study investigated whether or not a polymorphism in the gene encoding the surfactant protein A(SP-A) has any bearing on the individual susceptibility to the development of chronic obstructive pulmonary disease(COPD) in a genetically homogenous Korean population. Methods: The genotypes of 19 COPD patients and 20 healthy neonates as controls were tested using a polymerase chain reaction followed by restriction fragment length polymorphism analysis for the SP-A gene. Results: The specific frequencies of the 6A2 and 6A18 alleles of SP-A1 and the 1A2 allele of SP-A2 were much higher in the COPD group than control group (p<0.05). However, the frequencies of the 6A3 and 6A4 alleles of SP-A1 and the 1A0 allele of SP-A2 in the COPD group were significantly lower than the control group. In the COPD group, the frequencies of the +50 locus genotypes GG of SP-A1 and the +9 locus genotypes CC of SP-A2 were 85.0% and 60.6%, respectively, and 19.7% and 24.8% in the control group, respectively. The frequencies of the polymorphic genotypes or alleles showed a statistically significant difference between the COPD group and the control group (P<0.05). Conclusion: A genetic polymorphism in SP-A is associated with the development of COPD in the Korean population.
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