Search

Eun Chong Yoon,1 So-My Koo,1 Hye Yun Park,2 Ho Cheol Kim,3 Woo Jin Kim,4 Ki Uk Kim,5 Ki-Suck Jung,6 Kwang Ha Yoo,7 Hyoung Kyu Yoon,8 Hee-Young Yoon1 1Division of Allergy and Respiratory Diseases, Department of Internal Medicine, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea; 2Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; 3Department of Internal Medicine, Gyeongsang National University Changwon Hospital, Gyeongsang National University School of Medicine, Changwon, Republic of Korea; 4Department of Internal Medicine and Environmental Health Center, Kangwon National University, Chuncheon, Republic of Korea; 5Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; 6Department of Internal Medicine, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Republic of Korea; 7Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Republic of Korea; 8Department of Internal Medicine, Yeouido St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of KoreaCorrespondence: Hee-Young Yoon, Soonchunhyang University Seoul Hospital, 59, Daesagwan-ro, Yongsan-gu, Seoul, 04401, Republic of Korea, Tel +82-10-8728-6950, Fax +82-2-709-9554, Email yhyoung85@schmc.ac.krPurpose: Chronic obstructive pulmonary disease (COPD) is a respiratory disease characterized by chronic inflammation. Acute exacerbation of COPD (AECOPD) manifests as acute worsening of respiratory symptoms and is associated with high morbidity and mortality. The aim of the present study was to evaluate the predictive value of white blood count (WBC) and its derived inflammatory biomarkers for AECOPD.Methods: From the Korean COPD Subgroup Study cohort, a prospective and multicenter observational study, 826 patients who had baseline complete blood count (CBC) and 3-year AECOPD data were included. Follow-up CBC data at 1 (n = 385), 2 (n = 294), and 3 (n = 231) years were collected for available patients. The primary outcome was the occurrence of AECOPD at 3 years. The risk of AECOPD was evaluated using a binary logistic analysis.Results: The cumulative incidences of 12-, 24-, and 36-month AECOPD were 47.6%, 60.5%, and 67.6%, respectively. Patients with AECOPD at 3 years had higher baseline WBC counts, neutrophil counts, neutrophil/lymphocyte ratio (NLR), and neutrophil/monocyte ratio than those without AECOPD. Higher WBC count, neutrophil count, and NLR were associated with the 3-year occurrence of AECOPD in the univariate analysis, but only the higher neutrophil count was a significant risk factor (odds ratio [OR] = 1.468; 95% confidence interval [CI]: 1.024– 2.104) in the covariates-adjusted analysis. In the analysis of changes in inflammatory parameters, a decrease in the platelet count (OR = 0.502; 95% CI: 0.280– 0.902) and NLR (OR = 0.535; 95% CI: 0.294– 0.974) at 2 years and an increase in the eosinophil count (OR = 2.130; 95% CI: 1.027– 4.416) at 3 years were significantly associated with AECOPD in the adjusted analysis.Conclusion: Our data suggest that a high baseline WBC count, particularly neutrophil count, was associated with a higher incidence of long-term AECOPD.Keywords: blood cell count, blood platelets, eosinophils, lymphocytes, neutrophils, pulmonary disease, chronic obstructive

Sang Hee Lee,1,2 Haejung Lee,3 Yun Seong Kim,4 Hye-Kyung Park,5,6 Min Ki Lee,5,6 Ki Uk Kim5,6 1Department of Internal Medicine, Wonkwang University Sanbon Hospital, Gunpo-si, Republic of Korea; 2Department of Internal Medicine, Wonkwang University College of Medicine, Iksan, Republic of Korea; 3Department of Nursing, Pusan National University College of Nursing, Yangsan-si, Republic of Korea; 4Department of Internal Medicine, Pusan National University Yangsan Hospital, Yangsan-si, Republic of Korea; 5Department of Internal Medicine, Pusan National University Hospital, Busan, Republic of Korea; 6Medical Research Institute, Pusan National University Hospital, Busan, Republic of KoreaCorrespondence: Ki Uk KimDepartment of Internal Medicine, Pusan National University School of Medicine, 179 Gudeok-ro, Seo-gu, Busan 49241, Republic of KoreaTel +82-51-240-7804Fax +82-51-254-3127Email uk303@naver.comBackground: Disease-specific knowledge is associated with outcomes of patients, but the knowledge level of chronic obstructive pulmonary disease (COPD) patients is known to be low.Objective: We measured the level of disease-specific knowledge and defined factors associated with poor disease knowledge in COPD patients.Materials and Methods: A cross-sectional survey was performed in five hospitals in South Korea. At enrolment, all patients completed the Bristol COPD Knowledge Questionnaire (BCKQ), Satisfaction with Life Scale (SWLS), Personal Resource Questionnaire (PRQ), St. George’s Respiratory Questionnaire (SGRQ), 36-item Short-Form Health Survey (SF-36), and the Hospital Anxiety and Depression Scale (HADS). The data were analyzed via linear regression to identify factors associated with low-level knowledge of COPD.Results: A total of 245 COPD patients were enrolled in this study. The mean total BCKQ score was 28.1 (SD, 7.4). The lowest scores were seen for items exploring knowledge of “Oral steroids” and “Inhaled steroids”. In univariate analysis, higher level of education (r = 0.17), low income (r = 0.13), the post-bronchodilator FEV1, % predicted (r = − 0.24), the post-bronchodilator FEV1/FVC ratio (r = − 0.13), SWLS (r = 0.15), PRQ (r = 0.16), SF-36 MCS (r = 0.13), HADS-A (r = − 0.17), and HADS-D (r = − 0.28) scores correlated with the BCKQ score (all p < 0.05). FEV1 (r = − 0.25, p < 0.001) and HADS-D score (r = − 0.29, p < 0.001) were significantly associated with the total BCKQ score in multivariate analysis.Conclusion: Our Korean patients with COPD lacked knowledge on oral and inhaled steroid treatments. In particular, patients with higher-level lung function and/or depressive symptoms exhibited poorer disease-specific knowledge; such patients may require additional education.Keywords: chronic obstructive pulmonary disease, disease knowledge, lung function, depression

Sei Won Kim,1,* Chin Kook Rhee,2,* Ki Uk Kim,3 Sang Haak Lee,4 Hun Gyu Hwang,5 Yu Il Kim,6 Deog Kyeom Kim,7 Sang Do Lee,8 Yeon-Mok Oh,8 Hyoung Kyu Yoon1 On behalf of the KOLD Study Group 1Division of Pulmonary, Department of Internal Medicine, Yeouido St Mary’s Hospital, 2Division of Pulmonary, Allergy and Critical Care Medicine, Department of Internal Medicine, Seoul St Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, 3Department of Internal Medicine, Pusan National University, School of Medicine, Busan, 4Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, St Paul’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, 5Department of Internal Medicine, Soonchunhyang University Gumi Hospital, Gumi, 6Division of Pulmonology, Department of Internal Medicine, Chonnam National University Hospital, Gwangju, 7Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, SMG-SNU Boramae Medical Center, Seoul National University College of Medicine, 8Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea *These authors contributed equally to this work Background: Interleukin (IL)-33 promotes T helper (Th)2 immunity and systemic inflammation. The role of IL-33 in asthma has been widely investigated. IL-33 has also been suggested to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). This study investigated the clinical significance and usefulness of plasma IL-33 level in patients with COPD. Methods: A total of 307 patients with stable COPD from 15 centers, who were in the Korean Obstructive Lung Disease cohort, were enrolled in this study. Plasma IL-33 levels were measured by enzyme-linked immunosorbent assay. We analyzed the association between IL-33 level and other clinical characteristics related to COPD. We also examined the features of patients with COPD who exhibited high IL-33 levels. Results: IL-33 levels varied, but were very low in most patients. Eosinophil count was significantly correlated with a plasma IL-33 level. In addition, old age and current smoking were related to a low IL-33 level. Significantly more patients with a higher IL-33 level had chronic bronchitis compared with those with a low IL-33 level. Conclusion: Plasma IL-33 level in patients with stable COPD was related to eosinophil count and chronic bronchitis phenotype. Further studies are needed to identify the precise mechanisms of IL-33/ST2 pathway in patients with COPD. Keywords: biomarker, cytokine, interleukin-33, eosinophil, pathogenesis, chronic bronchitis

Metabolic reprogramming is an important cancer hallmark. However, the mechanisms driving metabolic phenotypes of cancer cells are unclear. Here, we show that the interferon-inducible (IFN-inducible) protein viperin drove metabolic alteration in cancer cells. Viperin expression was observed in various types of cancer and was inversely correlated with the survival rates of patients with gastric, lung, breast, renal, pancreatic, or brain cancer. By generating viperin knockdown or stably expressing cancer cells, we showed that viperin, but not a mutant lacking its iron-sulfur cluster-binding motif, increased lipogenesis and glycolysis via inhibition of fatty acid [beta]-oxidation in cancer cells. In the tumor microenvironment, deficiency of fatty acids and oxygen as well as production of IFNs upregulated viperin expression via the PI3K/AKT/mTOR/HIF-1[alpha] and JAK/STAT pathways. Moreover, viperin was primarily expressed in cancer stem-like cells (CSCs) and functioned to promote metabolic reprogramming and enhance CSC properties, thereby facilitating tumor growth in xenograft mouse models. Collectively, our data indicate that viperin-mediated metabolic alteration drives the metabolic phenotype and progression of cancer., Introduction Cancers are surrounded by a complex microenvironment that causes hypoxic and nutritional stress. Cancer cells reprogram metabolic pathways to support cancer proliferation, growth, metastasis, and survival within this harsh [...]