• Tuberculosis and Respiratory Diseases
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• v.86 no.3
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• pp.166-175
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• 2023

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. The lower airways contain a rich and diverse microbiome, which may play a significant regulatory role in both health and disease. In COPD, the microbiome becomes perturbed, causing dysbiosis. Increased representation of members in the Proteobacteria phylum and certain members in the Firmicutes phylum has been associated with increased risk of exacerbations and mortality. Therapies such as inhaled corticosteroids and azithromycin may modulate the airway microbiome or its metabolites in patients with COPD. This paper provides an up-to-date overview of the airway microbiome and its importance in the pathophysiology of COPD and as potential therapeutic target in the future.

• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.302-312
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• 2022

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disease. Not all patients with COPD respond to available drugs. Identifying respondents to therapy is critical to delivering the most appropriate treatment and avoiding unnecessary medication. Recognition of individual patients' dominant characteristics by phenotype is a useful tool to better understand their disease and tailor treatment accordingly. To look for a suitable phenotype, it is important to understand what makes COPD complex and heterogeneous. The pathology of COPD includes small airway disease and/or emphysema. Thus, COPD is not a single disease entity. In addition, there are two types (panlobular and centrilobular) of emphysema in COPD. The coexistence of different pathological subtypes could be the reason for the complexity and heterogeneity of COPD. Thus, it is necessary to look for the phenotype based on the difference in the underlying pathology. Review of the literature has shown that clinical manifestation and therapeutic response to pharmacological therapy are different depending on the presence of computed tomography-defined airway wall thickening in COPD patients. Defining the phenotype of COPD based on the underlying pathology is encouraging as most clinical manifestations can be distinguished by the presence of increased airway wall thickness. Pharmacological therapy has shown significant effect on COPD with airway wall thickening. However, it has limited use in COPD without an airway disease. The phenotype of COPD based on the underlying pathology can be a useful tool to better understand the disease and adjust treatment accordingly.

• Tuberculosis and Respiratory Diseases
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• v.78 no.1
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• pp.8-17
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• 2015

Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.230-240
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• 2017

Chronic obstructive pulmonary disease (COPD) results in high morbidity and mortality among patients both domestically and globally. The Korean clinical practice guideline for COPD was revised in 2014. It was drafted by the members of the Korean Academy of Tuberculosis and Respiratory Diseases, as well as participating members of the Health Insurance Review and Assessment Service, Korean Physicians' Association, and Korea Respiration Trouble Association. This revised guideline covers a wide range of topics, including the epidemiology, diagnosis, assessment, monitoring, management, exacerbation, and comorbidities of COPD in Korea. We drafted a guideline on COPD management by performing systematic reviews on the topic of management with the help of a meta-analysis expert. We expect this guideline will be helpful medical doctors treating patients with respiratory conditions, other health care professionals, and government personnel in South Korea.

• Tuberculosis and Respiratory Diseases
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• v.79 no.4
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• pp.241-247
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• 2016

Bronchodilators are the cornerstone of symptomatic chronic obstructive pulmonary disease (COPD) treatment. They are routinely recommended for symptom reduction, with a preference of long-acting over short-acting drugs. Bronchodilators are classified into two classes based on distinct modes of action, i.e., long-acting antimuscarinics (LAMA, once-daily and twice-daily), and long-acting ${\beta}2$-agonists (LABA, once-daily and twice-daily). In contrast to asthma management, evidence supports the efficacy of both classes of long-acting bronchodilators as monotherapy in preventing COPD exacerbations, with greater efficacy of LAMA drugs versus LABAs. Several novel LAMA/LABA fixed dose combination inhalers are currently approved for COPD maintenance treatment. These agents show superior symptom control to monotherapies, and some of these combinations have also demonstrated superior efficacy in exacerbation prevention versus monotherapies, or combinations of inhaled corticosteroids plus LABA. This review summarizes the current data on clinical effectiveness of bronchodilators alone or in combination to prevent exacerbations of COPD.

• The Journal of the Korean life insurance medical association
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• v.29 no.1
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• pp.12-15
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• 2010

Global prevalence of chronic obstructive pulmonary disease(COPD) is known to 5.6 ~ 9.8%. Then life insurance applicants from persons with COPD are frequently encountered, and the underwriter and insurance medical doctors are called on with some regularity to render assessments of the mortality risk associated with COPD. According to previous article which contains long-term follow up of COPD, mortality ratio and excess death rate were 230% and 29 per 1000, respectively. Nowadays molecular genetic methodology such as GWAS has been developed. So it might be possible that molecular diagnostic methods may be one of useful underwriting tools in the life insurance risk selection of COPD applicants.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.241-246
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• 2017

Chronic obstructive pulmonary disease (COPD) is an ambulatory care-sensitive condition, and effective treatment of outpatients can prevent worsening of the illness and hospitalization. Current COPD guidelines provide appropriate guidance for the diagnosis and treatment of patients with COPD. In fact, it has been shown that when appropriate guidance and treatment are performed, the morbidity and mortality rates of COPD patients are reduced. However, there is a gap between the clinical guidelines and the actual clinical treatment. Therefore, the Health Insurance Review and Assessment Service (HIRA) conducted an evaluation of the adequacy of COPD diagnosis and treatment using the Claims Database of HIRA. This review provides a summary of the COPD adequacy assessment results reported by the HIRA and some brief comments on the results.

• Tuberculosis and Respiratory Diseases
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• v.71 no.1
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• pp.1-7
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• 2011

Many findings suggest that chronic obstructive pulmonary disease (COPD) imposes an enormous burden on patients, health-care professionals and society. COPD contributes to morbidity and mortality and to a significant use of health-care resources. In spite of a higher prevalence of COPD in Korea, the result of COPD treatment is not effective. The purpose of this article was to review recent advances in the study of COPD in Korea with the aim of improving effective management. This review highlights articles pertaining to the following topics; prevalence, assessment of COPD, risk factors for hospitalization, co-morbid diseases, phenotypes, and treatment issues.

• Tuberculosis and Respiratory Diseases
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• v.83 no.3
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• pp.185-194
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• 2020

Blood eosinophil counts have emerged as a chronic obstructive pulmonary disease (COPD) biomarker that predict the effects of inhaled corticosteroids (ICS) in clinical practice. Post-hoc and prospective analysis of randomized control trials have shown that higher blood eosinophil counts at the start of the study predict a greater response to ICS. COPD patients with frequent exacerbations (2 or more moderate exacerbations/yr) or a history of hospitalization have a greater response to ICS. Ex-smokers also appear to have a greater ICS response. Blood eosinophil counts can be combined with clinical information such as exacerbation history and smoking status to enable a precision medicine approach to the use of ICS. Higher blood eosinophil counts are associated with increased eosinophilic lung inflammation, and other biological features that may contribute to the increased ICS response observed. Emerging data indicates that lower blood eosinophil counts are associated with an increased risk of bacterial infection, suggesting complex relationships between eosinophils, ICS response, and the airway microbiome.

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.68-72
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• 2022

Posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) are relatively uncommon neurological disorders. These two independent syndromes can be concurrent as a part of a continuum process; however, the specific mechanism is not well known. Although the relationship between RCVS and PRES is currently unclear, they could share a common pathophysiology. This case report aimed to determine the pathophysiology underlying the co-occurrence of PRES and RCVS in a patient with an acute exacerbation of chronic obstructive pulmonary disease.