• Clinical and Experimental Pediatrics
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• v.64 no.5
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• pp.229-238
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• 2021

Background: Bronchial hyperresponsiveness (BHR), an important physiological feature of asthma, is a prognostic marker of childhood asthma. Purpose: We aimed to investigate the factors associated with BHR in adolescents with childhood asthma. Methods: Two hundred and fifteen adolescents (≥13 years of age; 149 males, 66 females) who were diagnosed with asthma during childhood were enrolled, underwent methacholine challenge tests, and were divided into the BHR group (<25 mg/mL of provocation concentration causing a 20% fall in forced expiratory volume in 1 second [FEV₁] [PC₂₀], n=113) or non-BHR group (≥25 mg/mL of PC₂₀, n=102). We examined longitudinal changes in BHR and the risk factors for its persistence in the 108 adolescents for whom baseline data, including methacholine PC₂₀ at age 6 years, were available. Multivariate logistic regression analyses were performed to assess the factors associated with BHR in adolescents. Results: Mold sensitization (adjusted odds ratio [aOR], 5.569; P=0.005) and increased blood eosinophil count (aOR, 1.002; P=0.026) were independently associated with BHR in boys but not girls. The odds of BHR decreased by 32% with each 1-year increase in age in boys (aOR, 0.683; P=0.010) but not girls. A reduced FEV₁/forced vital capacity ratio (<90%) was independently related with BHR in female patients only (aOR, 7.500; P=0.007). BHR decreased with age throughout childhood. A low methacholine PC₂₀ at age 6 years was independently associated with persistent BHR throughout childhood in male and female patients, whereas early mold sensitization was a risk factor for persistent BHR in male patients only (aOR, 7.718; P=0.028). Conclusion: Our study revealed sex-specific differences in the factors associated with BHR in adolescents with childhood asthma. Our findings suggest the risk factors that might affect asthma transition from childhood to adolescence and adulthood.

• Tuberculosis and Respiratory Diseases
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• v.84 no.1
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• pp.22-34
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• 2021

The coronavirus pandemic, known as coronavirus disease 2019 (COVID-19), is an infectious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus first identified in patients from Wuhan, China. Since December 2019, SARS-CoV-2 has spread swiftly around the world, infected more than 25 million people, and caused more than 800,000 deaths in 188 countries. Chronic respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD) appear to be risk factors for COVID-19, however, their prevalence remains controversial. In fact, studies in China reported lower rates of chronic respiratory conditions in patients with COVID-19 than in the general population, while the trend is reversed in the United States and Europe. Although the underlying molecular mechanisms of a possible interaction between COVID-19 and chronic respiratory diseases remain unknown, some observations can help to elucidate them. Indeed, physiological changes, immune response, or medications used against SARS-CoV-2 may have a greater impact on patients with chronic respiratory conditions already debilitated by chronic inflammation, dyspnea, and the use of immunosuppressant drugs like corticosteroids. In this review, we discuss importance and the impact of COVID-19 on asthma and COPD patients, the possible available treatments, and patient management during the pandemic.

• Tuberculosis and Respiratory Diseases
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• v.77 no.6
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• pp.237-242
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• 2014

Asthma is a chronic inflammatory disease of the airway that comprises a variety of etiologies and inflammatory phenotypes. Clinically, there is a wide range of patients with varying severities and responses to individual drugs. The introduction of inhaled corticosteroid therapy has dramatically changed the treatment of asthma. Recent development of new therapies suggests the possibility of another breakthrough. These can be categorized as follows: anti-cytokine therapies that usually target eosinophilic inflammation, sublingual immunotherapy, and bronchial thermoplasty. In this paper, we will review the major articles related to asthma treatment that were published in 2013.

• Tuberculosis and Respiratory Diseases
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• v.63 no.3
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• pp.235-241
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• 2007

Background: Airway mucus hypersecretion plays an important role in the pathogenesis of asthma, and is associated with the induction of MUC5AC expression in airway secretion. The MUC5AC gene is highly polymorphic; however, there are few studies about the association between the polymorphisms of the MUC5AC gene and asthma susceptibility or asthma phenotypes. We have investigated the association of MUC5AC promoter polymorphisms with the risk of asthma and asthma phenotypes. Methods: We determined the genotypes of the MUC5AC promoter (-1274G>A) in 78 asthma patients and in 78 age, sex-matched control individuals in the Korean population. Genomic DNAs from blood were analyzed by PCR and RFLP (restriction fragment length polymorphism) determination. We examined $FEV_1$, total eosinophil count, serum IgE level, $PC_{20}$ and the presence of atopy (by a skin test) in asthma patients. Results: The mean age of the patients was $47.7{\pm}16.1$ years and 38.5% were men, and the mean $FEV_1$ was $84.4{\pm}22.3%$ of predicted in the asthma patients. The -1274G>A polymorphism of the MUC5AC promoter in asthma patients was not significantly different as compared with normal individuals (GG 57.7%, AG 34.6% and AA 7.7% in asthma patients vs. GG 56.4%, AG 38.5% and AA 5.1% in control subject, p = 0.752, Cod). Several clinical parameters in asthma patients such as $FEV_1$, total eosinophil count, serum IgE level, $PC_{20}$ and the presence of atopy, were not associated with the -1274G>A polymorphism of the MUC5AC promoter. Conclusion: The -1274G>A single nucleotide polymorphism (SNP) frequency of the MUC5AC promoter was not associated with asthma in a Korean population.

• Clinical and Experimental Pediatrics
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• v.50 no.4
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• pp.335-339
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• 2007

The link between upper airway disease (allergic rhinitis and sinusitis) and lower airway disease (asthma) has long been of interest to physicians. Many epidemiological and pharmacological studies have provided a better understanding of pathophysiologic interrelationship between allergic rhinitis and asthma. The vast majority of patients with asthma have allergic rhinitis, and rhinitis is a major independent risk factor for asthma in cross-sectional and longitudinal studies. The association between sinusitis and asthma has long been appreciated. Through the recent evidences, allergic rhinitis, sinusitis, and asthma may not be considered as different diseases but rather as the expression in different parts of the respiratory tract of same pathological process in nature. Various mechanisms have been proposed to explain the relationship between asthma and upper airway diseases, but the underlying mechanisms are not completely discovered. The implications for the one-airway hypothesis are important not only academically but also clinically for diagnostic and therapeutic purposes.

• Tuberculosis and Respiratory Diseases
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• v.81 no.4
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• pp.289-298
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• 2018

Background: Obstructive airway disease patients with increased variability of airflow and incompletely reversible airflow obstruction are often categorized as having asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS). ACOS is heterogeneous with two sub-phenotypes: asthma-ACOS and COPD-ACOS. The objective of this study was to determine the difference in risk of exacerbation between the two sub-phenotypes of ACOS. Methods: A total of 223 patients exhibiting incompletely reversible airflow obstruction with increased variability (spirometrically defined ACOS) were enrolled. These patients were divided into asthma-ACOS and COPD-ACOS according to their physician's diagnosis and smoking history of 10 pack-years. Within-group comparisons were made for asthma-ACOS versus COPD-ACOS and light smokers versus heavy smokers. Results: Compared to patients with COPD-ACOS, patients with asthma-ACOS experienced exacerbation more often despite their younger age, history of light smoking, and better lung function. While the light-smoking group showed better lung function, they made unscheduled outpatient clinic visits more frequently. On multivariate analysis, asthma-ACOS and poor inhaler compliance were significantly associated with more than two unscheduled clinic visits during the previous year. Conclusion: Spirometrically defined ACOS includes heterogeneous subgroups with different clinical features. Phenotyping of ACOS by physician's diagnosis could be significant in predicting future risk of exacerbation.

• The Journal of Internal Korean Medicine
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• v.29 no.1
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• pp.32-41
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• 2008

Background : Monocyte chemoattractant protein-1(MCP-1), one of the CC chemokines, appears to play a significant role in asthma pathogenesis. It was reported that polymorphism in the MCP-1(-2518 A/G promoter) was associated with asthma in Caucasians, but the association of this polymorphism and asthma patients in the Korean population has not yet been clarified. Objective : We investigated the possible association between 2 polymorphisms (-2518 A/G promoter and Cys35Cys) and asthma patients in a Korean population. Materials and Methods : DNA samples were obtained from 86 Korean asthma patients and 270 healthy controls. MCP-1 genomic variants (-2518 A/G promoter and Cys35Cys polymorphism) were detected by PCR-RFLP. Level of MCP-1 was measured by ELISA for each genotype (n=8) (AA, AG, GG) and allele types of -2518 A/G promoter polymorphism for control subjects. Results : The Cys35Cys polymorphism was associated with asthma patients in Korean population [genotype distribution ($X^{2}=16.011$, P<0.001)]. Comparison of the two groups revealed no detectable differences in genotype and allele frequencies of the -2518 A/G polymorphism. Haplotype frequencies analysis revealed significant difference $(X^{2}=51.70$, P<0.001). MCP-1 serum level of subjects with G genotype of -2518 A/G promoter polymorphism was statistically higher than that with AA genotype (P<0.05). Conclusion : Our data indicate that no association exists between the MCP-1 -2518 A/G polymorphism and asthma susceptibility in the Korean population. However, it is noteworthy that the high prevalence of the -2518 G allele in the Korean population suggests a potentially important ethnic variation in the regulation of MCP-1 production. This variation must be considered in gene-association studies in different ethnic populations.

• Molecules and Cells
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• v.27 no.2
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• pp.175-181
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• 2009

The myosin light chain kinase (MYLK) gene encodes both smooth muscle and nonmuscle cell isoforms. Recently, polymorphisms in MYLK have been reported to be associated with several diseases. To examine the genetic effects of polymorphisms on the risk of asthma and related phenotypes, we scrutinized MYLK by re-sequencing/genotyping and statistical analysis in Korean population (n = 1,015). Seventeen common polymorphisms located in or near exons, having pairwise $r^2$ values less than 0.25, were genotyped. Our statistical analysis did not replicate the associations with the risk of asthma and log-transformed total IgE levels observed among African descendant populations. However, two SNPs in intron 16 (+89872C> G and +92263T> C), which were in tight LD (|D'| = 0.99), revealed significant association with log-transformed blood eosinophil level even after correction multiple testing ($P=0.002/P^{corr}=0.01$ and $P=0.002/P^{corr}=0.01$, respectively). The log-transformed blood eosinophil levels were higher in individuals bearing the minor alleles for +89872C> G and +92263T> C than in those bearing other allele. In additional subgroup analysis, the genetic effects of both SNPs were much more apparent among asthmatic patients and atopic asthma patients. Among atopic asthma patients, the log-transformed blood eosinophil levels were proportionally increased by gene-dose dependent manner of in both +89872C> G and +92263T> C(P = 0.0002 and P = 0.00007, respectively). These findings suggest that MYLK polymorphisms might be among the genetic factors underlying differential increases of blood eosinophil levels among asthmatic patients. Further biological and/or functional studies are needed to confirm our results.

• Clinical and Experimental Pediatrics
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• v.55 no.9
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• pp.330-336
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• 2012

Purpose: Fractional exhaled nitric oxide (FeNO) and forced expiratory flow between 25% and 75% of vital capacity ($FEF_{25-75}$) are not included in routine monitoring of asthma control. We observed changes in FeNO level and $FEF_{25-75}$ after FeNO-based treatment with inhaled corticosteroid (ICS) in children with controlled asthma (CA). Methods: We recruited 148 children with asthma (age, 8 to 16 years) who had maintained asthma control and normal forced expiratory volume in the first second ($FEV_1$) without control medication for ${\geq}3$ months. Patients with FeNO levels >25 ppb were allocated to the ICS-treated (FeNO-based management) or untreated group (guideline-based management). Changes in spirometric values and FeNO levels from baseline were evaluated after 6 weeks. Results: Ninety-three patients had FeNO levels >25 ppb. These patients had lower $FEF_{25-75}$ % predicted values than those with FeNO levels ${\leq}25$ ppb (P<0.01). After 6 weeks, the geometric mean (GM) FeNO level in the ICS-treated group was 45% lower than the baseline value, and the mean percent increase in $FEF_{25-75}$ was 18.7% which was greater than that in other spirometric values. There was a negative correlation between percent changes in $FEF_{25-75}$ and FeNO (r=-0.368, P=0.001). In contrast, the GM FeNO and spirometric values were not significantly different from the baseline values in the untreated group. Conclusion: The anti-inflammatory treatment simultaneously improved the FeNO levels and $FEF_{25-75}$ in CA patients when their FeNO levels were >25 ppb.

• Allergy, Asthma & Respiratory Disease
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• v.6 no.6
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• pp.279-283
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• 2018

Asthma is considered a chronic inflammatory airway disease. Mounting evidence reports that patients with asthma are at significantly higher risk of developing communicable diseases such as invasive pneumococcal disease, Haemophilus influenza, varicella, measles, pertussis and tetanus. While impaired innate immunity may play a role in increased risk of developing these infections, suboptimal adaptive immune responses have also been reported to play a role in asthmatic subjects with regard to increased risk of infections. This review discusses the currently underrecognized immunological effect of asthma on antibody to vaccines and recommends that clinicians be aware of less optimal antibody production in response to vaccines in subjects with asthma.