S. Cho

Positive and negative associations of HLA class I alleles with allopurinol-induced SCARs in Koreans.

Recent investigations suggest genetic susceptibility of allopurinol-induced severe cutaneous adverse reactions (SCARs). However, the strength of association was variable according to phenotypes and ethnic backgrounds. To explore genetic markers for allopurinol-induced SCARs in Koreans, we genotyped human leukocyte antigen (HLA) class I alleles of 25 cases of allopurinol-induced SCARs (20 cases of drug-induced hypersensitivity syndrome and five cases of Stevens–Johnson syndrome/toxic epidermal necrolysis) and 57 patients tolerant to allopurinol. Frequencies of B*5801 [92.0 vs. 10.5%, Pc=2.45×10−11, odds ratio (OR)=97.8], Cw*0302 (92.0 vs. 12.3%, Pc=9.39×10−11, OR=82.1), and A*3303 (88.0 vs. 26.3%, Pc=3.31×10−6, OR=20.5) were significantly higher in SCARs compared with tolerant controls. In contrast, A*0201 was not found in SCARs patients despite relatively high frequency in tolerant controls (29.8%). We found strong positive association of HLA-B*5801 and negative association of HLA-A*0201 with the development of allopurinol-induced SCARs in the Korean population.

Additive role of tiotropium in severe asthmatics and Arg16Gly in ADRB2 as a potential marker to predict response

Background:  Recent findings have raised new interests about the use of anticholinergics, especially tiotropium, for the treatment of asthma. This study was performed to determine whether an additional improvement in lung function is obtained when tiotropium is administrated in addition to conventional therapies in severe asthmatics, and to identify factors capable of predicting the response to tiotropium, using a pharmacogenetic approach.

Allergen-specific conventional immunotherapy decreases immunoglobulin E-mediated basophil histamine releasability

Background Allergen‐specific immunotherapy has proven to be clinically effective in the treatment of patients with atopic asthma; however, the mechanisms are still unclear. Several noted immunological changes include an increase of the allergen‐specific IgG antibody, a reduction in the allergen‐specific IgE antibody subsequent to transient increase, an allergen‐specific T cell shift in cytokine production from Th2 to Th1, and a decrease in quantity and activity of basophils and mast cells.

Association of angiotensin I‐converting enzyme gene polymorphisms with aspirin intolerance in asthmatics

Background Aspirin‐intolerant asthma (AIA) refers to the development of bronchoconstriction in asthmatic individuals following the ingestion of aspirin or other non‐steroidal anti‐inflammatory drugs (NSAIDs). Angiotensin I‐converting enzyme (ACE), a membrane‐bound peptidase present in the lung, plays a pivotal role in the metabolism of the endogenous peptides involved in the pathogenesis of asthma.

Association between bronchodilating response to short‐acting β‐agonist and non‐synonymous single‐nucleotide polymorphisms of β2‐adrenoceptor gene

Background With β‐agonists being the most widely used agents in the treatment of asthma, in vitro studies reported that β2‐adrenergic receptor (ADRB2) polymorphisms are associated with agonist‐promoted down‐regulation.

Evaluation of cytokine mRNA in induced sputum from patients with allergic rhinitis: relationship to airway hyperresponsiveness.

Background:  Although airway hyperresponsiveness (AHR) is a characteristic feature of asthma, it is also frequently present in allergic rhinitis (AR). However, the pathogenesis of AHR is unclear and the roles of cytokines in the airway have not been well established in AR. We sought to compare cytokine mRNA levels in the sputum of AR patients with or without AHR and those of asthma patients, and to evaluate whether differences in cytokine levels are associated with the development of an abnormal airway response and the absence of respiratory symptoms in AR patients with AHR.

Predictors of bronchial hyperresponsiveness in chronic rhinosinusitis with nasal polyp.

Background:  Chronic rhinosinusitis with nasal polyposis (CRSNP) and asthma are inflammatory lesions of the respiratory epithelium. This study was conducted to evaluate predictive factors of bronchial hyperresponsiveness (BHR) in patients with CRSNP.

Association and functional relevance of E237G, a polymorphism of the high‐affinity immunoglobulin E‐receptor β chain gene, to airway hyper‐responsiveness

Background The hyper‐sensitivity reaction of IgE, with its high‐affinity receptors (FcɛRI), is central to the phenomenon of atopic diseases.

Distinct association of genetic variations of vascular endothelial growth factor, transforming growth factor-β, and fibroblast growth factor receptors with atopy and airway hyperresponsiveness

Background:  Recent studies showed that high levels of transforming growth factor (TGF)‐β1 in the airways reduced airway responsiveness, which was reversed in conditions of basic fibroblast growth factor (FGF2) deficiency, whereas high levels of vascular endothelial growth factor (VEGF) enhanced airway sensitization to allergens and airway hyperresponsiveness (AHR).

Original article: Evaluation of cytokine mRNA in induced sputum from patients with allergic rhinitis: relationship to airway hyperresponsiveness

Background:  Although airway hyperresponsiveness (AHR) is a characteristic feature of asthma, it is also frequently present in allergic rhinitis (AR). However, the pathogenesis of AHR is unclear and the roles of cytokines in the airway have not been well established in AR. We sought to compare cytokine mRNA levels in the sputum of AR patients with or without AHR and those of asthma patients, and to evaluate whether differences in cytokine levels are associated with the development of an abnormal airway response and the absence of respiratory symptoms in AR patients with AHR.