SummaryBackground and objective The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). Methods TBXA2R gene polymorphisms (TBXA2R1795T4C, TBXA2R1924T4C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method.Results The rare C allele frequency of TBXA2R1795T4C was significantly higher in AIA than in ATA (P 5 0.03) and the TBXA2R1795T4C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV 1 ) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P 5 0.009); AIA patients homozygous for the 1795 C allele had a greater percent fall of FEV 1 compared with individuals with TBXA2R1795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R1795T4C rare allele and HLA DPB1*0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P 5 0.008, odds ratio 5 5.3). Conclusion These results suggest that the polymorphism of TBXA2R1795T4C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

SummaryBackground Our previous study reported that more than 50% of toluene diisocyanate (TDI)-induced asthma patients had persistent asthmatic symptoms even after complete avoidance. Although specific IgE (sIgE) has been detected in a portion of patients with TDI-asthma, a recent investigation suggests that the presence of serum specific IgG (sIgG), not sIgE, is more closely associated with positive bronchoprovocation test (BPT) results. Objective To evaluate the possible role of sIgE and sIgG in predicting long-term prognosis of TDIasthma. Materials and methods Forty-one TDI-asthma patients whose diagnosis was confirmed by TDI-BPT, and 20 unexposed healthy controls were enrolled. Both sIgE and sIgG to TDI-human serum albumin (HSA) conjugate were detected by ELISA. All patients with persistent asthmatic symptoms took anti-asthmatic medications during the follow-up period (mean: 67.5 months) and were instructed to avoid exposure to TDI. Airway hyper-responsiveness to methacholine (AHM) was monitored every year during the study period. The patients were classified into three groups according to changing patterns of AHM and asthmatic symptoms as follows: group I, no improvement with persistent asthmatic symptoms (n 12); group II, partial improvement with persistent asthmatic symptoms (n 13); group III, in remission (n 16). Results Favourable prognosis was associated with a mild degree of AHM at initial diagnosis (P < 0.05). Although there were no significant differences in the prevalence of sIgE antibody to TDI-HSA conjugate among the three groups (P > 0.05), prevalence of sIgG in group I tended to be higher than in group II (0.05 < P < 0.1). However, the levels of sIgG were significantly higher in group I than in group II (P 0.05), whereas levels of sIgE were significantly higher in group II than in group I (P 0.014). No significant differences were noted in exposure duration, sex, age, atopic status, and total IgE level among the three groups (P > 0.05). Conclusion This study confirmed that a favourable outcome is related to a mild degree of AHM and to low levels of sIgG to predict persistent asthmatic symptoms, it also suggested that the presence of high serum-specific IgE at initial diagnosis may represent a better prognosis.