Mitsunobu F, Ashida K, Hosaki Y, Tsugeno H, Okamoto M, Nishida N, Nagata T, Tanizaki Y, Tanimoto M
Department of Medicine, Misasa Medical Center Second Department of Internal Medicine, Okayama University Medical School, Yamada, Misasa, Tottori, Japan.
Clin Exp Allergy. 2004 Jan;34(1):59-64. doi: 10.1111/j.1365-2222.2004.01844.x.
Smoking is the most important cause of chronic obstructive pulmonary disease (COPD). However, the influence of cigarette smoking on the pathogenesis of asthma in the elderly remains controversial. This study attempted to clarify the influence of cigarette smoking on elderly asthmatics.
Forty-eight asthmatics over 70 years old (25 ex-smokers and 23 never-smokers) and 20 patients with COPD over 70 years old (all ex-smokers) were studied to determine the influence of cigarette smoking on IgE-mediated allergy (total IgE, IgE antibodies against inhalant allergens, bronchial hyper-responsiveness (BHR), generation of leukotriene (LT) B4 and C4), pulmonary function, and the relative area of lung showing attenuation values less than -950 Hounsfield units (RA950) on high-resolution computed tomography scans.
The incidence of positive IgE antibodies against inhalant allergens, BHR, and the generation of leukotriene B4 (LTB4) by leucocytes were significantly increased in patients with a history of smoking compared with those without. Residual volume (%RV) was significantly increased, and diffusing capacity for carbon monoxide was significantly decreased in ex-smokers with asthma and COPD compared with never-smokers with asthma. Inspiratory RA950 and ratio of expiratory RA950 to inspiratory RA950 were significantly larger in asthmatics with a smoking history than in those without, and in COPD patients than in asthmatics.
Cigarette smoking enhances the production of IgE antibodies, BHR, and generation of LTB4 by leucocytes in elderly asthmatics. Increased hyper-inflation or emphysematous changes of the lungs expressed by increased RA950, closely related to %RV, was more frequently observed in ex-smokers compared with never-smokers.
吸烟是慢性阻塞性肺疾病（COPD）的最重要病因。然而，吸烟对老年人哮喘发病机制的影响仍存在争议。本研究试图阐明吸烟对老年哮喘患者的影响。
对48名70岁以上的哮喘患者（25名既往吸烟者和23名从不吸烟者）和20名70岁以上的COPD患者（均为既往吸烟者）进行研究，以确定吸烟对IgE介导的过敏反应（总IgE、针对吸入性过敏原的IgE抗体、支气管高反应性（BHR）、白三烯（LT）B4和C4的生成）、肺功能以及高分辨率计算机断层扫描中肺实质衰减值小于-950亨氏单位（RA950）的相对面积的影响。
与无吸烟史的患者相比，有吸烟史的患者中，针对吸入性过敏原的IgE抗体阳性、BHR以及白细胞生成白三烯B4（LTB4）的发生率显著增加。与无哮喘的从不吸烟者相比，有哮喘和COPD的既往吸烟者的残气量（%RV）显著增加，一氧化碳弥散量显著降低。有吸烟史的哮喘患者的吸气RA950以及呼气RA950与吸气RA950的比值均显著大于无吸烟史的患者，且在COPD患者中大于哮喘患者。
吸烟增强了老年哮喘患者中IgE抗体的产生、BHR以及白细胞生成LTB4的能力。与%RV密切相关的、由RA950增加所表示的肺过度充气或肺气肿改变在既往吸烟者中比从不吸烟者中更常见。
