Matsuse Hiroto
Nihon Arukoru Yakubutsu Igakkai Zasshi. 2016 Jun;51(3):214-220.
The purpose of the present review is to explain the mechanism of alcohol-induced asthma in Japanese. An oral ethanol provocation test was performed in Japanese asthmatics to measure pulmonary function, blood ethanol, acetaldehyde and histamine. Acetaldehyde dehydrogenase 2 (ALDH2) genotype was determined by polymerase chain reaction (PCR) and ethanol patch test. Human bronchi and mast cells were stimulated with acetaldehyde in vitro. Approximately half of the asthmatic subjects developed bronchoconstriction with concomitant increases in blood acetaldehyde and histamine, which was associated with genetically reduced ALDH2 activities. In vitro acetaldehyde stimulation induced bronchoconstriction and degranulation of human mast cells. Collectively, as a metabolite of alcohol, the elevation of acetaldehyde following alcohol consumption induces airway mast cells to release histamine, which result in exacerbation of asthma in susceptible population.
本综述的目的是解释日本人群中酒精诱发哮喘的机制。对日本哮喘患者进行口服乙醇激发试验，以测量肺功能、血液中的乙醇、乙醛和组胺。通过聚合酶链反应（PCR）和乙醇贴片试验确定乙醛脱氢酶2（ALDH2）基因型。在体外用乙醛刺激人支气管和肥大细胞。大约一半的哮喘受试者出现支气管收缩，同时血液中的乙醛和组胺增加，这与ALDH2活性的遗传降低有关。体外乙醛刺激可诱导人肥大细胞发生支气管收缩和脱颗粒。总的来说，作为酒精的一种代谢产物，饮酒后乙醛水平升高会诱导气道肥大细胞释放组胺，从而导致易感人群哮喘加重。
