哮喘联盟

   摘要
   目的：胃肠通透性(GIP)异常见于许多疾病，包括慢性肠道炎症性疾病如克罗恩病和非肠道免疫性疾病如糖尿病、多发性硬化症。虽然已有文献证实了在哮喘患者中有黏膜异常的消化障碍，但先前的研究仅仅只评估结肠的通透性，而忽视了小肠黏膜相关淋巴组织(MALT)丰富的区域。GIP的改变可能导致从肠腔进入体循环的致敏蛋白增加，从而启动并激活获得性免疫系统，并引起不恰当的过敏源致敏和/或诱发肠外炎症。本研究旨在评估中-重度成人哮喘患者中的胃肠通透性。
   方法：患者摄入一种复方糖溶液，并收集其尿液。采用高液相色谱法分析GIP。同时评估人口统计学特征、特应性(使用过敏源皮肤测试法评估)以及痰液细胞计数。
   结果：纳入14例中-重度哮喘患者，发现一半的患者GIP异常。GIP异常与痰液细胞计数无关，特应性与肠道通透性也无明显关联。
   结论：本研究证实了我们能够识别哮喘患者中免疫原性小肠MALT丰富区域的GIP异常。气道炎症和GIP增加关联性的缺乏表明这两个参数无因果关系，更确切的说是独立存在的，二者可在哮喘的发展和进程中独立或相继出现。
 

（苏楠 审校）
Clin Invest Med. 2014 Apr 1;37(2):E53.

 

High prevalence of abnormal gastrointestinal permeability in moderate-severe asthma.
 

Walker J, Dieleman L, Mah D, Park K, Meddings J, Vethanayagam D1.
 

ABSTRACT
PURPOSE: Abnormal gastrointestinal permeability (GIP) has been implicated in a number of diseases, including chronic intestinal inflammatory disorders such as Crohn's as well as non-intestinal immunologic diseases such as diabetes and multiple sclerosis. Although evidence in the literature demonstrates mucosal abnormalities of the digestive barrier in asthma, previous studies have assessed only colonic permeability, while ignoring the mucosal-associated lymphoid tissue (MALT) rich areas of the small intestine. Alterations in GIP may lead to increased entry of allergenic proteins from the gut lumen into the systemic circulation, thus priming and activating the adaptive immune system and leading to inappropriate allergen sensitization and/or deregulated extra-intestinal inflammation. This study examines GIP in adults with moderate to severe asthma.
METHODS: Patients ingested a mixed-sugar solution and urine was collected. GIP was assayed using high-performance liquid chromatography. Demographics, atopy (assessed by allergen skin testing) and sputum cell counts were also assessed.
RESULTS: Fourteen patients with moderate to severe asthma were studied, half of whom were found to have abnormal GIP. Abnormal GIP did not correlate with sputum cell counts and there was no apparent association between atopy and intestinal permeability.
CONCLUSION: This study demonstrated our ability to identify abnormal GIP in the MALT-rich, immunogenic small intestine of patients with asthma. The absence of a correlation between airway inflammation and increased GIP suggests that these two parameters are not causally linked, but rather define distinct entities that could separately or sequentially be involved with the development and propagation of asthma over time.
 

Clin Invest Med. 2014 Apr 1;37(2):E53.