摘要来源： 临床exp exp exp allergy。 2010年3月； 40（3）：486-93。 Epub 2009 10月7日。PMID： 19817752 19817752
A B Riemer
Abstract:BACKGROUND: Hypersensitivity reactions towards non-steroidal anti-inflammatory drugs (NSAID) are common, although true allergies are detectable only in患者亚组。当前的研究是通过病例观察提示的，患者经验在他的第二多氯芬酸和质子泵抑制剂药物的第二个过程之后，被发现了广义的荨麻疹，并被发现具有双氯芬酸特异性IgE。 During recent years, our group has been investigating the importance of gastric digestion in the development of food allergies, demonstrating anti-acid medication as a risk factor for sensitization against food proteins.
OBJECTIVE: Here, we aimed to investigate whether the mechanism of food allergy induction described can also be causative in NSAID过敏，使用双氯芬酸作为范式。
方法： 我们将BALB/C小鼠对患者药物摄入后建模的几种口服免疫治疗方法进行。双氯芬酸在各种剂量的情况下，单独或共价耦合白蛋白，将双氯芬酸施用。在抗体水平上评估免疫反应, and functionally examined by in vitro and in vivo crosslinking assays.
RESULTS: Only mice receiving albumin-coupled diclofenac under gastric acid suppression developed anti-diclofenac IgG1 and IgE, whereas no immune responses were induced by the drug alone or without胃酸抑制。抗体诱导的剂量取决于剂量，该组接受了较高剂量的药物，显示持续的抗二氯芬酸滴度。抗体在体内诱导的体外和阳性皮肤测试诱导的粒细胞脱粒。
结论： 胃酸抑制是一种抑制量的引起的机制，