Postprandial, or meal-related, symptoms, such as abdominal pain, early satiation, fullness or bloating, are often reported by patients with disorders of gut-brain interaction, including functional dyspepsia (FD) or irritable bowel syndrome (IBS). We propose that postprandial symptoms arise via a distinct pathophysiological process. A physiological or psychological insult, for example, acute enteric infection, leads to loss of tolerance to a previously tolerated oral food antigen. This enables interaction of both the microbiota and the food antigen itself with the immune system, causing a localised immunological response, with activation of eosinophils and mast cells, and release of inflammatory mediators, including histamine and cytokines. These have more widespread systemic effects, including triggering nociceptive nerves and altering mood. Dietary interventions, including a diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols, elimination of potential food antigens or gluten, IgG food sensitivity diets or salicylate restriction may benefit some patients with IBS or FD. This could be because the restriction of these foods or dietary components modulates this pathophysiological process. Similarly, drugs including proton pump inhibitors, histamine-receptor antagonists, mast cell stabilisers or even tricyclic or tetracyclic antidepressants, which have anti-histaminergic actions, all of which are potential treatments for FD and IBS, act on one or more of these mechanisms. It seems unlikely that food antigens driving intestinal immune activation are the entire explanation for postprandial symptoms in FD and IBS. In others, fermentation of intestinal carbohydrates, with gas release altering reflex responses, adverse reactions to food chemicals, central mechanisms or nocebo effects may dominate. However, if the concept that postprandial symptoms arise from food antigens driving an immune response in the gastrointestinal tract in a subset of patients is correct, it is paradigm-shifting, because if the choice of treatment were based on one or more of these therapeutic targets, patient outcomes may be improved.

中文翻译：

---

肠-脑相互作用障碍的餐后症状及其作为治疗目标的潜力


患有肠-脑相互作用障碍（包括功能性消化不良（FD）或肠易激综合征（IBS））的患者经常报告餐后或与膳食相关的症状，例如腹痛、早饱、饱腹感或腹胀。我们认为餐后症状是通过独特的病理生理过程产生的。生理或心理损伤，例如急性肠道感染，导致对先前耐受的口服食物抗原的耐受性丧失。这使得微生物群和食物抗原本身与免疫系统相互作用，引起局部免疫反应，激活嗜酸性粒细胞和肥大细胞，并释放炎症介质，包括组胺和细胞因子。这些具有更广泛的系统影响，包括触发伤害性神经和改变情绪。饮食干预措施，包括低可发酵寡糖、二糖、单糖和多元醇的饮食、消除潜在的食物抗原或麸质、IgG 食物敏感性饮食或限制水杨酸盐，可能会使一些 IBS 或 FD 患者受益。这可能是因为这些食物或饮食成分的限制调节了这种病理生理过程。同样，具有抗组胺能作用的药物，包括质子泵抑制剂、组胺受体拮抗剂、肥大细胞稳定剂，甚至三环或四环抗抑郁药，所有这些药物都是治疗 FD 和 IBS 的潜在方法，作用于这些机制中的一种或多种。驱动肠道免疫激活的食物抗原似乎不太可能是 FD 和 IBS 餐后症状的全部解释。 在其他情况下，肠道碳水化合物的发酵、气体释放改变反射反应、对食品化学品的不良反应、中枢机制或反安慰剂效应可能占主导地位。然而，如果餐后症状是由食物抗原在一部分患者胃肠道中驱动免疫反应引起的这一概念是正确的，那么这就是范式转变，因为如果治疗的选择是基于一个或多个这些治疗目标，患者的治疗效果可能会得到改善。