Leeds Gastroenterology Institute, St James's University Hospital, Leeds, UK
Deakin University-Geelong Waterfront Campus, Geelong, Victoria, Australia.
Gut. 2024 Jun 6;73(7):1199-1211. doi: 10.1136/gutjnl-2023-331833.
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.
餐后（或与进食相关）症状，如腹痛、早饱、饱胀或腹胀，常发生于胃肠道-大脑交互障碍患者中，包括功能性消化不良（FD）或肠易激综合征（IBS）。我们提出，餐后症状是通过一种独特的病理生理过程产生的。例如，急性肠道感染等生理性或心理性损伤会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都能与免疫系统相互作用，引起局部免疫反应，嗜酸性粒细胞和肥大细胞被激活，并释放炎症介质，包括组胺和细胞因子。这些具有更广泛的全身效应，包括触发伤害性神经并改变情绪。饮食干预，包括低发酵寡糖、双糖、单糖和多元醇饮食，消除潜在的食物抗原或麸质，IgG 食物敏感性饮食或水杨酸盐限制，可能对一些 IBS 或 FD 患者有益。这可能是因为限制这些食物或饮食成分可以调节这种病理生理过程。同样，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在内的药物，具有抗组胺作用，所有这些都是 FD 和 IBS 的潜在治疗药物，都作用于这些机制中的一个或多个。似乎推动肠道免疫激活的食物抗原并不是 FD 和 IBS 餐后症状的全部解释。在其他情况下，肠道碳水化合物发酵，气体释放改变反射反应、食物化学物质的不良反应、中枢机制或反安慰剂效应可能占主导地位。然而，如果餐后症状是由于食物抗原在胃肠道中引发免疫反应而产生的这一概念适用于一部分患者，那么这将是一个范式转变，因为如果治疗选择基于这些治疗靶点中的一个或多个，那么患者的治疗结果可能会得到改善。
