Duodenal hypersensitivity to acid in patients with functional dyspepsia-pathogenesis and evaluation

Abstract

Functional dyspepsia (FD) is a subcategory of the functional gastrointestinal disorders according to the Rome III classification of functional gastroduodenal disorders. FD is characterized by the presence of symptoms that are believed to be associated with gastroduodenal lesions, particularly epigastric pain or burning, postprandial fullness, or early satiation, without the evidence of organic disease likely to explain the onset of these symptoms. Generally, multiple factors are considered to be involved in the onset of dyspeptic symptoms in patients with FD. Among these factors, acid is thought to be more important because proton pump inhibitors (PPIs) and histamine 2 (H2)-receptor antagonists have been proposed to be effective therapies for a subset of patients with FD. Although manometric methods, scintigraphic methods, electrogastrography and ultrasonography have been used to evaluate enterokinesis, a practical method for evaluating duodenal hypersensitivity to acid has not been reported. Recently, we attempted to evaluate duodenal hypersensitivity to acid and gastric motility by duodenal acidification using transnasal endoscopy. Using this method, we could simultaneously evaluate both dyspeptic symptoms and gastric motility in healthy volunteers. Furthermore, we evaluated duodenal hypersensitivity to acid in healthy volunteers and in patients with FD, and we reported that duodenal acidification induced dyspeptic symptoms more significantly in patients with FD than in healthy volunteers.

Predictors of the clinical effects of pirfenidone on idiopathic pulmonary fibrosis

“…Although gastroscopy was not performed on any of our cases, we do not believe anorexia occurred from gastroduodenal ulcers, as it spontaneously resolved after pirfenidone discontinuation. PPIs and H2RAs do not directly activate gastric motility; however, they are known to improve postprandial fullness and early satiation observed in functional dyspepsia without organic disease [22] through attenuating duodenal hypersensitivity to acids [23]. It is reported that PPI monotherapy improves dysmotility-like symptoms significantly better than that of H2RAs plus mosapride in functional dyspepsia [24].…”

Effects of Alkaline‐Reduced Drinking Water on Irritable Bowel Syndrome with Diarrhea: A Randomized Double‐Blind, Placebo‐Controlled Pilot Study

“…Interestingly, just infusing a small amount (0.1 mol/L) of acid into the stomach can aggravate indigestion in most people [ 28 ]. In addition, acidification of the duodenum exacerbates dyspeptic symptoms by inducing proximal gastric relaxation and inhibiting gastric accommodation to a meal [ 29 ]. In one animal study, duodenal acidification-induced gastric hypersensitivity could be the cause of dyspepsia in patients with IBS and serotonin 5-HT3 receptors play a key role [ 30 ].…”

Characterization of a reproducible gastric pain model using oral capsaicin titration in healthy volunteers

“…Evidence supporting the stomach rather than the duodenum as the main source of symptoms includes the rapid resolution of symptoms when water is ingested (11,19,20), and the endoscopic observation of pooled capsaicin in the gastric corpus but not beyond after oral ingestion (11). However, with the present understanding of the pathophysiology of FD, this may not be of prime importance, as both gastric and duodenal mechanisms are probably involved (3,56,57). Another potential confounder is the open capsaicin dose titration on study days 2 and 3, whereas the titration on day 1 was nocebo‐controlled and visually blinded.…”