Gastric Perception Thresholds Are Low and Sensory Neuropeptide Levels High in <i>Helicobacter pylori-</i>Positive Functional Dyspepsia

Abstract

Background and Aims: In functional dyspepsia (FD) decreased perception levels can be shown on gastric distension. Substance P (SP) and calcitonin gene-related peptide (CGRP) are involved in the sensitization of afferent neuronal pathways due to chronic inflammation. The role of Helicobacter pylori-induced gastric mucosal inflammation in the pathogenesis of FD is controversial. The aim of this study was to assess whether FD patients have altered mucosal concentrations of CGRP and SP, and to investigate whether this is associated with visceral hypersensitivity or H. pylori infection. Methods: Gastrointestinal symptoms, H. pylori status, perception thresholds at gastric balloon distension, and gastric mucosal concentrations of CGRP and SP were determined in 13 FD patients and 18 healthy controls (HC). Results: In H. pylori-positive FD patients discomfort and pain thresholds on gastric distension were lower compared to other groups. Antral mucosal levels of CGRP and SP were higher in H. pylori-positive subjects. In FD significantly negative correlations between discomfort and pain thresholds and antral mucosal concentrations of CGRP and SP were observed. Conclusions: In FD low perception thresholds on gastric distension are associated with high levels of CGRP and SP in the antrum, suggesting that sensory neuropeptides are involved in FD pathophysiology.

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

“…Similarly, Mönnikes et al [126] showed that discomfort and pain thresholds on gastric distension were lower in patients with functional dyspepsia that were H. pylori-positive. These patients also showed higher antral mucosal levels of CGRP and SP, which negatively correlated with the levels of discomfort and pain thresholds, demonstrating the role of the brain-gut axis in hypersensitivity and SP and CGRP involvement in the sensitization of afferent neuronal pathways, which result from chronic inflammation [84,126] . Similar inflammation-related changes in sensory-motor function have been observed in subjects with intestinal mucosal inflammation [9,11,123] .…”

“…H. pylori infection may increase sympathetic ANS activity via induction of gastritis and overproduction of systemic inflammatory mediators through a pathogenburden mechanism [61] . Increased ANS activity is related to symptom thresholds in patients with peptic ulcers [38][39]121] , in acid-sensitive and insensitive patients with non-cardiac chest pain [67] , in patients with non-specific disorders of esophageal motility [132] , as well as in individuals with functional dyspepsia [9,21,42,66,76,94,126,133] and IBS [134] . Such a pathway is also considered as one of the causes of pain in H. pylori-infected patients with fibromyalgia [96] .…”

The study on the role of inflammatory cells and mediators in post-infectious functional dyspepsia

“…Functional dyspepsia is a multifactorial disorder with many potential mechanisms having been purported to play roles in symptom generation including abnormalities in gastric motor function, visceral hypersensitivity, neurotransmitter imbalance, inflammation and psychological dysfunction [3]. Helicobacter pylori (H. pylori) is present in some patients with functional dyspepsia but H. pylori eradication therapy has a positive effect in only about 10% of H. pylori positive non-ulcer dyspepsia patients [4,5].…”

A life-threatening complication of a life-saving manoeuvre

“…Acute inflammatory cell-induced hyperalgesia has been associated with increased neural expression of the pro-nociceptive neuropeptide, substance P. 13 In functional dyspepsia, pain was found to correlate with substance P and not inflammation. 23 Our previous work showed an association of increased b-endorphin expression with reduced visceral sensitivity. 12 Furthermore, patients with IBD exhibited abnormal expression of these neuropeptides in the rectal mucosa.…”