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Frontiers in Cellular and Infection... 2021In recent years, increasing studies have been conducted on the mechanism of gut microbiota in neuropsychiatric diseases and non-neuropsychiatric diseases. The academic... (Review)
Review
In recent years, increasing studies have been conducted on the mechanism of gut microbiota in neuropsychiatric diseases and non-neuropsychiatric diseases. The academic community has also recognized the existence of the microbiota-gut-brain axis. Chronic pain has always been an urgent difficulty for human beings, which often causes anxiety, depression, and other mental symptoms, seriously affecting people's quality of life. Hyperalgesia is one of the main adverse reactions of chronic pain. The mechanism of gut microbiota in hyperalgesia has been extensively studied, providing a new target for pain treatment. Enterochromaffin cells, as the chief sentinel for sensing gut microbiota and its metabolites, can play an important role in the interaction between the gut microbiota and hyperalgesia through paracrine or neural pathways. Therefore, this systematic review describes the role of gut microbiota in the pathological mechanism of hyperalgesia, learns about the role of enterochromaffin cell receptors and secretions in hyperalgesia, and provides a new strategy for pain treatment by targeting enterochromaffin cells through restoring disturbed gut microbiota or supplementing probiotics.
Topics: Brain; Enterochromaffin Cells; Gastrointestinal Microbiome; Humans; Hyperalgesia; Probiotics; Quality of Life
PubMed: 34722345
DOI: 10.3389/fcimb.2021.760076 -
Neurogastroenterology and Motility Apr 2018Functional dyspepsia (FD) is a gastrointestinal disorder of unknown etiology. Although micro-inflammation appears to be important in the pathogenesis, studies evaluating... (Meta-Analysis)
Meta-Analysis
Functional dyspepsia (FD) is a gastrointestinal disorder of unknown etiology. Although micro-inflammation appears to be important in the pathogenesis, studies evaluating immune activation in FD have been inconsistent. A systematic review of literature and meta-analysis was performed to compare immunologic cell counts and cytokine levels in the mucosa and peripheral blood of individuals with FD and healthy controls. PubMed, Embase, and the Cochrane library were searched. Data on immunologic cell counts and cytokines levels among individuals with FD and control groups were extracted and compared by calculating standard mean differences (SMD). Thirty-seven studies met the inclusion criteria. Mast cell (SMD = 0.94, 95%CI 0.26-1.62, P = .007) and eosinophil counts (SMD = 0.36, 95%CI 0.06-0.68, P = .03) in the stomach were increased, among individuals with FD compared to controls. Similarly, mast cell (SMD = 0.66, 95%CI 0.20-1.13, P = 0.005) and eosinophil (SMD = 0.95, 95%CI 0.66-1.24; P < .001) counts in the duodenum were also increased in those with FD compared to controls. In a subgroup analysis, elevated eosinophil counts in the duodenum were observed in both post-prandial distress syndrome (SMD = 0.97, 95%CI 0.46-1.47, P = .0002) and epigastric pain syndrome subtypes (SMD = 1.16, 95%CI 0.48-1.83, P = .0008). No differences in mucosal intraepithelial lymphocyte, enterochromaffin cell, and neutrophil counts, as well as, peripheral interlukin-6 (IL-6) and IL-10 levels were observed among individuals with FD and controls. Micro-inflammation in the form of local immune cell infiltration, particularly eosinophils and mast cells, characterizes the pathogenesis of FD.
Topics: Duodenum; Dyspepsia; Eosinophils; Humans; Inflammation; Inflammation Mediators; Mast Cells
PubMed: 29392796
DOI: 10.1111/nmo.13304 -
Alimentary Pharmacology & Therapeutics Sep 2015Proton pump inhibitors (PPIs) have a well-established safety profile. However, concerns have been raised about a potential relationship between PPI-induced... (Review)
Review
BACKGROUND
Proton pump inhibitors (PPIs) have a well-established safety profile. However, concerns have been raised about a potential relationship between PPI-induced hypergastrinaemia and the development of enterochromaffin-like (ECL) cell hyperplasia, neuroendocrine tumours and gastric cancer during long-term therapy.
AIM
To review the effects of long-term PPI use on serum gastrin levels and gastric histopathology.
METHODS
A systematic literature search was conducted in PubMed on 21 April 2015 to identify studies reporting the effects of long-term (defined as >3 years) PPI use on gastrin levels and gastric histopathology.
RESULTS
A total of 16 studies (1920 patients) met the inclusion criteria. During long-term PPI therapy, mean gastrin levels rose to one to three times the upper limit of the normal range (~100 pg/mL), and an increased prevalence of ECL cell hyperplasia was observed (+7.8-52.0%). Helicobacter pylori-positive patients had a significantly increased risk of developing ECL linear/micronodular hyperplasia compared with H. pylori-negative patients [OR: 2.45 (95% CI: 1.47-4.10), P = 0.0006]; however, no evidence of neoplastic changes was found. The risk of corpus atrophy was markedly higher in H. pylori-positive patients than in H. pylori-negative patients [OR: 11.45 (95% CI: 6.25-20.99), P < 0.00001]. Not a single case of gastric adenocarcinoma was found.
CONCLUSIONS
Long-term PPI therapy induced moderate hypergastrinaemia in most patients and an increased prevalence of ECL cell hyperplasia. H. pylori-positive patients receiving long-term PPI therapy were exposed to a higher risk of corpus atrophy than H. pylori-negative patients. No neuroendocrine tumours or gastric cancers were found.
Topics: Drug Administration Schedule; Enterochromaffin-like Cells; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Neuroendocrine Tumors; Proton Pump Inhibitors; Risk Factors; Stomach Neoplasms
PubMed: 26177572
DOI: 10.1111/apt.13324 -
Journal of Digestive Diseases Sep 2016To systematically review the available data on cytokine and immune cells in the peripheral blood and mucosal biopsy samples from patients with irritable bowel syndrome... (Review)
Review
OBJECTIVE
To systematically review the available data on cytokine and immune cells in the peripheral blood and mucosal biopsy samples from patients with irritable bowel syndrome (IBS).
METHODS
From a review of the literature, data on cytokines and immune cells that had been assayed in at least three independent studies were collated and trends examined.
RESULTS
Levels of interleukin (IL)-10 tended to be decreased and those of IL-6, IL-8, tumor necrosis factor-α and IL-1β increased in the systemic circulation in IBS, while in the mucosa, IL-10 was decreased and IL-8, mast cells, enterochromaffin cells and CD3 T lymphocytes were increased. However, these findings were not consistent across all studies and, in some instances, were limited to certain IBS sub-populations.
CONCLUSIONS
The interpretation of this literature is limited by several factors, such as the intrinsic heterogeneity of IBS and a lack of standardization in study design. While a number of intriguing immunological observations have been made in IBS, more work is needed before a compelling case can be made for a role for immune-mediated events in the etiology of IBS.
Topics: Cytokines; Enterochromaffin Cells; Humans; Immunity, Mucosal; Inflammation Mediators; Intestinal Mucosa; Irritable Bowel Syndrome; Mast Cells; T-Lymphocyte Subsets
PubMed: 27426409
DOI: 10.1111/1751-2980.12379 -
The Cochrane Database of Systematic... Dec 2014Proton pump inhibitors (PPIs) are the most effective drugs to reduce gastric acid secretion. PPIs are one of the most commonly prescribed classes of medications... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Proton pump inhibitors (PPIs) are the most effective drugs to reduce gastric acid secretion. PPIs are one of the most commonly prescribed classes of medications worldwide. Apart from short-term application, maintenance therapy with PPIs is recommended and increasingly used in certain diseases, such as Zollinger-Ellison syndrome and gastro-oesophageal reflux disease, especially for people with erosive oesophagitis or Barrett's oesophagus. Although PPIs are generally safe, their efficacy and safety of long-term use remains unclear. The question of whether the long-term use of PPIs could promote the development of gastric pre-malignant lesions has been widely investigated, but results are inconsistent. Limited insight on this problem leads to a dilemma in decision making for long-term PPI prescription.
OBJECTIVES
To compare the development or progression of gastric pre-malignant lesions, such as atrophic gastritis, intestinal metaplasia, enterochromaffin-like (ECL) cell hyperplasia, and dysplasia, in people taking long-term (six months or greater) PPI maintenance therapy.
SEARCH METHODS
We searched the following databases (from inception to 6 August 2013): the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, and CINAHL. In addition, we searched the reference lists of included trials and contacted experts in the field.
SELECTION CRITERIA
We searched for randomised controlled trials (RCTs) in adults (aged 18 years or greater) concerning the effects of long-term (six months or greater) PPI use on gastric mucosa changes, confirmed by endoscopy or biopsy sampling (or both).
DATA COLLECTION AND ANALYSIS
Two review authors independently performed selection of eligible trials, assessment of trial quality, and data extraction. We calculated odds ratios (OR) for analysis of dichotomous data and mean differences for continuous data, with 95% confidence intervals (CI).
MAIN RESULTS
We included seven trials (1789 participants). Four studies had high risk of bias and the risk of bias in the other three trials was unclear. In addition, it was difficult to assess possible reporting bias. We pooled 1070 participants from four RCTs to evaluate corporal atrophy development revealing an insignificantly increased OR of 1.50 (95% CI 0.59 to 3.80; P value = 0.39; low-quality evidence) for long-term PPI users relative to non-PPI users. In five eligible trials, corporal intestinal metaplasia was assessed among 1408 participants, also with uncertain results (OR 1.46; 95% CI 0.43 to 5.03; P value = 0.55; low-quality evidence). However, by pooling data of 1705 participants from six RCTs, our meta-analysis showed that participants with PPI maintenance treatment were more likely to experience either diffuse (simple) (OR 5.01; 95% CI 1.54 to 16.26; P value = 0.007; very-low-quality evidence) or linear/micronodular (focal) ECL hyperplasia (OR 3.98; 95% CI 1.31 to 12.16; P value = 0.02; low-quality evidence) than controls. No participant showed any dysplastic or neoplastic change in any included studies.
AUTHORS' CONCLUSIONS
There is presently no clear evidence that the long-term use of PPIs can cause or accelerate the progression of corpus gastric atrophy or intestinal metaplasia, although results were imprecise. People with PPI maintenance treatment may have a higher possibility of experiencing either diffuse (simple) or linear/micronodular (focal) ECL cell hyperplasia. However, the clinical importance of this outcome is currently uncertain.
Topics: Enterochromaffin-like Cells; Gastritis, Atrophic; Humans; Hyperplasia; Intestines; Maintenance Chemotherapy; Metaplasia; Precancerous Conditions; Proton Pump Inhibitors; Randomized Controlled Trials as Topic; Stomach Neoplasms; Time Factors
PubMed: 25464111
DOI: 10.1002/14651858.CD010623.pub2