The DOI matches its Crossref record; 162 of the 163 references it cites were found in a registry or an index; 6 of the 99 sources its claims cite were checked for support.
Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified
Open accessAbstract
., dysbiosis). The gut microbiota is a complex ecosystem in which microbes coexist and interact with the human host. Indeed, the resident gut bacteria are needed for multiple vital functions, such as nutrient and drug metabolism, the production of energy, defense against pathogens, the modulation of the immune system and support of the integrity of the gut mucosal barrier. The bacteria are collected in communities that vary in density and composition within each segment of the gastrointestinal (GI) tract. Therefore, every change in the gut ecosystem has been connected to an increased susceptibility or exacerbation of various GI disorders. The aim of this review is to summarize the recently available data on PPI-related microbiota alterations in each segment of the GI tract and to analyze the possible involvement of PPIs in the pathogenesis of several specific GI diseases.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This narrative review summarizes evidence that proton pump inhibitors, through long-term acid suppression, alter gut microbiota composition across the gastrointestinal tract and may contribute to dysbiosis-associated diseases. It concludes that PPIs should be used only when strictly necessary and that further prospective studies are needed to clarify health impacts.
Key findings
- PPIs reduce gastric acid and alter microbiota in each GI segment; a four-week esomeprazole study in healthy volunteers increased *Fusobacterium* and *Leptotrichia* in the periodontal pocket, decreased *Neisseria* and *Veillonella* in saliva, and increased *Streptococcus* in fecal samples.
- In the stomach, *Streptococcaceae* were the most abundant family during PPI therapy; hypochlorhydria reduced microbial diversity and increased nitrate/nitrite reductase bacterial functions. One study reported up to 2.4 times greater gastric cancer risk in long-term PPI users even after *H. pylori* eradication, though other meta-analyses did not confirm this risk.
- Chronic PPIs strongly impact the small intestine and can cause small intestinal bacterial overgrowth, defined as more than 10^5 bacteria per ml of upper gut aspirate; PPI-induced dysbiosis may increase risk of hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis. In rats, PPIs reduced jejunal *Actinobacteria* and *Bifidobacteria* spp. and exacerbated NSAID-induced enteropathy.
- In the colon, PPIs decrease commensal bacteria and microbial diversity and increase oral bacteria in stool; they are associated with increased *Clostridium difficile* infection and other enteric infections and may predispose to IBS. Post-infectious IBS occurs in 10%-30% of patients after infectious gastroenteritis, while many studies found no direct correlation between PPI use and colorectal cancer.
Methods
- Design: narrative review.
- Data or sample: no primary data; synthesizes published literature on PPI-related microbiota alterations in each GI tract segment and specific GI diseases.
- Main analysis: narrative synthesis; no systematic search strategy, databases, inclusion/exclusion criteria, or quantitative meta-analysis are reported.
Limitations
- The paper states that further prospective studies are necessary to define how PPI-induced microbial changes impact human health, that confirmation in humans is needed for the role of dysbiosis in NSAID enteropathy, and that the validity of probiotic prevention remains to be seen.
- The paper notes ongoing uncertainty: the role of PPIs in gastric cancer development is under debate, IBD microbial data are not fully elucidated, and many studies have not found a direct correlation between PPI use and colorectal cancer.
- Evident from the text: as a narrative review, it lacks a systematic search, formal quality appraisal, and meta-analysis, so findings are synthesized without formal bias assessment.
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Claims the paper makes
49 Not checked yet · 4 Own interpretation · 3 Partly supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“because their long-term use significantly decreases the risk of the progression to high-grade dysplasia and EAC[50-52]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
- Not checked yetcites [50] source
- Partly supportedcites [51] sourceExperimental — accuracy not yet measured
The Results describe a cohort with non-dysplastic BE at baseline and report a significant association between PPI prescriptions and lower risk of high-grade dysplasia or EAC (adjusted HR 0.39). Prescriptions filled for at least 36 months were associated with a greater reduction, but the paper describes the duration response as a trend. The Discussion concludes only that PPI therapy may reduce incidence; this observational study does not establish that long-term use itself significantly decreases progression risk. (LLM, conf=0.86)
- Partly supportedcites [52] sourceExperimental — accuracy not yet measured
The Results (PPI use and risk of advanced neoplasia) report a statistically significant association between PPI use and lower risk of oesophageal adenocarcinoma and/or high-grade dysplasia in patients with Barrett’s oesophagus. But the duration–response analysis gives long-term use (>2–3 years) an adjusted OR of 0.45 with a 95% CI of 0.19–1.06, so it does not establish a statistically significant long-term effect. The analysis also includes patients with low-grade dysplasia, rather than only non-dysplastic Barrett’s oesophagus, and reports an association rather than proving that PPIs cause the reduction. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“PPIs have also been reported to exacerbate the mucosal damage caused by non-steroidal anti-inflammatory drugs (NSAIDs) in the distal portion of the small bowel to the ligament of Treitz[95,96]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > SMALL INTESTINE
What the sources say
- Partly supportedcites [95] sourceExperimental — accuracy not yet measured
The section “PPIs EXACERBATE NSAID-INDUCED MUCOSAL LESIONS IN THE SMALL INTESTINE” reports that adding PPIs to NSAIDs is associated with more small-intestinal mucosal lesions than NSAIDs alone. The passages do not establish the claim’s more specific anatomical boundary at the ligament of Treitz. Page numbers were not provided in our copy. (LLM, conf=0.82)
- Partly supportedcites [96] sourceExperimental — accuracy not yet measured
The ‘Risks associated with long-term use of PPIs’ section reports that PPIs increased the incidence and severity of NSAID-induced small-intestine injury. The copy does not locate that injury in the distal small bowel or define its extent by the ligament of Treitz. (LLM, conf=0.85)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Partly supported
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In the paper
“The consequence of this invasion is the promotion of NF-κB signaling and the expression of several cytokines, such as IL-6, IL-8, IL-10, IL-18 and TNF-α.”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
What the sources say
- Supportedcites [147] source
The ‘Underlying Mechanisms of F. nucleatum Pathogenesis in CRC’ section says F. nucleatum promotes NF-κB expression or activation and increases IL-6, IL-8, IL-10, IL-18 and TNF-α. Its Figure 1 caption links FadA-mediated invasion with increased levels of the same inflammatory mediators. The section describes more than one signaling pathway, but supports the claim’s overall association. (LLM, conf=0.93)
- Partly supportedcites [150] sourceExperimental — accuracy not yet measured
The Introduction’s “Fusobacterium nucleatum” section says invasive isolates evoke increased TNF-α expression. It does not link F. nucleatum invasion to NF-κB signaling or to expression of IL-6, IL-8, IL-10, and IL-18; the Introduction’s “Toll-like receptors” section discusses NF-κB activation by pathogens generally, not by F. nucleatum specifically. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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- Supported
None of the sources cited for this claim have been checked yet.
In the paper
“Changes in this microbial equilibrium that is, dysbiosis can promote and influence the course of many intestinal and extra-intestinal diseases[14-16].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > INTRODUCTION
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This bacterium could have a role in EAC, promoting the metaplastic processes in the early stages of cancer through an increase in the interleukin (IL)-18 expression and downregulation of transforming growth factor beta 1, nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 signaling involved in the EAC cascade[42-44].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“The use of PPIs is generally well tolerated, although their long-term use exposes patients to an increased risk of developing extra-intestinal disorders[6-8]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > INTRODUCTION
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“likely due to PPI-driven gastric hypo-chlorhydria, which can cause also significant changes in gut microbiota composition[9-11]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > INTRODUCTION
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A recent epidemiological study revealed that, in the absence of other risk factors, the long-term use of PPIs is associated with an increased risk of EAC[48].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
- Not checked yetcites [48] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In both these conditions, a significant enrichment of Campylobacter concisus has been reported[42,43].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“and other meta-analyses not confirming such a risk[65,66]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
What the sources say
- Not checked yetcites [65] source
- Not checked yetcites [66] Eslami L, Nasseri-Moghaddam S. Meta-analyses: Does long-term PPI use increase the risk of gastric premalignant lesions? Arch Iran Med 2013; 16: 449-458
plain- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 27
- Probably not a substantial claim. 5
In the paper
“One study showed that, in healthy volunteers, a four-week esomeprazole administration of PPI caused an increase of Fusobacterium and Leptotrichia in the periodontal pocket, associated with a decrease of Neisseria and Veillonella in saliva and a parallel increase of Streptococcus in fecal samples”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ORAL CAVITY
What the sources say
- Not checked yetcites [34] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“PPIs are the first-choice treatment for acid-related disorders such as bleeding, peptic ulcers, gastroesophageal reflux, erosive esophagitis (ERD) and certain dyspepsia subtypes[2-5].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > INTRODUCTION
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“It is likely that this switch in favor of Gram-negative bacteria could cause an LPS-mediated activation of innate immunity, inducing a dangerous cycle of dysbiosis-inflammation-dysbiosis and mucosal damage[38].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
- Not checked yetcites [38] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Proton pump inhibitors (PPIs) are acid-suppressive agents and are among the most widely used and over-used drugs in the world[1].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > INTRODUCTION
What the sources say
- Not checked yetcites [1] source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The gut microbiota has a key role in metabolic, nutritional, physiological, defensive and immunological processes in the human body, and its composition is closely connected to individuals’ health and the diseases they experience[12,13].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > INTRODUCTION
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Based on these data, the oral cavity could represent a potential source of microbiota information related to oral and non-oral disorders; it could also be an important indicator of dysbiosis in other areas of the GI tract.”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ORAL CAVITY
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“PPI treatment can alter esophageal microbiota, causing an increase in the abundance of Firmicutes and a decrease in the abundance of Bacteroidetes and Proteobacteria[47].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
- Not checked yetcites [47] source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“two types of microbiota have been identified in the esophagus: Type I, present in healthy subjects, is characterized by a predominance of Gram-positive taxa (especially Streptococcus), whereas type II, associated with ERD and Barrett esophagus (BE), is constituted by a predominance of Gram-negative taxa”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The distal tract is mostly colonized by Firmicutes, followed by Bacteroidetes, Actinobacteria, Proteobacteria and Fusobacteria, with the most represented genera being Streptococcus, followed by Prevotella and Veillonella[35].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
- Not checked yetcites [35] source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“this suggests that PPIs may cause both oral and gut microbiota alterations[34]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ORAL CAVITY
What the sources say
- Not checked yetcites [34] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Both ERD and BE are considered precursor conditions to esophageal adenocarcinoma (EAC)[41].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > ESOPHAGUS
What the sources say
- Not checked yetcites [41] source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“with some studies and meta-analyses reporting an increased risk of developing GC in long-term PPI users[62,63] up to 2.4 times greater, even after Helicobacter pylori (H. pylori) eradication, according to a recent study[64]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The primary abundance of Streptococcaceae was also demonstrated in dyspeptic patients during PPI treatment, suggesting that this ecological switch in favor of Streptococcaceae could be an independent indicator of gastric dysbiosis due to these drugs[59].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
What the sources say
- Not checked yetcites [59] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Moreover, germ-free mice are less susceptible to intestinal lesions induced by NSAIDs and it has been documented that NSAID-induced enteropathy is transferable via microbiota[98,101,102].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > SMALL INTESTINE
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“H. pylori infection can lead to antrum-predominant gastritis, in which the oxyntic mucosa is not inflamed but a gastrin-driven increase in acid output occurs, along with the possible development of duodenal ulcer[67,68].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It is important to keep in mind that hypochlorhydria promotes a reduction in microbial diversity and the growth of microbes that have genotoxic potential, with an increase in the nitrate/nitrite reductase bacterial functions involved in cancer development[60].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
What the sources say
- Not checked yetcites [60] source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition, when the infection does spread to the oxyntic mucosa, it causes pangastritis, which is associated with hypochloridria, and is responsible for the development of chronic atrophic gastritis, intestinal metaplasia and, finally, dysplasia and GC[69,70].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Chronic treatment with PPIs strongly impacts small intestine microbiota and, in particular, causes small intestinal bacterial overgrowth (SIBO), likely due to the loss of the gastric acid defensive barrier[81-83].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > SMALL INTESTINE
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Moreover, PPIs augmented the expression of bacteria with beta-glucuronidases activity, and this microbial imbalance could promote the spread of NSAIDs into enterohepatic circulation, increasing bile cytotoxicity and subsequently causing ulcerative lesions[99,100].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > SMALL INTESTINE
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“The gastric microbiota is composed mainly of Firmicutes, Bacteroidetes, Proteo-bacteria and Actinobacteria, with the most abundant genera being Streptococcus, followed by Veillonella, Prevotella, Fusobacterium and Rothia[54].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
What the sources say
- Not checked yetcites [54] source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“PPIs have unfavorable effects on gastric functions and host defensive mechanisms, causing delayed gastric emptying, decreased gastric mucus viscosity, increased bacterial load and increased bacterial translocation[55-57].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > STOMACH
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, the gastric hypochlorhydria caused by PPIs favors the survival and migration of oral bacteria in lower areas of the GI tract, with a possible establishment of a pro-inflammatory microenvironment.”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > CONCLUSION
hedgeddirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“PPIs by reducing gastric acid secretion can produce profound changes in the colonic microbiota, mainly characterized by a decrease in the abundance of commensal bacteria, which is associated with a reduction in microbial diversity and an increase of oral bacteria in the stool[108,109].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Even if not fully clarified, it has been hypothesized that, in CDI, a reduction in alpha diversity and a decrease in the abundance of bacteria of the Ruminococcoceae associated with an increase in the Enterobacteriaceae, Enterococcoceae and Lactobacillaceae families observed during long-term PPI treatment could facilitate the onset of infection[109].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
What the sources say
- Not checked yetcites [109] source
hedgedconditional- Asserted: fails — The authors may not put it forward as true.
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Probably not a substantial claim. The authors may not put it forward as true.
None of the sources cited for this claim have been checked yet.
In the paper
“As previously stated, the long-term PPI use facilitates the induction of enteric infection, and, through secondary changes in microbiota composition, these drugs may influence gut–brain axis functions, prompting IBS onset[117,118].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
What the sources say
- Not checked yetcites [117] source
- Not checked yetcites [118] Carabotti M, Scirocco A, Maselli MA, Severi C. The gut-brain axis: Interactions between enteric microbiota, central and enteric nervous systems. Ann Gastroenterol 2015; 28: 203-209
hedgedconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“This microorganism has two adhesion proteins, FapA and FadA, the latter of which mediates the invasion of the bacterium into the intestinal epithelium.”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“PPIs can influence the onset of enteric infections, resulting in an increased risk of Clostridium difficile infection (CDI), as well as Salmonella, Campylobacter and diarrheagenic Escherichia coli (E. coli)[110-113].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The net result of these changes is the creation of a pro-inflammatory milieu for tumor growth, favored by the FapA-mediated suppression of T cells’ cytotoxic activity[147,150].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“F. nucleatum is a commensal anaerobic bacterium of the oral cavity associated with periodontal disorders, and it has been found in large quantities in CRC[147].”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
What the sources say
- Not checked yetcites [147] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The evidence indicates that PPIs which are widely used in gastroenterology clinical practice likely through their acid-antisecretory effects, are able to modify the host microbiota in each segment of the GI tract and can contribute to dysbiosis development; this dysbiosis can, in turn, facilitate the onset of certain GI disorders.”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > CONCLUSION
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“The IBS dysbiosis mostly consists of a reduction in alpha diversity and an imbalance between microbial groups, represented by a scarce amount Bifidobacteria and Lactobacilli members and an increase in potentially pathogenic Enterobacteriaceae, such as E. coli[127,128]”
§ Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified > COLON
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper relies on this without support.
Gastric dysbiosis occurs as a result of H. pylori-related gastritis.
“Gastric dysbiosis occurs as a result of H. pylori-related gastritis.”
The paper relies on this without support.
H. pylori pro-inflammatory activity affects the luminal microenvironment and modifies the gastric microbiota.
“H. pylori pro-inflammatory activity affects the luminal microenvironment and modifies the gastric microbiota.”
The paper relies on this without support.
Depending on the site of H. pylori colonization, the dysbiosis can be associated with either an increase or decrease in acid secretion, which further influences gastric microbiota composition.
“It is noteworthy that, depending on the site of H. pylori colonization, the dysbiosis can be associated with either an increase or decrease in acid secretion, which further influences gastric microbiota composition.”
The paper relies on this without support.
This dysbiosis has also been shown to be related to the occurrence of HE and SBP, implying a poor prognosis and disease progression.
“This dysbiosis has also been shown to be related to the occurrence of HE and SBP, implying a poor prognosis and disease progression.”
Claims other papers make about this one
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The cited source says what the claim attributes to it.
In the citing paper
“Outcomes vary, with some studies showing no association.”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [446]
In the citing paper
“Another group of drugs that has been shown to cause dysbiosis and is associated with cognitive decline is the proton pump inhibitors (PPI) (446, 447).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [446]
Citations
Cites
Enterotypes of the human gut microbiome
MetaHIT Consortium (additional members), Arumugam, M., Raes, J., Pelletier, E., Le Paslier, D., Yamada, T., Mende, D. R., Fernandes, G. R., Tap, J., Bruls, T., et al. (2011) · Nature · doi:10.1038/nature09944 · Cited by 7,548
Revised Estimates for the Number of Human and Bacteria Cells in the Body
Sender, R., Fuchs, S., & Milo, R. (2016) · PLOS Biology · doi:10.1371/journal.pbio.1002533 · Cited by 5,425
Introduction to the human gut microbiota
Thursby, E., & Juge, N. (2017) · Biochemical Journal · doi:10.1042/bcj20160510 · Cited by 3,600
Dewhirst, F. E., Chen, T., Izard, J., Paster, B. J., Tanner, A. C. R., Yu, W.-H., Lakshmanan, A., & Wade, W. G. (2010) · Journal of Bacteriology · doi:10.1128/jb.00542-10 · Cited by 3,352
Defining the normal bacterial flora of the oral cavity
Aas, J. A., Paster, B. J., Stokes, L. N., Olsen, I., & Dewhirst, F. E. (2005) · Journal of Clinical Microbiology · doi:10.1128/jcm.43.11.5721-5732.2005 · Cited by 3,092
Management of Helicobacter pylori infection—the Maastricht V/Florence Consensus Report
Malfertheiner, P., Mégraud, F., O'Morain, C. A., Gisbert, J. P., Kuipers, E. J., Axon, A. T. R., Bazzoli, F., Gasbarrini, A., Atherton, J. C., Graham, D. Y., et al. (2016) · Gut · doi:10.1136/gutjnl-2016-312288 · Cited by 3,023
Role of the normal gut microbiota
Jandhyala, S. M. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i29.8787 · Cited by 3,001
The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems.
(2015) · PubMed Central · Cited by 2,540
Self-citationPathogenesis of Helicobacter pylori Infection
Kusters, J. G., van Vliet, A. H. M., & Kuipers, E. J. (2006) · Clinical Microbiology Reviews · doi:10.1128/cmr.00054-05 · Cited by 2,526
The gut microbiota and host health: a new clinical frontier
Marchesi, J. R., Adams, D. H., Fava, F., Hermes, G. D. A., Hirschfield, G. M., Hold, G., Quraishi, M. N., Kinross, J., Smidt, H., Tuohy, K. M., et al. (2016) · Gut · doi:10.1136/gutjnl-2015-309990 · Cited by 2,302
Occlusal Caries: Biological Approach for Its Diagnosis and Management
Carvalho, J. C., Dige, I., Mačhiulskienė, V., Qvist, V., Bakhshandeh, A., Parolo, C. C. F., & Maltz, M. (2016) · Caries Research · doi:10.1159/000448662 · Cited by 2,159
Vilstrup, H., Amodio, P., Bajaj, J. S., Córdoba, J., Ferenci, P., Mullen, K. D., Weißenborn, K., & Wong, P. Y. N. (2014) · Hepatology · doi:10.1002/hep.27210 · Cited by 2,065
Machiels, K., Joossens, M., Sabino, J., De Preter, V., Arijs, I., Eeckhaut, V., Ballet, V., Claes, K., Van Immerseel, F., Verbeke, K., et al. (2014) · Gut · doi:10.1136/gutjnl-2013-304833 · Cited by 1,904
Dysbiosis of the gut microbiota in disease
Carding, S., Verbeke, K., Vipond, D. T., Corfe, B. M., & Owen, L. J. (2015) · Microbial Ecology in Health & Disease · doi:10.3402/mehd.v26.26191 · Cited by 1,710
Darfeuille-Michaud, A., Boudeau, J., Bulois, P., Neut, C., Glasser, A.-L., Barnich, N., Bringer, M.-A., Swidsinski, A., Beaugerie, L., & Colombel, J.-F. (2004) · Gastroenterology · doi:10.1053/j.gastro.2004.04.061 · Cited by 1,566
ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus
Shaheen, N. J., Falk, G. W., Iyer, P. G., & Gerson, L. B. (2015) · The American Journal of Gastroenterology · doi:10.1038/ajg.2015.322 · Cited by 1,498
Proton pump inhibitors affect the gut microbiome
Imhann, F., Bonder, M. J., Vich Vila, A., Fu, J., Mujagic, Z., Vork, L., Tigchelaar, E. F., Jankipersadsing, S. A., Cenit, M. C., Harmsen, H. J. M., et al. (2016) · Gut · doi:10.1136/gutjnl-2015-310376 · Cited by 1,371
Proteobacteria: A Common Factor in Human Diseases
Rizzatti, G., Lopetuso, L. R., Gibiino, G., Binda, C., & Gasbarrini, A. (2017) · BioMed Research International · doi:10.1155/2017/9351507 · Cited by 1,308
Systemic Diseases Caused by Oral Infection
Li, X., Kolltveit, K. M., Tronstad, L., & Olsen, I. (2000) · Clinical Microbiology Reviews · doi:10.1128/cmr.13.4.547 · Cited by 1,292
Updated Guidelines for the Diagnosis and Treatment of Gastroesophageal Reflux Disease
DeVault, K. R., & Castell, D. O. (2005) · The American Journal of Gastroenterology · doi:10.1111/j.1572-0241.2005.41217.x · Cited by 1,130
Current Understanding of Dysbiosis in Disease in Human and Animal Models
DeGruttola, A. K., Low, D., Mizoguchi, A., & Mizoguchi, E. (2016) · Inflammatory Bowel Diseases · doi:10.1097/mib.0000000000000750 · Cited by 1,122
Altered profile of human gut microbiome is associated with cirrhosis and its complications
Bajaj, J. S., Heuman, D. M., Hylemon, P. B., Sanyal, A. J., White, M. B., Monteith, P., Noble, N. A., Unser, A. B., Daita, K., Fisher, A. R., et al. (2014) · Journal of Hepatology · doi:10.1016/j.jhep.2013.12.019 · Cited by 1,099
Comparative Analysis of Human Gut Microbiota by Barcoded Pyrosequencing
Andersson, A. F., Lindberg, M., Jakobsson, H. E., Bäckhed, F., Nyrén, P., & Engstrand, L. G. (2008) · PLoS ONE · doi:10.1371/journal.pone.0002836 · Cited by 1,079
Segata, N., Haake, S. K., Mannon, P., Lemon, K. P., Waldron, L., Gevers, D., Huttenhower, C., & Izard, J. (2012) · Genome Biology · doi:10.1186/gb-2012-13-6-r42 · Cited by 1,076
Dysbiosis of the faecal microbiota in patients with Crohn’s disease and their unaffected relatives
Joossens, M., Huys, G., Cnockaert, M., De Preter, V., Verbeke, K., Rutgeerts, P., Vandamme, P., & Vermeire, S. (2011) · Gut · doi:10.1136/gut.2010.223263 · Cited by 1,063
Human Gut Microbiome and Risk for Colorectal Cancer
Ahn, J., Sinha, R., Pei, Z., Dominianni, C., Wu, J., Shi, J., Goedert, J. J., Hayes, R. B., & Yang, L. (2013) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/djt300 · Cited by 947
The genetics and immunopathogenesis of inflammatory bowel disease
Cho, J. H. (2008) · Nature Reviews Immunology · doi:10.1038/nri2340 · Cited by 940
Proton pump inhibitors alter the composition of the gut microbiota
Jackson, M. A., Goodrich, J. K., Maxan, M.-E., Freedberg, D. E., Abrams, J. A., Poole, A. C., Sutter, J. L., Welter, D., Ley, R. E., Bell, J. T., et al. (2016) · Gut · doi:10.1136/gutjnl-2015-310861 · Cited by 895
IBD—what role do Proteobacteria play?
Mukhopadhya, I., Hansen, R., El-Omar, E. M., & Hold, G. L. (2012) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2012.14 · Cited by 810
The gut microbiota and inflammatory bowel disease
Matsuoka, K., & Kanai, T. (2015) · Seminars in Immunopathology · doi:10.1007/s00281-014-0454-4 · Cited by 804
The Intestinal Microbiota in Colorectal Cancer.
Tilg, H., Adolph, T. E., Gerner, R. R., & Moschen, A. R. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.03.004 · Cited by 777
The efficacy of probiotics in the treatment of irritable bowel syndrome: a systematic review
Moayyedi, P., Ford, A. C., Talley, N. J., Cremonini, F., Foxx-Orenstein, A. E., Brandt, L. J., & Quigley, E. M. M. (2010) · Gut · doi:10.1136/gut.2008.167270 · Cited by 728
Intestinal microbiota in human health and disease: the impact of probiotics
Gerritsen, J., Smidt, H., Rijkers, G. T., & de Vos, W. M. (2011) · Genes & Nutrition · doi:10.1007/s12263-011-0229-7 · Cited by 724
Gastric microbial community profiling reveals a dysbiotic cancer-associated microbiota
Ferreira, R. M., Pereira-Marques, J., Pinto-Ribeiro, I., Costa, J. L., Carneiro, F., Machado, J. C., & Figueiredo, C. (2018) · Gut · doi:10.1136/gutjnl-2017-314205 · Cited by 697
Mucosal microbiome dysbiosis in gastric carcinogenesis
Coker, O. O., Dai, Z., Nie, Y., Zhao, G., Cao, L., Nakatsu, G., Wu, W. K., Wong, S. H., Chen, Z., Sung, J. J. Y., et al. (2018) · Gut · doi:10.1136/gutjnl-2017-314281 · Cited by 695
Shen, Z.-H., Zhu, C.-X., Quan, Y.-S., Yang, Z.-Y., Wu, S., Luo, W.-W., Tan, B., & Wang, X.-Y. (2018) · World Journal of Gastroenterology · doi:10.3748/wjg.v24.i1.5 · Cited by 646
Systematic review of the risk of enteric infection in patients taking acid suppression
Leonard, J., Marshall, J. K., & Moayyedi, P. (2007) · The American Journal of Gastroenterology · doi:10.1111/j.1572-0241.2007.01275.x · Cited by 633
Small intestinal bacterial overgrowth syndrome
Bures, J. (2010) · World Journal of Gastroenterology · doi:10.3748/wjg.v16.i24.2978 · Cited by 620
Ford, A. C., Forman, D., Hunt, R. H., Yuan, Y., & Moayyedi, P. (2014) · BMJ · doi:10.1136/bmj.g3174 · Cited by 585
Human oral microbiota and its modulation for oral health
Zhang, Y., Wang, X., Li, H., Ni, C., Du, Z., & Yan, F. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.01.146 · Cited by 582
Clostridium difficile-associated diarrhea and proton pump inhibitor therapy: a meta-analysis
Janarthanan, S., Ditah, I., Adler, D. G., & Ehrinpreis, M. N. (2012) · American Journal of Gastroenterology · doi:10.1038/ajg.2012.179 · Cited by 538
Bacterial biota in the human distal esophagus
Pei, Z., Bini, E. J., Yang, L., Zhou, M., Francois, F., & Blaser, M. J. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0306398101 · Cited by 501
Flanagan, L., Schmid, J., Ebert, M., Soucek, P., Kunicka, T., Liska, V., Bruha, J., Neary, P., Dezeeuw, N., Tommasino, M., et al. (2014) · European Journal of Clinical Microbiology & Infectious Diseases · doi:10.1007/s10096-014-2081-3 · Cited by 498
Han, Y. W., & Wang, X. (2013) · Journal of Dental Research · doi:10.1177/0022034513487559 · Cited by 489
Bavishi, C., & DuPont, H. L. (2011) · Alimentary Pharmacology & Therapeutics · doi:10.1111/j.1365-2036.2011.04874.x · Cited by 480
Gut Microbiota and Inflammation
Håkansson, Å., & Molin, G. (2011) · Nutrients · doi:10.3390/nu3060637 · Cited by 477
for the SIF-AIGO-FIMMG Group, Scarpignato, C., on behalf of the Italian Society of Pharmacology, T. I. A. O. H. G., Gatta, L., Zullo, A., & Blandizzi, C. (2016) · BMC Medicine · doi:10.1186/s12916-016-0718-z · Cited by 469
THABANE, M., KOTTACHCHI, D. T., & MARSHALL, J. K. (2007) · Alimentary Pharmacology & Therapeutics · doi:10.1111/j.1365-2036.2007.03399.x · Cited by 466
Proton Pump Inhibitors Exacerbate NSAID-Induced Small Intestinal Injury by Inducing Dysbiosis
Wallace, J. L., Syer, S., Denou, E., de Palma, G., Vong, L., McKnight, W., Jury, J., Bolla, M., Bercik, P., Collins, S. M., et al. (2011) · Gastroenterology · doi:10.1053/j.gastro.2011.06.075 · Cited by 460
Human Microbiome Fusobacterium Nucleatum in Esophageal Cancer Tissue Is Associated with Prognosis
Yamamura, K., Baba, Y., Nakagawa, S., Mima, K., Miyake, K., Nakamura, K., Sawayama, H., Kinoshita, K., Ishimoto, T., Iwatsuki, M., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-1786 · Cited by 457
Cheung, K. S., Chan, E. W., Wong, A. Y. S., Chen, L., Wong, I. C. K., & Leung, W. K. (2018) · Gut · doi:10.1136/gutjnl-2017-314605 · Cited by 455
Use of acid-suppressive drugs and risk of pneumonia: a systematic review and meta-analysis
Eom, C.-S., Jeon, C. Y., Lim, J.-W., Cho, E.-G., Park, S. M., & Lee, K.-S. (2011) · Canadian Medical Association Journal · doi:10.1503/cmaj.092129 · Cited by 393
Pathogenesis and immune mechanisms of chronic inflammatory bowel diseases.
Sartor, R. B. (1997) · PubMed · Cited by 391
Role of Oral Microbiota in Cancer Development
Karpiński, T. M. M. (2019) · Microorganisms · doi:10.3390/microorganisms7010020 · Cited by 381
Wang, M., Ahrné, S., Jeppsson, B. W., & Molin, G. (2005) · FEMS Microbiology Ecology · doi:10.1016/j.femsec.2005.03.012 · Cited by 373
History of Helicobacter pylori , duodenal ulcer, gastric ulcer and gastric cancer
Graham, D. Y. (2014) · World Journal of Gastroenterology · doi:10.3748/wjg.v20.i18.5191 · Cited by 357
Proton Pump Inhibitor Use and the Risk of Small Intestinal Bacterial Overgrowth: A Meta-analysis
Lo, W., & Chan, W. W. (2013) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2012.12.011 · Cited by 353
Gut Microbiome Dysbiosis and Immunometabolism: New Frontiers for Treatment of Metabolic Diseases
Belizário, J. E., Faintuch, J., & Garay-Malpartida, M. (2018) · Mediators of Inflammation · doi:10.1155/2018/2037838 · Cited by 341
Freedberg, D. E., Toussaint, N. C., Chen, S. P., Ratner, A. J., Whittier, S., Wang, T. C., Wang, H. H., & Abrams, J. A. (2015) · Gastroenterology · doi:10.1053/j.gastro.2015.06.043 · Cited by 322
Gut microbiota role in irritable bowel syndrome: New therapeutic strategies
Distrutti, E., Monaldi, L., Ricci, P., & Fiorucci, S. (2016) · World Journal of Gastroenterology · doi:10.3748/wjg.v22.i7.2219 · Cited by 320
Resistance of germfree rats to indomethacin-induced intestinal lesions
Robert, A., & Asano, T. (1977) · Prostaglandins · doi:10.1016/0090-6980(77)90178-2 · Cited by 312
Marshall, J. K., Thabane, M., Garg, A. X., Clark, W., Salvadori, M., & Collins, S. M. (2006) · Gastroenterology · doi:10.1053/j.gastro.2006.05.053 · Cited by 304
Arweiler, N. B., & Netuschil, L. (2016) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-31248-4_4 · Cited by 302
Singh, S., Garg, S. K., Singh, P. P., Iyer, P. G., & El-Serag, H. B. (2014) · Gut · doi:10.1136/gutjnl-2013-305997 · Cited by 298
Proton-pump inhibitors: understanding the complications and risks
Malfertheiner, P., Kandulski, A., & Venerito, M. (2017) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2017.117 · Cited by 297
Acquiring and maintaining a normal oral microbiome: current perspective
Zaura, E., Nicu, E. A., Krom, B. P., & Keijser, B. J. F. (2014) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2014.00085 · Cited by 293
Helicobacter pylori and gastric carcinogenesis
Hatakeyama, M. (2009) · Journal of Gastroenterology · doi:10.1007/s00535-009-0014-1 · Cited by 291
Trifan, A., Stanciu, C., Girleanu, I., Stoica, O. C., Singeap, A. M., Maxim, R., Chiriac, S. A., Ciobica, A., & Boiculese, L. (2017) · World Journal of Gastroenterology · doi:10.3748/wjg.v23.i35.6500 · Cited by 286
Gastrin and colorectal cancer: A prospective study
Thorburn*, C. M., Friedman‡, G. D., Dickinson§, C. J., Vogelman∥, J. H., Orentreich∥, N., & Parsonnet*, #. (1998) · Gastroenterology · doi:10.1016/s0016-5085(98)70193-3 · Cited by 267
Fusobacterium nucleatum and colorectal cancer: A review
Shang, F.-M., & Liu, H.-L. (2018) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v10.i3.71 · Cited by 258
Oral microbiome and oral and gastrointestinal cancer risk
Ahn, J., Chen, C. Y., & Hayes, R. B. (2012) · Cancer Causes & Control · doi:10.1007/s10552-011-9892-7 · Cited by 246
Helicobacter pylori and gastric carcinogenesis.
Corréa, P. (1995) · PubMed · Cited by 242
Mylonaki, M., Langmead, L., Pantes, A., Johnson, F., & Rampton, D. S. (2004) · European Journal of Gastroenterology & Hepatology · doi:10.1097/01.meg.0000131040.38607.09 · Cited by 241
A Clinician's Primer on the Role of the Microbiome in Human Health and Disease
Khanna, S., & Tosh, P. K. (2014) · Mayo Clinic Proceedings · doi:10.1016/j.mayocp.2013.10.011 · Cited by 237
Intestinal microecology and quality of life in irritable bowel syndrome patients
Si, J.-M. (2004) · World Journal of Gastroenterology · doi:10.3748/wjg.v10.i12.1802 · Cited by 218
Blackett, K. L., Siddhi, S. S., Cleary, S., Steed, H., Miller, M. H., Macfarlane, S., Macfarlane, G. T., & Dillon, J. F. (2013) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.12317 · Cited by 211
Wacklin, P., Kaukinen, K., Tuovinen, E. A., Collin, P., Lindfors, K., Partanen, J., Mäki, M., & Mättö, J. (2013) · Inflammatory Bowel Diseases · doi:10.1097/mib.0b013e31828029a9 · Cited by 210
Dyspepsia and the microbiome: time to focus on the small intestine
Zhong, L., Shanahan, E. R., Raj, A., Koloski, N. A., Fletcher, L., Morrison, M., Walker, M. M., Talley, N. J., & Holtmann, G. (2017) · Gut · doi:10.1136/gutjnl-2016-312574 · Cited by 210
Parsons, B. N., Ijaz, U. Z., D’Amore, R., Burkitt, M. D., Eccles, R., Lenzi, L., Duckworth, C. A., Moore, A. R., Tiszlavicz, L., Varro, A., et al. (2017) · PLOS Pathogens · doi:10.1371/journal.ppat.1006653 · Cited by 210
Gut microbiota and colorectal cancer
Gao, R., Gao, Z., Huang, L., & Qin, H. (2017) · European Journal of Clinical Microbiology & Infectious Diseases · doi:10.1007/s10096-016-2881-8 · Cited by 205
Brusselaers, N., Wahlin, K., Engstrand, L., & Lagergren, J. (2017) · BMJ Open · doi:10.1136/bmjopen-2017-017739 · Cited by 204
Gupta, A., Dhiman, R. K., Kumari, S., Rana, S., Agarwal, R., Duseja, A., & Chawla, Y. (2010) · Journal of Hepatology · doi:10.1016/j.jhep.2010.05.017 · Cited by 202
The Impact of Proton Pump Inhibitors on the Human Gastrointestinal Microbiome
Freedberg, D. E., Lebwohl, B., & Abrams, J. A. (2014) · Clinics in Laboratory Medicine · doi:10.1016/j.cll.2014.08.008 · Cited by 199
Bouhnik, Y., Alain, S., Attar, A., Flourié, B., Raskine, L., Sanson-Le Pors, M. J., & Rambaud, J.-C. (1999) · American Journal of Gastroenterology · doi:10.1111/j.1572-0241.1999.01016.x · Cited by 199
Microbiome, Metabolome and Inflammatory Bowel Disease
Ahmed, I., Roy, B. C., Khan, S., Septer, S. S., & Umar, S. (2016) · Microorganisms · doi:10.3390/microorganisms4020020 · Cited by 199
The influence of proton pump inhibitors and other commonly used medication on the gut microbiota
Imhann, F., Vila, A. V., Bonder, M. J., Manosalva, A. G. L., Koonen, D. P. Y., Fu, J., Wijmenga, C., Zhernakova, A., & Weersma, R. K. (2017) · Gut Microbes · doi:10.1080/19490976.2017.1284732 · Cited by 198
Yang, L., Francois, F., & Pei, Z. (2012) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-11-0934 · Cited by 192
Dam, G., Vilstrup, H., Watson, H., & Jepsen, P. (2016) · Hepatology · doi:10.1002/hep.28737 · Cited by 190
Microbial Colonization of the Upper Gastrointestinal Tract in Patients with Barrett's Esophagus
Macfarlane, S., Furrie, E., Macfarlane, G. T., & Dillon, J. F. (2007) · Clinical Infectious Diseases · doi:10.1086/518578 · Cited by 184
Do NSAIDs, Antibiotics, Infections, or Stress Trigger Flares in IBD?
Singh, S., Graff, L. A., & Bernstein, C. N. (2009) · The American Journal of Gastroenterology · doi:10.1038/ajg.2009.15 · Cited by 181
Wandall, J. H. (1992) · Gut · doi:10.1136/gut.33.5.617 · Cited by 179
Review article: dietary fibre in the era of microbiome science
O’Grady, J., O’Connor, E. M., & Shanahan, F. (2019) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.15129 · Cited by 179
Amir, I., Konikoff, F. M., Oppenheim, M., Gophna, U., & Half, E. E. (2014) · Environmental Microbiology · doi:10.1111/1462-2920.12285 · Cited by 176
A non-endoscopic device to sample the oesophageal microbiota: a case-control study
Elliott, D. R. F., Walker, A. W., O’Donovan, M., Parkhill, J., & Fitzgerald, R. C. (2016) · The Lancet. Gastroenterology & hepatology · doi:10.1016/s2468-1253(16)30086-3 · Cited by 166
Cook, M. B., Corley, D. A., Murray, L. J., Liao, L. M., Kamangar, F., Ye, W., Gammon, M. D., Risch, H. A., Casson, A. G., Freedman, N. D., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0103508 · Cited by 165
Influence of Proton-Pump Inhibitors on the Luminal Microbiota in the Gastrointestinal Tract
Tsuda, A., Suda, W., Morita, H., Takanashi, K., Takagi, A., Koga, Y., & Hattori, M. (2015) · Clinical and Translational Gastroenterology · doi:10.1038/ctg.2015.20 · Cited by 164
Medication Usage and the Risk of Neoplasia in Patients With Barrett's Esophagus
Nguyen, D. M., El-Serag, H. B., Henderson, L., Stein, D., Bhattacharyya, A., & Sampliner, R. E. (2009) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2009.06.001 · Cited by 159
Linking Gut Microbiota to Colorectal Cancer
Raskov, H., Burcharth, J., & Pommergaard, H. (2017) · Journal of Cancer · doi:10.7150/jca.20497 · Cited by 158
Sokol, H., Lepage, P., Seksik, P., Dore, J. M., & Marteau, P. R. (2006) · Journal of Clinical Microbiology · doi:10.1128/jcm.02600-05 · Cited by 140
Proton Pump Inhibitor Use and Risk of Colorectal Cancer: A Population-Based, Case–Control Study
Robertson, D. J., Larsson, H., Friis, S., Pedersen, L., Baron, J. A., & Sørensen, H. T. (2007) · Gastroenterology · doi:10.1053/j.gastro.2007.06.014 · Cited by 139
The esophageal microbiota in health and disease
Di Pilato, V., Freschi, G., Ringressi, M. N., Pallecchi, L., Rossolini, G. M., & Bechi, P. (2016) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.13127 · Cited by 139
The Gastric and Intestinal Microbiome: Role of Proton Pump Inhibitors
Minalyan, A., Gabrielyan, L., Scott, D. R., Jacobs, J. P., & Pisegna, J. R. (2017) · Current Gastroenterology Reports · doi:10.1007/s11894-017-0577-6 · Cited by 134
Long-term proton pump inhibitor (PPI) use and the development of gastric pre-malignant lesions
Song, H., Zhu, J., & Lu, D. (2014) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd010623.pub2 · Cited by 132
Meta‐analysis: proton‐pump inhibition in high‐risk patients with acute peptic ulcer bleeding
Bardou, M., Toubouti, Y., Benhaberou‐Brun, D., Rahme, E., & Barkun, A. N. (2005) · Alimentary Pharmacology & Therapeutics · doi:10.1111/j.1365-2036.2005.02391.x · Cited by 132
Huang, J.-Q., & Hunt, R. H. (2001) · Best Practice & Research Clinical Gastroenterology · doi:10.1053/bega.2001.0184 · Cited by 127
The human jejunum has an endogenous microbiota that differs from those in the oral cavity and colon
Sundin, O. H., Mendoza‐Ladd, A., Zeng, M., Díaz-Arévalo, D., Morales, E., Fagan, B. M., Ordoñez, J., Velez, P., Antony, N., & McCallum, R. W. (2017) · BMC Microbiology · doi:10.1186/s12866-017-1059-6 · Cited by 126
Chronic Proton Pump Inhibitor Therapy and the Risk of Colorectal Cancer
Yang, Y., Hennessy, S., Propert, K., Hwang, W., Sedarat, A., & Lewis, J. D. (2007) · Gastroenterology · doi:10.1053/j.gastro.2007.06.022 · Cited by 125
Review of the gut microbiome and esophageal cancer: Pathogenesis and potential clinical implications
Baba, Y., Iwatsuki, M., Yoshida, N., Watanabe, M., & Baba, H. (2017) · Annals of Gastroenterological Surgery · doi:10.1002/ags3.12014 · Cited by 123
Takagi, T., Naito, Y., Inoue, R., Kashiwagi, S., Uchiyama, K., Mizushima, K., Tsuchiya, S., Okayama, T., Dohi, O., Yoshida, N., et al. (2018) · Journal of Clinical Biochemistry and Nutrition · doi:10.3164/jcbn.17-78 · Cited by 121
Acid Suppression Therapy: Where Do We Go from Here?
Scarpignato, C., Pelosini, I., & Di Mario, F. (2006) · Digestive Diseases · doi:10.1159/000091298 · Cited by 119
Gwee, K.-A., Goh, V., Lima, G., & Setia, S. (2018) · Journal of Pain Research · doi:10.2147/jpr.s156938 · Cited by 117
López, R. L., Burgos, M. J. G., Gálvez, A., & Pulido, R. P. (2016) · Apmis · doi:10.1111/apm.12609 · Cited by 116
Recent developments in the pathophysiology of irritable bowel syndrome
El-Salhy, M. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i25.7621 · Cited by 111
Uejima, M., Kinouchi, T., Kataoka, K., Hiraoka, I., & Ohnishi, Y. (1996) · Microbiology and Immunology · doi:10.1111/j.1348-0421.1996.tb01108.x · Cited by 110
Acid suppressive drugs and gastric cancer: A meta-analysis of observational studies
Ahn, J. S. (2013) · World Journal of Gastroenterology · doi:10.3748/wjg.v19.i16.2560 · Cited by 109
Nardelli, S., Gioia, S., Ridola, L., Farcomeni, A., Merli, M., & Riggio, O. (2019) · Hepatology · doi:10.1002/hep.30304 · Cited by 109
Effects of Proton Pump Inhibitors on the Gastric Mucosa-Associated Microbiota in Dyspeptic Patients
Paroni Sterbini, F., Palladini, A., Masucci, L., Cannistraci, C. V., Pastorino, R., Ianiro, G., Bugli, F., Martini, C., Ricciardi, W., Gasbarrini, A., et al. (2016) · Applied and Environmental Microbiology · doi:10.1128/aem.01437-16 · Cited by 108
Kiank, C., Taché, Y., & Larauche, M. H. (2009) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2009.08.006 · Cited by 107
The use of proton pump inhibitors in treating and preventing NSAID-induced mucosal damage
Scheiman, J. M. (2013) · Arthritis Research & Therapy · doi:10.1186/ar4177 · Cited by 106
Risk Factors for the Development of Esophageal Adenocarcinoma in Barrett's Esophagus
de Jonge, P. J. F., Steyerberg, E. W., Kuipers, E. J., Honkoop, P., Wolters, L. M. M., Kerkhof, M., van Dekken, H., & Siersema, P. D. (2006) · The American Journal of Gastroenterology · doi:10.1111/j.1572-0241.2006.00626.x · Cited by 104
Postinfectious Irritable Bowel Syndrome
Ericsson, C. D., Hatz, C., & DuPont, A. W. (2008) · Clinical Infectious Diseases · doi:10.1086/526774 · Cited by 103
Oral microbiome alterations of healthy volunteers with proton pump inhibitor
Mishiro, T., Oka, K., Kuroki, Y., Takahashi, M., Tatsumi, K., Saitoh, T., Tobita, H., Ishimura, N., Sato, S., Ishihara, S., et al. (2018) · Journal of Gastroenterology and Hepatology · doi:10.1111/jgh.14040 · Cited by 96
Spiegel, B. M. R., Chey, W. D., & Chang, L. (2008) · The American Journal of Gastroenterology · doi:10.1111/j.1572-0241.2008.01992.x · Cited by 95
Colorectal Cancer: Looking for Answers in the Microbiota
Jobin, C. (2013) · Cancer Discovery · doi:10.1158/2159-8290.cd-13-0042 · Cited by 92
Marlicz, W., Łoniewski, I., Grimes, D. S., & Quigley, E. M. (2014) · Mayo Clinic Proceedings · doi:10.1016/j.mayocp.2014.07.015 · Cited by 91
Species Level Description of the Human Ileal Bacterial Microbiota
Villmones, H. C., Haug, E. S., Ulvestad, E., Grude, N., Stenstad, T., Halland, A., & Kommedal, Ø. (2018) · Scientific Reports · doi:10.1038/s41598-018-23198-5 · Cited by 91
Hypergastrinemia Is Associated with Increased Risk of Distal Colon Adenomas
Georgopoulos, S. D., Polymeros, D., Triantafyllou, K., Spiliadi, C., Mentis, A., Karamanolis, D. G., & Ladas, S. D. (2006) · Digestion · doi:10.1159/000096593 · Cited by 90
Probiotic therapy for irritable bowel syndrome.
Aragon, G., Graham, D. B., Borum, M. L., & Doman, D. B. (2010) · PubMed Central · Cited by 89
Adverse outcomes of long-term use of proton pump inhibitors: a systematic review and meta-analysis
Islam, M. M., Poly, T. N., Walther, B. A., Dubey, N. K., Anggraini Ningrum, D. N., Shabbir, S.-A., & (Jack) Li, Y.-C. (2018) · European Journal of Gastroenterology & Hepatology · doi:10.1097/meg.0000000000001198 · Cited by 88
Proton Pump Inhibitors and the Risk of Colorectal Cancer
van Soest, E. M., van Rossum, L. G. M., Dieleman, J. P., van Oijen, M. G. H., Siersema, P. D., Sturkenboom, M. C. J. M., & Kuipers, E. J. (2008) · The American Journal of Gastroenterology · doi:10.1111/j.1572-0241.2007.01665.x · Cited by 80
NSAID enteropathy and bacteria: a complicated relationship
Syer, S. D., Blackler, R. W., Martin, R., de Palma, G., Rossi, L., Verdu, E., Bercik, P., Surette, M. G., Aucouturier, A., Langella, P., et al. (2015) · Journal of Gastroenterology · doi:10.1007/s00535-014-1032-1 · Cited by 80
Maintenance proton pump inhibition therapy and risk of oesophageal cancer
Brusselaers, N., Engstrand, L., & Lagergren, J. (2018) · Cancer Epidemiology · doi:10.1016/j.canep.2018.02.004 · Cited by 80
Fan, X., & Sellin, J. H. (2009) · Alimentary Pharmacology & Therapeutics · doi:10.1111/j.1365-2036.2009.03970.x · Cited by 77
What are the effects of proton pump inhibitors on the small intestine?
Fujimori, S. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i22.6817 · Cited by 70
Watt, E., Gemmell, M., Berry, S., Glaire, M. A., Farquharson, F. M., Louis, P., Murray, G. I., El-Omar, E. M., & Hold, G. L. (2016) · Microbiome · doi:10.1186/s40168-016-0207-9 · Cited by 69
Proton Pump Inhibitors: Risks and Rewards and Emerging Consequences to the Gut Microbiome
Singh, A., Cresci, G., & Kirby, D. F. (2018) · Nutrition in Clinical Practice · doi:10.1002/ncp.10181 · Cited by 69
Hydrogen sulphide protects against NSAID ‐enteropathy through modulation of bile and the microbiota
Blackler, R. W., Motta, J., Manko, A., Workentine, M., Bercik, P., Surette, M. G., & Wallace, J. L. (2015) · British Journal of Pharmacology · doi:10.1111/bph.12961 · Cited by 66
Sharma, V. K., Leontiadis, G. I., & Howden, C. W. (2001) · Alimentary Pharmacology & Therapeutics · doi:10.1046/j.1365-2036.2001.00904.x · Cited by 64
Is Campylobacter to esophageal adenocarcinoma as Helicobacter is to gastric adenocarcinoma?
Kaakoush, N. O., Castaño-Rodríguez, N., Man, S. M., & Mitchell, H. M. (2015) · Trends in Microbiology · doi:10.1016/j.tim.2015.03.009 · Cited by 62
Liang, S., Xu, L., Zhang, D., & Wu, Z. (2016) · The Turkish Journal of Gastroenterology · doi:10.5152/tjg.2016.15375 · Cited by 62
Shah, R., Richardson, P. A., Yu, H., Kramer, J. R., & Hou, J. K. (2017) · Digestion · doi:10.1159/000455008 · Cited by 58
Drugs that inhibit gastric acid secretion may alter the course of inflammatory bowel disease
Juillerat, P., Schneeweiß, S., Cook, E. F., Ananthakrishnan, A. N., Mogun, H., & Korzenik, J. R. (2012) · Alimentary Pharmacology & Therapeutics · doi:10.1111/j.1365-2036.2012.05173.x · Cited by 54
de la Coba Ortiz, C., Argüelles Arias, F., Martín de Argila de Prados, C., Júdez Gutiérrez, J., Linares Rodríguez, A., Ortega Alonso, A., Rodríguez de Santiago, E., Rodríguez-Téllez, M., Vera Mendoza, M. I., Aguilera Castro, L., et al. (2016) · Revista Española de Enfermedades Digestivas · doi:10.17235/reed.2016.4232/2016 · Cited by 54
The microbiome of the oral mucosa in irritable bowel syndrome
Fourie, N. H., Wang, D., Abey, S. K., Sherwin, L. B., Joseph, P. V., Rahim-Williams, B., Ferguson, E. G., & Henderson, W. A. (2016) · Gut Microbes · doi:10.1080/19490976.2016.1162363 · Cited by 53
The Colonic Microbiota and Colonic Disease
Shanahan, F. (2012) · Current Gastroenterology Reports · doi:10.1007/s11894-012-0281-5 · Cited by 49
Microbiome and potential targets for chemoprevention of esophageal adenocarcinoma
Neto, A. G., Whitaker, A., & Pei, Z. (2015) · Seminars in Oncology · doi:10.1053/j.seminoncol.2015.09.005 · Cited by 48
Meta-analyses: does long-term PPI use increase the risk of gastric premalignant lesions?
Eslami, L., & Nasseri‐Moghaddam, S. (2013) · PubMed · Cited by 47
Recent insights into the pathogenesis of hepatic encephalopathy and treatments
Sturgeon, J. P., & Shawcross, D. L. (2013) · Expert Review of Gastroenterology & Hepatology · doi:10.1586/17474124.2014.858598 · Cited by 46
Sung, J., Kim, N., Lee, J., Hwang, Y.-J., Kim, H. W., Chung, J. W., Kim, J.-W., & Lee, D. H. (2018) · Gut and Liver · doi:10.5009/gnl17063 · Cited by 39
OESOPHAGEAL MICROBIAL FLORA IN CARCINOMA OF THE OESOPHAGUS
Lau, W. F., Wong, J., & Ong, K. (1981) · Australian and New Zealand Journal of Surgery · doi:10.1111/j.1445-2197.1981.tb05905.x · Cited by 38
Bruno, G., Rocco, G., Zaccari, P., Porowska, B., Mascellino, M. T., & Severi, C. (2018) · Canadian Journal of Infectious Diseases and Medical Microbiology · doi:10.1155/2018/6237239 · Cited by 32
Self-citationZhu, J., Qi, X., Yu, H., Yoshida, E. M., Mendez-Sanchez, N., Zhang, X., Wang, R., Deng, H., Li, J., Han, D., et al. (2018) · United European Gastroenterology Journal · doi:10.1177/2050640618773564 · Cited by 28
Dave, M., Johnson, L. A., Walk, S. T., Young, V. B., Stidham, R. W., Chaudhary, M. N., Funnell, J. A., & Higgins, P. (2011) · Gut · doi:10.1136/gut.2010.224337 · Cited by 24
Proton-pump inhibitors for the treatment of functional dyspepsia
Suzuki, H., Okada, S., & Hibi, T. (2011) · Therapeutic Advances in Gastroenterology · doi:10.1177/1756283x11398735 · Cited by 22
The gut microbiota era marches on
Guarner, F. (2014) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2014.156 · Cited by 19
Is irritable bowel syndrome an infectious disease?
Thompson, J. R. (2016) · World Journal of Gastroenterology · doi:10.3748/wjg.v22.i4.1331 · Cited by 19
Schmulson, M. J., & Frati-Munari, A. C. (2019) · Revista de Gastroenterología de México · doi:10.1016/j.rgmx.2018.02.008 · Cited by 14
Gastrin and Colon Cancer: A Unifying Hypothesis
Joshi, S. N., & Gardner, J. D. (2008) · Digestive Diseases · doi:10.1159/000171567 · Cited by 13
Schmulson, M. J., & Frati-Munari, A. C. (2018) · Revista de Gastroenterología de México (English Edition) · doi:10.1016/j.rgmxen.2018.05.011 · Cited by 10
Relationship between infectious gastroenteritis and irritable bowel syndrome
Kanazawa, M., & Fukudo, S. (2013) · Clinical Journal of Gastroenterology · doi:10.1007/s12328-013-0444-4 · Cited by 9
The microbiome as a potential biomarker for oesophageal adenocarcinoma
Abrams, J. A. (2017) · The Lancet Gastroenterology & Hepatology · doi:10.1016/s2468-1253(16)30177-7 · Cited by 7
Agreus, L., Xia, H. H. ‐., & Alley, N. J. T. (1997) · Alimentary Pharmacology & Therapeutics · doi:10.1046/j.1365-2036.1997.00255.x · Cited by 3
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Metadata
- Authors
- Bruno, G., Zaccari, P., Rocco, G., Scalese, G., Panetta, C., Porowska, B., Pontone, S., & Severi, C.
- Affiliations
- University of Otago (NZ)
- Corresponding author
- Pontone, Stefano
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2019-06-14
- Volume
- 25
- Issue
- 22
- Pages
- 2706-2719
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC6580352
- OpenAlex
- W2950297440
- Semantic Scholar
- 8c9a916b6bbfed0cf31d78d22613750fe17a7b02
- Cited by
- 258
- References
- 163
- Citations by year
- 2026: 19 · 2025: 31 · 2024: 46 · 2023: 62 · 2022: 31 · 2021: 37 · 2020: 27 · 2019: 4
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Gastroenterology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by-nc)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Gastroenterology › Helicobacter pylori-related gastroenterology studies
- Keywords
- proton pump inhibitors, gut dysbiosis, gut microbiota, gastrointestinal diseases, gut mucosal barrier, immunomodulation, pathogenesis
- MeSH terms
- Gastrointestinal Microbiome, Achlorhydria, Bacteria, Gastric Acid, Gastric Mucosa, Humans, Intestinal Mucosa, Proton Pump Inhibitors, Dysbiosis
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