Dyspepsia and the microbiome: time to focus on the small intestine

Zhong, Laurie; Shanahan, Erin R.; Raj, Ashok; Koloski, Natasha A.; Fletcher, Linda M.; Morrison, Mark; Walker, Marjorie M.; Talley, Nicholas J.; Holtmann, Gerald

doi:10.1136/gutjnl-2016-312574

Cited by 161 publications

(156 citation statements)

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“…In patients with functional dyspepsia with slow gastric emptying or impaired fundic accommodation, it is conceivable that neuronal or muscle diseases -in addition to a preceding or concomitant infection or on their own -could explain the pathogenesis and acute onset 232 . Most excitingly, new information documenting subtle duodenal inflammation (notably, duodenal eosinophilia in a subset of patients with PDS), increased duodenal mucosal perme ability, a disturbed duodenal microbiota, impaired enteric nervous system reflexes and evidence of systemic alterations (for example, increased levels of circulating cytokines and small-intestinal T cells) have shifted interest from the stomach to the upper small intestine 103 .…”

Section: Discussionmentioning

confidence: 99%

“…in the gastric microbiota was inversely associated with the severity of PDS symptoms in a small study 101 . Another small study analysed the composition of the gastric microbiota in patients with functional dyspepsia and reported that Bacteroidetes were more abundant than Proteobacteria compared with healthy controls, and Acidobacteria were absent 102 , whereas another study described an altered duodenal microbiota with a predominance of species typically found in the oral microbiota 103 . These results warrant further studies on the role of the microbiota in functional dyspepsia.…”

Section: Intestinal Microbiotamentioning

confidence: 99%

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Functional dyspepsia

Enck¹,

Azpiroz

Boeckxstaens

et al. 2017

Nat Rev Dis Primers

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| Functional dyspepsia is one of the most prevalent functional gastrointestinal disorders. Functional dyspepsia comprises three subtypes with presumed different pathophysiology and aetiology: postprandial distress syndrome (PDS), epigastric pain syndrome (EPS) and a subtype with overlapping PDS and EPS features. Functional dyspepsia symptoms can be caused by disturbed gastric motility (for example, inadequate fundic accommodation or delayed gastric emptying), gastric sensation (for example, sensations associated with hypersensitivity to gas and bloating) or gastric and duodenal inflammation. A genetic predisposition is probable but less evident than in other functional gastrointestinal disorders, such as irritable bowel syndrome (IBS). Psychiatric comorbidity and psychopathological state and trait characteristics could also play a part, although they are not specific to functional dyspepsia and are less pronounced than in IBS. Possible differential diagnoses include Helicobacter pylori infection and peptic ulceration. Pharmacological therapy is mostly based on the subtype of functional dyspepsia, such as prokinetic and fundus-relaxing drugs for PDS and acid-suppressive drugs for EPS, whereas centrally active neuromodulators and herbal drugs play a minor part. Psychotherapy is effective only in a small subset of patients, whereas quality of life can be severely affected in nearly all patients. Future therapies might include novel compounds that attempt to treat the underlying gastric and duodenal inflammation. NATURE REVIEWS | DISEASE PRIMERS VOLUME 3 | ARTICLE NUMBER 17081 | 1 PRIMER © 2 0 1 7 M a c m i l l a n P u b l i s h e r s L i m i t e d , p a r t o f S p r i n g e r N a t u r e . A l l r i g h t s r e s e r v e d .standard therapy for gastro -oesophageal reflux disease. Paediatric dyspeptic symptoms are being addressed in a separate classification effort 10 . This Primer covers functional dyspepsia in adults only, although we sporadically refer to paediatric functional dyspepsia when similarities exist. EpidemiologyThe population prevalence of functional dyspepsia is quite variable across the globe, with overall high numbers (10-40%) in Western countries and low numbers (5-30%) in Asia, independent of the respective functional dyspepsia definitions 11 . A large-scale health and nutrition survey from France 12 (which involved >35,000 people) identified that 15% of individuals had suspected functional dyspepsia, 28% had irritable bowel syndrome (IBS) and 6% had both. The population of patients who are affected by both IBS and functional dyspepsia has been reported to range between 10% and 27% in previous studies 13 and to approach 30% in popu lation samples; it could be even higher in specific populations 14,15 . This observation has given rise to the term 'overlap syndrome' (REF. 13), which calls into question the sensitivity and specificity of the Rome criteria, at least for IBS and functional dyspepsia. This argument is also supported by the observation that patients with functional dyspepsia m...

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Section: Discussionmentioning

confidence: 99%

Section: Intestinal Microbiotamentioning

confidence: 99%

Functional dyspepsia

Enck¹,

Azpiroz

Boeckxstaens

et al. 2017

Nat Rev Dis Primers

Self Cite

253

247

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“…[15][16][17]38 Intestinal microbiota play an important role in the maintenance of host health by providing energy, nutrients, and immunological protection and its imbalance can provoke various GI symptoms and disease. 39 Because H.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, sequencing analysis of gut microbiota showed that H. pylori was not alone in the stomach and the interaction of H. pylori with those microorganisms might play a role in H. pylori-associated functional dyspepsia. 16,17 In this study, we hypothesize that H. pylori infected patients diagnosed as FD might have dysbiosis of the gut microbiota. Most of them would also have irritable bowel syndrome (IBS).…”

Section: Introductionmentioning

confidence: 99%

IsHelicobacter pyloriAssociated Functional Dyspepsia Correlated With Dysbiosis?

Kim

Chung

Kim

et al. 2017

J Neurogastroenterol Motil

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Background/AimsTo assess the long-term effect of Helicobacter pylori eradication on symptomatic improvement according to the type of antibiotic and the duration of treatment in H. pylori-associated functional dyspepsia. MethodsWe searched Pubmed, Embase, CINAHL, and the Cochrane library databases for randomized controlled trials written in English and undertaken up to August 2016 that met our eligibility criteria. The search methodology used combinations of the following keywords: Helicobacter pylori OR H. pylori OR HP; dyspepsia OR functional dyspepsia OR non-ulcer dyspepsia; eradication OR cure OR treatment. The study outcome was the summary odds ratio (OR) for symptomatic improvement in H. pylori-associated functional dyspepsia with successful eradication therapy. Subgroup analyses were performed based on the type of antibiotic, and the duration of treatment, whether or not patients had symptoms of irritable bowel syndrome, and on race. ResultsSixteen randomized controlled trials met the inclusion criteria. The summary OR for symptomatic improvement in patients in our eradication group was 1.33 (95% confidence interval [CI], 1.16-1.54; P < 0.01). In a subgroup analysis on type of antibiotic, symptomatic improvement with metronidazole-containing regimen (OR, 1.87; 95% CI, 1.26-2.77) was better than treatment with clarithromycin (OR, 1.29; 95% CI, 1.11-1.50). H. pylori eradication therapy given for 10-14 days was the more effective for symptom improvement than 7-day therapy. When the studies excluding irritable bowel syndrome cases were analyzed, there were no therapeutic effects of H. pylori eradication on symptomatic improvement. ConclusionsIn the clinical setting, the most effective H. pylori eradication regimen for functional dyspepsia to provide relief of symptoms is a metronidazole-based treatment regimen for at least 10 days. The explanation for this is that H. pylori-associated functional dyspepsia could be associated with dysbiosis.

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“…In this context, emerging information in relation to the gut microbiome becomes relevant. Bacteria colonizing the gut mucosa can alter mucosal inflammation and sensory function and can impair quality of life [10]. On the basis of these and similar data, unraveling the mechanisms that cause functional gastrointestinal disorders and developing the therapies that will specifically target the underlying pathological mechanisms appears to be closer to fruition.…”

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confidence: 99%