Gastroduodenal “Dysbiosis”: a New Clinical Entity

Shah, Ayesha; Morrison, Mark; Holtmann, Gerald

doi:10.1007/s11938-018-0207-x

Cited by 26 publications

(31 citation statements)

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“…While the duodenal bacterial load as measured by qPCR revealed significant differences between groups, the rate of positive glucose breath tests was not different across the different patient groups and controls. This could be potentially explained by the poor sensitivity and specificity of glucose breath test 47 . It is well recognised that false positive results can occur in conditions associated with rapid gastrointestinal transit, loss of small intestinal absorptive surface, altered gastrointestinal tract anatomy, which allows some glucose loads to escape the small bowel absorption and subsequently get fermented in the colon 15,48 …”

Section: Discussionmentioning

confidence: 99%

Duodenal bacterial load as determined by quantitative polymerase chain reaction in asymptomatic controls, functional gastrointestinal disorders and inflammatory bowel disease

Shah

Talley

Koloski

et al. 2020

Aliment Pharmacol Ther

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Summary Background Small intestinal bacterial overgrowth may play a role in gastrointestinal and non‐gastrointestinal diseases. Aims To use quantitative polymerase chain reaction (qPCR) to determine and compare bacterial loads of duodenal biopsies in asymptomatic controls, and patients with functional gastrointestinal disorders (FGIDs) and inflammatory bowel disease (IBD) including ulcerative colitis (UC) and Crohn’s disease (CD). To define effects of gastric acid inhibition on bacterial load, explore links of bacterial load and gastrointestinal symptoms in response to a standardised nutrient challenge and compare bacterial load with glucose breath test results. Methods In 237 patients (63 controls, 84 FGID and 90 IBD), we collected mucosal samples under aseptic conditions during endoscopy extracted and total DNA. Bacterial load metric was calculated utilising qPCR measurements of the bacterial 16S rRNA gene, normalised to human beta‐actin expression. Standard glucose breath test and nutrient challenge test were performed. Results The duodenal microbial load was higher in patients with FGID (0.22 ± 0.03) than controls (0.07 ± 0.05; P = 0.007) and patients with UC (0.01 ± 0.05) or CD (0.02 ± 0.09), (P = 0.0001). While patients treated with proton pump inhibitors (PPI) had significantly higher bacterial loads than non‐users (P < 0.05), this did not explain differences between patient groups and controls. Bacterial load was significantly (r = 0.21, P < 0.016) associated with the symptom response to standardised nutrient challenge test. Methane, but not hydrogen values on glucose breath test were associated with bacterial load measured utilising qPCR. Conclusions Utilising qPCR, a diagnosis of FGID and treatment with PPI were independently associated with increased bacterial loads. Increased bacterial loads are associated with an augmented symptom response to a standardised nutrient challenge.

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Section: Discussionmentioning

confidence: 99%

Duodenal bacterial load as determined by quantitative polymerase chain reaction in asymptomatic controls, functional gastrointestinal disorders and inflammatory bowel disease

Shah

Talley

Koloski

et al. 2020

Aliment Pharmacol Ther

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“…A growing body of scientific evidence highlights the importance of the small intestine microbiome in normal human physiology and response to dietary interventions [2,3]. Alterations in the small intestine microbiome are implicated in a number of human disorders, such as malnutrition [4,5], obesity, and metabolic disease [6], inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) [7][8][9], and drug side effects [10]. Despite the apparent importance of the small intestine microbiome in human health, it remains understudied and poorly characterized largely because of the procedural and logistical complexities associated with its sampling in humans (methods are too invasive and require specialized healthcare facilities).…”

Section: Introductionmentioning

confidence: 99%

Self-reinoculation with fecal flora changes microbiota density and composition leading to an altered bile-acid profile in the mouse small intestine

2020

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Background: The upper gastrointestinal tract plays a prominent role in human physiology as the primary site for enzymatic digestion and nutrient absorption, immune sampling, and drug uptake. Alterations to the small intestine microbiome have been implicated in various human diseases, such as non-alcoholic steatohepatitis and inflammatory bowel conditions. Yet, the physiological and functional roles of the small intestine microbiota in humans remain poorly characterized because of the complexities associated with its sampling. Rodent models are used extensively in microbiome research and enable the spatial, temporal, compositional, and functional interrogation of the gastrointestinal microbiota and its effects on the host physiology and disease phenotype. Classical, culture-based studies have documented that fecal microbial self-reinoculation (via coprophagy) affects the composition and abundance of microbes in the murine proximal gastrointestinal tract. This pervasive selfreinoculation behavior could be a particularly relevant study factor when investigating small intestine microbiota. Modern microbiome studies either do not take self-reinoculation into account, or assume that approaches such as single housing mice or housing on wire mesh floors eliminate it. These assumptions have not been rigorously tested with modern tools. Here, we used quantitative 16S rRNA gene amplicon sequencing, quantitative microbial functional gene content inference, and metabolomic analyses of bile acids to evaluate the effects of selfreinoculation on microbial loads, composition, and function in the murine upper gastrointestinal tract.Results: In coprophagic mice, continuous self-exposure to the fecal flora had substantial quantitative and qualitative effects on the upper gastrointestinal microbiome. These differences in microbial abundance and community composition were associated with an altered profile of the small intestine bile acid pool, and, importantly, could not be inferred from analyzing large intestine or stool samples. Overall, the patterns observed in the small intestine of non-coprophagic mice (reduced total microbial load, low abundance of anaerobic microbiota, and bile acids predominantly in the conjugated form) resemble those typically seen in the human small intestine.Conclusions: Future studies need to take self-reinoculation into account when using mouse models to evaluate gastrointestinal microbial colonization and function in relation to xenobiotic transformation and pharmacokinetics or in the context of physiological states and diseases linked to small intestine microbiome and to small intestine dysbiosis.

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“…3 The current gold standard for diagnosing SIBO remains small bowel aspirate and culture, however in clinical practice breath testing has largely replaced culture methods given the simplicity and noninvasive nature of these tests. 3 Breath tests are based on the principle that human cells do not produce hydrogen and/or methane gas 4 and presence of these gases in the human breath indicates the metabolism of (non-digested) carbohydrates by gut microbes. 5 Although certain Clostridium and Bacteroides spp.…”

Section: Introductionmentioning

confidence: 99%

“…Hence, we decided to conduct a systematic review and meta-analysis to (1) assess and compare the prevalence of methane positive SIBO in patients with IBS and IBD (and their subtypes) and healthy controls; (2) explore the link between diagnostic modality (type of breath test) and variations in methane SIBO prevalence in patients with IBS and IBD; (3) assess the association between proton pump inhibitor (PPI) use and methane positivity on breath test; (4) assess the link between transit time and methane positivity on breath tests and; (5) assess the effect of antibiotic therapy on symptom improvement in patients with methane positive SIBO.…”

Section: Introductionmentioning

confidence: 99%

Methane positive small intestinal bacterial overgrowth in inflammatory bowel disease and irritable bowel syndrome: A systematic review and meta-analysis

et al. 2021

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Several studies reported a potential role of methane producing archaea in the pathophysiology of irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). We conducted a systematic review and meta-analysis to assess the prevalence of methane positive small intestinal bacterial overgrowth (SIBO) in IBS and IBD compared with controls. MEDLINE (PubMed) and Embase electronic databases were searched from inception until March 2021 for case-control and prevalence studies reporting SIBO in IBS and IBD. We extracted data from published studies and calculated pooled prevalence of SIBO in IBS or IBD, odds ratios (OR), and 95% CIs, utilizing a random effects model. The final dataset included 17 independent studies assessing the prevalence of methane positive SIBO in 1,653 IBS-patients and 713 controls, and 7 studies assessing the prevalence of methane positive SIBO in 626 IBD-patients and 497 controls, all utilizing breath test for SIBO diagnosis. Prevalence of methane positive SIBO in IBS and IBD was 25.0% (95% CI 18.8-32.4) and 5.6% (95% CI 2.6-11.8), respectively. Methane positive SIBO in IBS was not increased compared to controls (OR = 1.2, 95% CI 0.8-1.7, P = .37) but was significantly more prevalent in IBS-C as compared to IBS-D (OR = 3.1, 95% CI 1.7-5.6, P = .0001). The prevalence of methane-positive SIBO in patients with IBD was 3-fold lower at 7.4% (95% CI 5.4-9.8) compared to 23.5% (95% CI 19.8-27.5) in controls. The prevalence of methane positive SIBO was significantly lower in Crohn's disease as compared to ulcerative colitis, (5.3%, 95% CI 3.0-8.5 vs. 20.2%, 95% CI 12.8-29.4). This systematic review and meta-analysis suggests methane positivity on breath testing is positively associated with IBS-C and inversely with IBD. However, the quality of evidence is low largely due to clinical heterogeneity of the studies. Thus, causality is uncertain and further studies are required.

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Gastroduodenal “Dysbiosis”: a New Clinical Entity

Cited by 26 publications

References 100 publications

Duodenal bacterial load as determined by quantitative polymerase chain reaction in asymptomatic controls, functional gastrointestinal disorders and inflammatory bowel disease

Duodenal bacterial load as determined by quantitative polymerase chain reaction in asymptomatic controls, functional gastrointestinal disorders and inflammatory bowel disease

Self-reinoculation with fecal flora changes microbiota density and composition leading to an altered bile-acid profile in the mouse small intestine

Methane positive small intestinal bacterial overgrowth in inflammatory bowel disease and irritable bowel syndrome: A systematic review and meta-analysis

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