Fig 3 - available from: BMC Gastroenterology
This content is subject to copyright. Terms and conditions apply.
Duodenum inflammatory changes by VCE0. a Erosion of proximal duodenum (circled) Prior to HP eradication. b Erosions in proximal duodenum (circled) Post HP eradication
Source publication
Background
Helicobacter pylori (HP) infection is present in about 50% of the global population, and is associated with chronic gastritis, peptic disease and gastric malignancies. HP prevalence in Crohn’s disease (CD) patients was shown to be low compared to the general population, and its influence on disease activity is yet to be determined. Our a...
Similar publications
Purpose:
The aim of this study was to investigate the diagnostic efficacy and image quality of magnetic resonance enterography (MRE) using oral mannitol solution for the evaluation Crohn disease (CD).
Materials and methods:
We retrospectively evaluated MRE examinations of 153 patients with an assumed or definitive diagnosis of CD. There were 65...
Citations
... [15] Conflicting evidence from human and animal studies supports Helicobacter as an agent causing IBD. [16][17][18][19][20][21][22] Pediatric data on this aspect are limited and based on a small sample. Some studies have suggested negative association of H pylori infection in children with IBD, [23] while others disagreed. ...
Background:
Available literature has reported the association of Helicobacter pylori (H pylori) infection with inflammatory bowel disease (IBD) in adults. However, only a few studies have addressed the disease in children.
Aim:
To ascertain the correlation of H pylori infection with IBD among children.
Methods:
The aim of this systematic review and meta-analysis is to assess the association between H pylori infection and IBD in children. We searched databases including Cochrane, EMBASE, Google Scholar, PubMed, Medline, and Web of Science to select relevant studies. Ultimately, based on predetermined inclusion criteria, we included 6 studies that met the requirements. Review Manager and Stata software were used to extract and analyze the data from the relevant studies. In the methods, we employed both qualitative and quantitative approaches for comprehensive analysis. Qualitative analysis involved describing study designs, sample characteristics, and results, while quantitative analysis involved statistical tests such as calculating pooled risk ratios and 95% confidence intervals to evaluate the association between H pylori infection and IBD in children. Lastly, by combining the results of the individual studies, our objective is to provide a comprehensive understanding of the relationship between H pylori infection and IBD in children.
Results:
In totality, we involved 2236 participants that were recruited in 6 studies. We detected no significant difference in H pylori prevalence (9.8% vs 12.7%, P = .12) by comparing the children IBD group to controls. Among the IBD children, we estimated odds ratio (OR) of H pylori infection to 0.62 [(95% confidence interval (CI) of 0.34-1.12)]. In children suffering from ulcerative colitis (UC) and Crohn disease (CD), the H pylori infection rates were higher than in those with IBD-unclassified (IBDU).When analyzed stratified by disease of study design, In CD group [OR = 1.42, 95% CI: 0.72-2.80)] (I2 = 0%, P = .64). but no significant difference in CD group.
Conclusions:
No correlation was found between H pylori infection and the occurrence of IBD in children.
... In a patient group with 56 cases and quiescent Crohn disease, it was shown that fecal calprotectin levels did not change significantly with H pylori eradication. 26 There were only six H pylori positive patients which lead them to avoid coming to a clear conclusion. ...
Background:
Fecal calprotectin is an important inflammatory marker in intestinal diseases and is not routinely used in the upper gastrointestinal system disorders. The aim of this study was to show whether there is a relationship between fecal calprotectin levels and Helicobacter pylori (H pylori) gastritis in children and to determine the association of fecal calprotectin levels with gastric biopsy results in terms of chronic inflammation and neutrophil activity.
Methods:
Patients with the complaints of the upper gastrointestinal system (epigastric pain, heartburn, nausea and vomiting) who were planned to undergo endoscopy were enrolled prospectively. The presence of H pylori was defined according to the gastric antrum biopsy results. Fecal calprotectin level was tested in the stool sample of the patients. The fecal calprotectin levels, upper gastrointestinal endoscopy and gastric biopsy results of 89 patients were evaluated.
Results:
H pylori was found to be positive in the gastric biopsies of 51 (57.3%) patients. In the H pylori positive group mean fecal calprotectin level was 74.8 ± 67 μg/g, and in the H pylori negative group mean fecal calprotectin level was 52.7 ± 46 μg/g and the difference was significant (p= 0.039). We also found a significant relationship between fecal calprotectin levels and gastric neutrophil activity grades (p= 0.034).
Conclusions:
Mean fecal calprotectin levels were found to be higher in H pylori positive subjects in our study. Fecal calprotectin levels were correlated with gastric neutrophil activity grades. Fecal calprotectin represents gastric neutrophilic inflammation. When interpreting a high fecal calprotectin level, H pylori infection should be kept in mind.
... H. pylori is found in approximately 50% of the world's population [6]. People may become infected in their early childhood, with the infection persisting throughout their lifetime. ...
Background
Helicobacter pylori (H. pylori) eradication can reduce the prevalence of gastric cancer. However, whether H. pylori eradication therapy should be performed in infected patients, especially in asymptomatic cases, is still controversial.
Aims
The aims of this study were to determine whether H. pylori screening and eradication could prevent gastric cancer in a cost-effective way, and further whether eradication therapy should be administered to asymptomatic individuals.
Methods
Cost-effectiveness analysis was performed using a Markov model. We established two groups, each with 10,000 hypothetical Chinese individuals at the age of 40 years. Clinical outcomes and cost of H. pylori eradication were compared between the eradication and control groups.
Results
There was a lower morbidity with gastric cancer in the eradication group than in the control group, which was most significant after running the model for 15 years. The eradication group experienced an average of 34.64 quality-adjusted life years (QALYs) per person, and the average cost was US $1706.52 per person. The control group exhibited an average of 32.63 QALYs per person, and the average cost was US $2045.10 per person. The cost-effectiveness analysis showed that eradication saved $1539 per LY per person and $168.45 per QALY per person.
Conclusions
H. pylori screening and eradication therapy effectively reduces the morbidity of gastric cancer and cancer-related costs in asymptomatic infected individuals. Therefore, we believe that H. pylori eradication can prevent gastric cancer in a cost-effective way.
... H. pylori is the most important cause of DU (8)(9)(10)(11). At present, more than 50% of the world population is infected with H. pylori (18,19), and there were high H. pylori infection rates in various age groups in this study. It has been reported that H. pylori infection mainly occurs in the duodenal bulb (20), and it is very rare below the descending segment. ...
Background/aims:
This study aimed to investigate the differences and relevance of various common duodenal diseases in different parts in the aspects of age, gender, helicobacter pylori (H. pylori) infection, application of nonsteroidal anti-inflammatory drugs (NSAIDs), smoking, or alcohol consumption.
Materials and methods:
The medical records of various duodenal diseases were collected and tested for difference using the χ2 test or the Fisher exact probability method.
Results:
1) The proportions of duodenal ulcer (DU), inflammation, and duodenal bulb diseases in the adult group (A) (47.98%, 36.70%, and 66.63%) were higher than those in the elderly group (E) (41.38%, 29.83%, and 56.82%), but the proportions of duodenal diverticulum (DD) and tumor diseases in the descending and ascending segments (2.95%, 1.43%, 9.14%, and 0.14%) were lower than those in group E (13.73%, 3.69%, 19.41%, and 0.76%) (p<0.001). 2) The positive rate of H. pylori (63.64%) in the duodenal bulb diseases was higher than that in the bulb-descending segment (53.75%), but the application rate of NSAIDs (16.44%) in the duodenal bulb-descending diseases was lower than that in the descending segment (24.81%) (p<0.001).
Conclusion:
1) DU, inflammation, and duodenal bulb diseases are common in adults, but DD and tumor diseases in the descending and ascending segments are more common in the elderly. 2) Compared with the duodenal bulb-descending diseases, the application of NSAIDs has greater impact on the diseases in the descending segment, and the rate of H. pylori infection is higher in duodenal bulb diseases.
... pylori) having spiral (shape), gram negative (micro aerophilic) bacterium, usually found in humans 'gastric mucosa, which can live for decades (Safavi, 2016). H. pylori is the gastric pathogen affecting more than 50% of the world population (Lahat et al., 2017). Most of them remain asymptomatic in whole life and survive without any major clinical outcomes (Lahat et al., 2017). ...
... H. pylori is the gastric pathogen affecting more than 50% of the world population (Lahat et al., 2017). Most of them remain asymptomatic in whole life and survive without any major clinical outcomes (Lahat et al., 2017). H. pylori commonly induce the upper gastrointestional (GI) disease such as induction of peptic ulcer (duodenal and gastric), gastric cancer, gastric mucosal linked lymphoid tissue lymphoma and chronic gastritis (Wyle, 1991). ...
Objective
H. pylori have gradually acquired resistance to the commonly used antibiotics because of their use in many parasitic and anaerobic infections, which leads to treatment failure of various gastric and duodenal diseases associated with H. pylori infection. The present research work aimed to isolate and characterize the bioactive compound from the methanol extract of stem of Berberis aristata DC. This is traditionally used for the treatment of dyspepsia, dysentery and diarrhea against antibiotic-resistant gastric pathogen H. pylori.
Methods
The in vitro antimicrobial activity of Berberine an active isolated compound from methanol extract of stem of Berberis aristata DC against drug-resistant H. pylori strain isolated from North Indian GERD patients. The H. pylori strain was only collected from those, who were devoid of any kind of anti-H. Pylori therapy. The methodology was in determining the Minimum inhibition concentration (MIC) using the microdilution method and disk diffusion method.
Results
H. pylori isolate was included in this study. Berberine from methanol extract of stem of Berberis aristata DC showed its potency on H. pylori-infected isolated from GERD patients with a maximum inhibition at 0.000075 μg/ml.
Conclusion
Prevalence of metronidazole resistance ranges between 50 and 90% in developing countries including India. The emergence of dual drug resistance was reported in various studies. This study suggests that Berberine an isolated compound from methanol extract of stem of Berberis aristata DC used commonly known as Daru Haldi potentially active for the treatment of drug-resistant H. pylori infection. Berberine from methanol extract of stem of Berberis aristata DC with a concentration of 0.000075 μg/ml shows a positive effect safely and effectively.
... Three cases of Crohn's diseases exacerbation after H. pylori eradication have been already described [78,79]. At contrary, eradication of the bacteria did not significantly change disease activity measures or the presence of gastro-duodenitis in a small cohort study of six patients with quiescent Crohn's disease [80]. Further studies are needed to reveal the relationship between H. pylori eradication and IBD onset or progression. ...
Helicobacter pylori is a bacterium that selectively infects the gastric epithelium of half of the world population. The microbiome, community of microorganisms gained major interest over the last years, due to its modification associated to health and disease states. Even if most of these descriptions have focused on chronic disorders, this review describes the impact of the intestinal bacterial microbiome on host response to Helicobacter associated diseases. Microbiome has a direct impact on host cells, major barrier of the gastro-intestinal tract, but also an indirect impact on immune system stimulation, by enhancing or decreasing non-specific or adaptive response. In microbial infections, especially in precancerous lesions induced by Helicobacter pylori infection, these modifications could lead to different outcome. Associated to data focusing on the microbiome, transcriptomic analyses of the eukaryote response would lead to a complete understanding of these complex interactions and will allow to characterize innovative biomarkers and personalized therapies.
... Moreover, the eradication success rate was comparable to that in previous reports in which eradication therapy was performed for patients without IBD. 23 Although the influence of eradication therapy was prospectively observed in only 6 CD patients and unchanged disease activity was reported, 24 this was small study without control arm and no UC patients were included. Our present report clearly described the disease activity of both CD and UC patients after H. pylori eradication in larger cohort with control arm. ...
Background/aims:
The influences of Helicobacter pylori eradication therapy on the disease course of inflammatory bowel disease (IBD) are still unclear. We therefore conducted a multicenter, retrospective cohort study to evaluate the safety of H. pylori eradication therapy for IBD patients.
Methods:
IBD patients with H. pylori eradication from 2005 to 2015 (eradication group) and control patients (non-eradication group; 2 paired IBD patients without H. pylori eradication matched with each eradicated patient) were included. IBD exacerbation (increased/additional IBD drug or IBD-associated hospitalization/surgery) and disease improvement based on the physicians' global assessment were investigated at baseline, and at 2 and 6 months after eradication or observation.
Results:
A total of 429 IBD (378 ulcerative colitis, 51 Crohn's disease) patients, comprising 144 patients in the eradication group and 285 patients in the non-eradication group, were enrolled at 25 institutions. IBD exacerbation was comparable between groups (eradication group: 8.3% at 2 months [odds ratio, 1.76; 95% confidence interval, 0.78-3.92; P=0.170], 11.8% at 6 months [odds ratio, 1.60; 95% confidence interval, 0.81-3.11; P=0.172]). Based on the physicians' global assessment at 2 months, none of the patients in the eradication group improved, whereas 3.2% of the patients in the non-eradication group improved (P=0.019). Multivariate analysis revealed that active disease at baseline, but not H. pylori eradication, was an independent factor for IBD exacerbation during 2 months' observation period. The overall eradication rate was 84.0%-comparable to previous reports in non-IBD patients.
Conclusions:
H. pylori eradication therapy does not alter the short-term disease activity of IBD.
... 6 Recent data focussing on H. pylori involvement in the pathogenesis of IBD is gaining attention. [6][7][8][9] Various mechanisms have been proposed that link H. pylori to IBD, including induction of alterations in gastric and intestinal permeability via various immunological pathways, or via induction of antigenic material absorption with subsequent loss of self-tolerance. 10 In the context of gastritis, the histopathology of the gastric mucosa infected with H. pylori is understood to strongly stimulate mucosal inflammation, thereby causing an inflammatory response characterised by an influx of neutrophils, mononuclear cells, and T helper 1 (Th1) cells that destroy intracellular pathogens. ...
... However, as H. pylori does not exist intracellularly, the Th1 response results in endothelial damage to the host's gastric mucosa and is incapable of pathogen clearance. 13 Several studies have reported that the prevalence of H. pylori infection is lower in patients with IBD compared to controls, 7,8,10,14,15 and this inverse relationship prompted investigations and shifted the focus of research to the potential protective role of H. pylori in the development of IBD. By colonising the gastric mucosa, H. pylori has acquired a series of attributes, primarily a downregulation of the host's immune system to evade both the innate and acquired immune system and prevent pathogen clearance. ...
... 6,20 Notwithstanding this, a recent meta-analysis found that the protective effect of H. pylori was not influenced by previous use of amino salicylates or corticosteroids; however, antibiotics amplified this negative association. 7 Secondly, it is possible that immunological alterations of the gut mucosa induced by IBD could prevent H. pylori colonisation. 8 Lastly, it has been proposed that H. pylori infection shifts the equilibrium between Th1 and Th2 immune responses to a Th2-dominant pattern. ...
Since it was first identified in 1982, Helicobacter pylori has continued to draw attention far beyond its role in peptic ulcer disease and is now associated with a myriad of immune-mediated diseases, both inside the gastrointestinal tract (GIT), such as mucosa-associated lymphoid tissue lymphoma, and systemic diseases, such as H. pylori-associated immune thrombocytopenia. This association has ignited research into the mechanisms of H. pylori pathogenicity, especially regarding its role within a multitude of diseases outside the GIT. Despite controversies, a growing body of evidence has begun to establish potential associations between H. pylori and extragastric GIT pathologies; H. pylori has recently been associated with luminal diseases, such as inflammatory bowel diseases and coeliac disease, as well as pancreatic, hepatobiliary, and malignant diseases of the GIT. Despite the lack of conclusive evidence regarding the mechanisms of these relationships, studies have found strong associations, like the case of H. pylori and coeliac disease, while others have not discovered such connections. In addition, while studies have established positive associations between H. pylori and various extragastric diseases, other studies have found the pathogen to play a protective role in disease development. This review comments on the latest evidence that addresses the role of H. pylori in non-gastric gastrointestinal diseases, and establishes the nature of these relationships and the implications of H. pylori eradication from a clinical perspective.
... Demographic data were acquired from reviews of medical records, phone interviews and face-to-face interviews. For each patient, the information collected included: Sex, age, initial diagnosis age, disease extent, disease activity score at diagnosis (using the CD activity index and the UC activity index) (17,18) and treatment history. For family members, the information collected included the following: Sex, age, residence, immigration status, education, occupation, marital status, smoking status, history of other autoimmune diseases, vaccination history and possession of pet animals. ...
The prevalence of inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is increasing markedly in China. The present study performed pedigree analysis of 4 families with a history of IBD and investigated the association of genetic and environmental factors with susceptibility to IBD. A total of 10 IBD patients (8 CD patients and 2 UC patients) and 90 family members were included in the present study. The clinical characteristics of familial subjects were compared with those of patients with sporadic IBD. Previously reported mutations, namely interleukin-10 receptor (IL10R)-A Thr84Ile, IL10RA Gly141Arg, IL10RB Trp159X, X-linked inhibitor of apoptosis (XIAP) Cys203Tyr, nucleotide-binding oligomerization domain-containing protein 2 (NOD2) Arg702Trp, NOD2 Gly908Arg and NOD2 Leu1007fsinsC, were screened in the patients with IBD, and selected demographic factors were compared between the patients and their unaffected family members. It was observed that single-gene and multi-gene inheritance patterns contributed to IBD in Chinese families. Based on data from the registry system, the ratio of patients with a family history of IBD was 1.25%, which was lower than that in the Western population. First-degree relatives were found to be more susceptible to IBD, and siblings were affected more frequently. Furthermore, the median age of diagnosis was younger in familial patients than in sporadic patients (29.0 vs. 36.0 for CD; 35.5 vs. 41.0 for UC). However, none of the 7 susceptibility loci were present in any of the familial patients. Immigration was a significant risk factor of IBD (odds ratio: 4.667; 95% confidence interval: 1.165-18.690; P=0.021). In conclusion, genetic heterogeneity exits between Chinese families with IBD and the Western population. The present findings suggest that genetic background and environmental factors serve a role in the pathogenesis of IBD.
Possible association has been suggested between Helicobacter pylori (H. pylori) infection and some of the lower gastrointestinal (GI) tract diseases. Previous studies have demonstrated that H. pylori infection might be associated with an increased risk of colorectal cancer/adenoma, while it seems to harbor a protective role in the development of inflammatory bowel disease. Some of them suggest possible differences in the association according to race/ethnicity. There are also a few studies on the effect of H. pylori eradication treatment on the development or aggravation of these diseases. Plausible mechanisms include both direct and indirect effects of H. pylori, such as influencing the host immune response and changing the intestinal microbiota, leading to the pathologic condition of the gut. However, the majority of the studies on this subject have the limitation of being simple epidemiologic studies, and definite proof for causal relationship or exact underlying mechanism has not been clearly demonstrated in most conditions yet. In this chapter, we will review the previous literature on the association between H. pylori infection and some lower GI tract diseases and discuss possible underlying mechanisms.
