Association between Helicobacter pylori and its eradication and the development of cancer
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SUBMITTER: Loosen S
PROVIDER: S-EPMC11344509 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:Aims/introductionIt is suspected that Helicobacter pylori is associated with extradigestive diseases including diabetes. So far, a number of studies have examined the association between H. pylori and diabetes, and the results were conflicting. The aim of the present study was to examine the association between H. pylori infection, eradication and diabetes.Materials and methodsThe present cross-sectional study was carried out using data from annual health checkups carried out at the Toranomon Hospital Health Management Center. The status of H. pylori infection, determined by serum antibodies and history of eradication, was categorized into three groups as "never," "current" and "past." The association between H. pylori infection and diabetes was examined using logistic regression.ResultsOf 21,634 participants, 6,530 (30.2%) had a current or past history of H. pylori infection, and 1,184 (5.5%) were identified as having diabetes. Multivariate adjusted odds ratios for diabetes compared with the "never" group were 1.36 (95% confidence interval 1.10-1.67) for the "current" group and 0.92 (95% confidence interval 0.79-1.07) for the "past" group. The association between H. pylori infection and diabetes was also observed among participants without a history of eradication.ConclusionsWe found that current H. pylori infection was associated with an increased risk of diabetes, and the increased risk was not observed among participants after eradication. The results were concordant with the hypothesis that H. pylori infection increases the risk of diabetes. Further studies are necessary to validate the present results.
| S-EPMC6717903 | biostudies-literature
Project description:The evidences on the association of Helicobacter pylori (H. pylori) to coronary heart diseases (CHD) are conflicting. In order to answer this important but yet unanswered clinical health issue, a large cohort study such as big data from the Taiwan National Health Insurance Research Database should be more convincing. Therefore, we aimed to make use of these big data source to analyze and clarify the relevance of H. pylori eradication and CHD risks. We looked through a total of 208196 patients with peptic ulcer diseases (PUD) from the years of 2000 to 2011. First, 3713 patients who received H. pylori eradication within 365 days of the index date were defined as the group A. We randomly selected the same number of patients as cohort A from 55249 non-eradication patients to be the comparison group B using propensity scores (including age, gender and comorbidity) so that we could control the confounding variables of CHD and mortality. Importantly, we perform sensitivity analysis for the time-dependent association between H. pylori eradication and risk of CHD, interactions between patient demographic characteristics and therapy by age (≥ or < 65 years old). The results showed that a trend of decreased association of CHD in patients with early eradication was observed compared to those without eradication (2.58% vs. 3.35%, p = 0.0905). The mortality rate was lower in early eradication subgroup compared to cohort B (2.86% vs. 4.43%, p = 0.0033). Interestingly, there was also significant difference observed in composite end-points for CHD and death in the early eradication subgroup (0.16% vs.0.57%, p = 0.0133). Further, the cumulative CHD rate was significantly lower in younger patients (< 65 years old) with H. pylori eradication therapy started < 1 year compared to those patients without eradication at all (p = 0.0384); the treatment did not appear to have an effect in older patients (≥ 65 years old) (p = 0.1963). Multivariate analysis showed that hypertension and renal diseases were risk factors for CHD in patients without eradication whilst younger age (< 65 years old) initiated with H. pylori therapy was a protective factor. In conclusion, the trend of decrease in CHD occurrence after early H. pylori eradication in addition to the significant decrease in composite end points for CHD and death, the significantly lower cumulative CHD rate in younger patients < 65 years old with H. pylori treated within 365 days suggested that there was positive association between H. pylori eradication and CHD.
| S-EPMC5749777 | biostudies-literature
Project description:Background and aimNodular gastritis is caused by Helicobacter pylori infection and is associated with the development of diffuse-type gastric cancer. This study examined the clinical characteristics of patients with nodular gastritis, including cancer incidence before and after H. pylori eradication.MethodsThis was a retrospective study of patients who underwent upper endoscopy and were positive for H. pylori infection. We examined the clinical findings and follow-up data after H. pylori eradication in patients with and without nodular gastritis.ResultsOf the 674 patients with H. pylori infections, nodular gastritis was observed in 114 (17%). It was more prevalent in women (69%) and young adults. Among patients with nodular gastritis, six (5%) had gastric cancer, all of which were of the diffuse type. Among the 19 (4%) patients with gastric cancer and no nodular gastritis, 16 had intestinal-type cancer. White spot aggregates in the corpus, a specific finding in patients with nodular gastritis, were more frequently observed in patients with gastric cancer than in those without (83% vs 26%, P = 0.0025). Of 82 patients with nodular gastritis who had H. pylori eradicated successfully, none developed gastric cancer over a 3-year follow-up period, while 7 (3%) of 220 patients without nodular gastritis developed gastric cancer after H. pylori eradication.ConclusionsIn patients with nodular gastritis, white spot aggregates in the corpus may indicate a higher risk of developing diffuse-type gastric cancer. Nodular gastritis may be an indication for eradication therapy to reduce the risk of cancer development after H. pylori eradication.
| S-EPMC6207053 | biostudies-literature
Project description:BackgroundPancreatic cancer is one of the most troublesome malignancies with dismal prognosis. H. pylori has been recognized as a type I carcinogen. Several studies have evaluated the association between H. pylori infection and pancreatic cancer development, however, the conclusions are inconsistent.MethodsLiterature search was carried out in PubMed, EMBASE, Cochrane Library and CNKI databases to identify eligible researches. We performed overall meta-analysis of all studies included and subgroup analysis based on regional distribution. Quality of the studies (assessed by Newcastle-Ottawa quality assessment scale for case-control studies) and CagA+ strains of H. pylori were taken into consideration, and we conducted additional analyses including high-quality researches and those concerning CagA+ H. pylori respectively.Results9 studies involving 3033 subjects (1083 pancreatic cancer cases, 1950 controls) were included. Summary OR and 95%CI of the overall meta-analysis of all included studies were 1.47 and 1.22-1.77, pooled data of the 4 high-quality studies were OR 1.28, 95%CI 1.01-1.63. OR of the 5 studies examined CagA+ strains was 1.42, corresponding 95%CI was 0.79 to 2.57. Summary estimates of subgroup analysis based on regional distribution are as follows, Europe group: OR 1.56, 95%CI 1.15-2.10; East Asia group: OR 2.01, 95%CI 1.33-3.02; North America group: OR 1.17, 95%CI 0.87-1.58. There was not obvious heterogeneity across the 9 studies. No publication bias was detected.ConclusionH. pylori infection is significantly, albeit weakly, associated with pancreatic cancer development. The association is prominent in Europe and East Asia, but not in North America. CagA+ H. pylori strains appear not to be associated with pancreatic cancer. However, more studies, especially prospective studies, are needed to validate our results.
| S-EPMC3784458 | biostudies-literature
Project description:BackgroundThe effect of H. pylori eradication in gastric cancer prevention can be attributed to the improvement of atrophic gastritis, which is a known risk of gastric cancer. However, gastric cancer has also been diagnosed after long-term H. pylori eradication. This study aimed to clarify the association between gastric atrophy and gastric cancer after H. pylori eradication, including its clinicopathological features.MethodsA total of 55 consecutive patients with 64 early gastric cancers (EGCs) diagnosed after H. pylori eradication were enrolled. The degree of endoscopic atrophy and the histological degrees of mononuclear cell infiltration, atrophy, and metaplasia in the corpus and adjacent mucosa of the EGCs were determined and scored.ResultsThe majority of EGCs (63/64) were located within the endoscopically assessed atrophic mucosa or along the atrophic border. The adjacent mucosa of the EGCs presented significantly higher degrees of all histological parameters than in the corpus (mononuclear cell infiltration, 0.86+/-0.09 vs. 0.51+/-0.11, P = 0.016; atrophy, 1.77+/-0.13 vs. 0.65+/-0.14, P<0.0001; metaplasia, 1.68+/-0.13 vs. 0.48+/-0.1, P<0.0001). The degree of endoscopic atrophy improved in the patients with longer post-H. pylori eradication periods; however, this trend was not observed for the histological parameters, and high degrees of atrophy and metaplasia were observed in the adjacent mucosa of the EGCs compared with the corpus during all periods (all P<0.05). The histological degrees of atrophy and metaplasia in the adjacent mucosa were particularly higher in the patients who underwent eradication due to gastric ulcers.ConclusionsSevere gastric atrophy remained in the adjacent mucosa of the EGCs after H. pylori eradication, which may be linked to gastric carcinogenesis.
| S-EPMC5051933 | biostudies-literature
Project description:BackgroundH. pylori virulence factors, especially vacA and cagA are important in gastroduodenal disease pathogenesis and affect cure rates. This meta-analysis aimed to clarify the association between vacA or cagA status and eradication outcome of H. pylori infection.MethodsA literature search was performed using electronic databases to identify studies. Twenty-six prospective studies were determined eligible. Meta-analytical techniques were conducted to calculate eradication rates and pooled relative ratios (RR).ResultsThe eradication rate was greater approximately 10% in vacA s1 compared with vacA s2 infected patients, and the pooled RR was 1.164 (95%CI: 1.040-1.303, P = 0.008). A significant association existed between vacA s1 and higher eradication rates in Europe (RR: 1.203, 95%CI: 1.003-1.442, P = 0.046) and Asia (RR: 1.187, 95%CI: 1.028-1.371, P = 0.020), in triple therapy patients (RR: 1.175, 95%CI: 1.012-1.365, P = 0.035). Eradication rates were similar for vacA m1 and m2 genotypes (RR: 0.981, 95%CI: 0.891-1.080, P = 0.690), whereas they were higher by approximately 8% in cagA-positive compared with cagA-negative infected patients, with a pooled RR of 1.094 (95%CI: 1.025-1.168, P = 0.007). A significant association existed between cagA-positive and increased eradication rates in Europe (RR: 1.138, 95%CI: 1.000-1.295, P = 0.049) and Asia (RR: 1.118, 95%CI: 1.051-1.190, P<0.001), in using PCR (RR: 1.232, 95%CI: 1.142-1.329, P<0.001) and protein chips (RR: 1.200, 95%CI: 1.060-1.359, P = 0.004), in triple therapy patients (RR: 1.090, 95%CI: 1.006-1.181, P = 0.034).ConclusionsEvidence indicates that infection with vacA s1, cagA-positive strains, but not vacA s2, cagA-negative, is more conducive to H. pylori eradication.
| S-EPMC5426689 | biostudies-literature
Project description:Background: Penicillins inhibit cell wall synthesis; therefore, H. pylori must be dividing for these antibiotics to be effective. Identifying growth responses to varying medium pH may allow design of more effective treatment regimens. Aim: To determine the effect of acidity on bacterial growth and the bactericidal efficacy of ampicillin. Methods: H. pylori were incubated in dialysis chambers suspended in 1.5L of media at various pHs with 5mM urea, with or without ampicillin, for 4, 8 or 16 hours, thus mimicking unbuffered gastric juice. Changes in gene expression, viability and survival were determined. The bacterial load of H. pylori infected gerbils was determined with and without profound acid inhibition. Results: At pH 3.0, but not at pH 4.5 or 7.4, there was decreased expression of ~400 genes, including many cell envelope biosynthesis, cell division genes and penicillin-binding proteins. In the presence of ampicillin, viability and survival declined at pH 4.5 and 7.4 but not at pH 3.0. Profound acid inhibition of H. pylori infected gerbils increased the antral bacterial load >3 fold, showing that elevation of intragastric pH stimulated growth. Conclusions: Ampicillin is bactericidal at pH 4.5 and 7.4, but not at pH 3.0, due to decreased expression of cell envelope and division genes at pH 3.0. Therefore, at pH 3.0, the pH at the gastric surface, the bacteria are non-dividing and persist with ampicillin treatment. A more effective inhibitor of acid secretion that maintains gastric pH near neutrality for 24 hours/day should enhance the efficacy of triple therapy and of amoxicillin, even allowing dual therapy for H. pylori eradication.
2012-09-30 | GSE39512 | GEO
Project description:Helicobacter pylori (HP) is a common infection of the gastrointestinal system that is usually related to peptic ulcers. However, recent studies have revealed relationships between HP and many other diseases. Although the exact mechanism is unknown, HP can prevent the absorption of certain drugs. A high prevalence of HP has been found in patients with Parkinson's disease, and this bacterium causes motor fluctuations by affecting the absorption of levodopa, which is the main drug used to treat Parkinson's disease. Eradicating HP from patients with Parkinson's disease by applying antibiotic treatment will increase the absorption of levodopa and decrease their motor fluctuations.
| S-EPMC4828559 | biostudies-other
Project description:Background/aimsAlthough undifferentiated gastric cancer (UGC) diagnosed after Helicobacter pylori eradication (HPE) carries a poor prognosis, characteristics of post-HPE UGC have not been evaluated in detail because of its low incidence. Therefore, we compared the clinicopathologic characteristics of UGC and differentiated gastric cancers (DGC) diagnosed after successful HPE.MethodsGC lesions from patients who had successfully completed HPE and who had undergone upper gastrointestinal endoscopy between January 2004 and March 2016 were analyzed. Tumors were divided into DGC and UGC groups. Clinicopathologic factors of background and tumor characteristics were compared using univariate and multiple logistic analyses.ResultsA total of 129 tumors from 115 patients were evaluated; 113 tumors were in the DGC group and 16 in the UGC group. Depressed-type tumors (P = 0.024) and sub-submucosal invasion (P<0.001) were significantly higher in the UGC group. The UGC group had larger tumor diameters (25.9±7.3 mm) than the DGC group (13.2±10.2 mm) (P<0.001). Multivariate analysis showed that female sex (odds ratio [OR] 3.24, 95%CI:1.02-10.37; P = 0.047) and absent follow-up (OR 4.99, 95%CI:1.60-15.57; P = 0.006) were significant independent risk factors for UGC. The DGC group showed a gradually decreasing temporal trend by trend test (P = 0.015), while the UGC group showed a relatively constant incidence over time, although the number of cases was small.ConclusionUGC was diagnosed even after long time spans following HPE, although the number of cases was small. Female sex, and especially absent follow-up, were risks for post-HPE UGC, suggesting that diligent long-term follow-up after HPE is essential.
| S-EPMC10065271 | biostudies-literature
Project description:It is difficult to confirm the accurate cutoff value to diagnose Helicobacter pylori (Hp) infection using commercial serology kits. It is reported that there were many cases with present/past infection that even the serum Hp-IgG antibody (HpAb) titers were below the cutoff value (e.g., 10 U/mL for E-Plate®), suggesting that we might overlook many gastric cancer (GC). We investigated an association between gastric cancer risk and serum Helicobacter pylori antibody titers.We conducted a primary screening between 2014 and 2015. We performed gastroendoscopy if HpAb titers were ≥3.0 U/mL (i.e., more than measurable limit, E-Plate). These patients were divided into two groups: HpAb = 3.0-9.9 U/mL ("negative-high" group) and HpAb ≥ 10 U/mL; cutoff value ("over-10 U/mL" group). Hp infection status was investigated, and the number of GC patients was counted.Among the 3321 subjects in the primary screening, 56.9% (1891/3321) showed HpAb titers ≥3.0 U/mL; 1314 patients underwent gastroendoscopy. Ten were GC. 421 patients were "negative-high" group; two were GC. After evaluating 381 patients for Hp infection, 22.6%/60.6% was with present/past infection among the "negative-high" group.We also found a correlation between HpAb titers and Hp infection status. "Negative-high" group has a risk of GC.
| S-EPMC5485312 | biostudies-other