scholarly journals Helicobacter pylori cagA Status and Gastric Mucosa-associated Lymphoid Tissue Lymphoma: a Systematic Review and Meta-analysis

2021 ◽  
Author(s):  
Mohsen Karbaalei ◽  
Amirhossein Sahebkar ◽  
Yoshio Yamaoka ◽  
Masoud Keikha
Keyword(s):  
Systematic Review ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Lymphoid Tissue ◽  
Meta Analysis ◽  
Publication Date ◽  
Inverse Association ◽  
High Grade ◽  
H Pylori

Abstract Background: Recent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is estimated that approximately 0.1% of people infected with H. pylori develop gastric MALT. However, the role of the CagA antigen, the highest causative agent of H. pylori, in increasing the risk of gastric MALT remains unclear and controversial. A systematic review and meta-analysis were conducted to evaluate the effect of cagA status on the development of gastric MALT.Methods: All articles evaluating the status of the cagA gene in the development of gastric MALT were collected using systematic searches in online databases, including PubMed, Scopus, Embase, and Google Scholar, regardless of publication date. The association between cagA and gastric MALT was assessed using the odds ratio (OR) summary. In addition, a random-effects model was used in cases with significant heterogeneity.Results: A total of 10 studies met our inclusion criteria, among which 1,860 patients participated. We observed a meaningful association between cagA status and gastric MALT, especially in Western countries (OR: 1.30; 0.90–1.87 with 95% CIs). However, the heterogeneity was significant; therefore, the results should be interpreted with caution. Surprisingly, a strong positive association was observed between cagA status and high-grade lymphomas (OR: 6.43; 2.45–16.84 with 95% CIs). In addition, no study has evaluated the correlation between cagA and vacA, but we observed an inverse association between vacA and gastric MALT risk (OR: 0.92; 0.57–1.50 with 95% CIs). Conclusion: CagA may not play a significant role in the early stages of gastric MALT, but it can be translocated to B cells and affect the development of high-grade lymphomas.

Nuclear Expression of BCL10 or Nuclear Factor Kappa B Predicts Helicobacter pylori–Independent Status of Early-Stage, High-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphomas

2004 ◽  
Vol 22 (17) ◽  
pp. 3491-3497 ◽  
Author(s):  
Sung-Hsin Kuo ◽  
Li-Tzong Chen ◽  
Kun-Huei Yeh ◽  
Ming-Shiang Wu ◽  
Hui-Chen Hsu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Lymphoid Tissue ◽  
Nuclear Factor Kappa B ◽  
Early Stage ◽  
Gastric Malt Lymphoma ◽  
Nuclear Factor ◽  
High Grade ◽  
Nuclear Expression ◽  
H Pylori

Purpose A high percentage of early-stage, high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas remain Helicobacter pylori dependent. t(11;18)(q21;q21), a genetic aberration highly predictive of H pylori–independent status in low-grade gastric MALT lymphoma, is rarely detected in its high-grade counterpart. This study examined whether nuclear expression of BCL10 or nuclear factor kappa B (NF-κB) is useful in predicting H pylori–independent status in patients with stage IE high-grade gastric MALT lymphomas. Patients and Methods Twenty-two patients who had participated in a prospective study of H pylori eradication for stage IE high-grade gastric MALT lymphomas were studied. The expression of BCL10 and NF-κB in pretreatment paraffin-embedded lymphoma tissues was evaluated by immunohistochemistry and confocal immunofluorescence microscopy. The presence of t(11;18)(q21;q21) was identified by a multiplex reverse transcriptase polymerase chain reaction of the API2-MALT1 chimeric transcript. Results Aberrant nuclear expression of BCL10 was detected in seven (87.5%) of eight H pylori–independent and in none of 14 H pylori–dependent high-grade gastric MALT lymphomas (P < .001). All seven patients with nuclear BCL10 expression had nuclear expression of NF-κB, compared with only two of 15 patients without nuclear BCL10 expression (P = .002). As a single variable, the frequency of nuclear expression of NF-κB was also significantly higher in H pylori–independent tumors than in H pylori–dependent tumors (seven of eight [87.5%] v two of 15 [12.3%]; P = .002). The API2-MALT1 fusion transcript was detected in only one (12.5%) of eight H pylori–independent lymphomas. Conclusion Nuclear expression of BCL10 or NF-κB is highly predictive of H pylori–independent status in high-grade gastric MALT lymphoma, and coexpression of these two markers in the nuclei is frequent.

scholarly journals Two-Way Relationship Between Helicobacter Pylori Infection and Periodontitis: Results from A Systematic Review and Meta-Analysis

2020 ◽  
pp. 1-7
Author(s):  
Felipe Rodolfo ◽  
Silvania Conceição Furtado ◽  
Alessandro Luiz Araújo Bentes Leal ◽  
Any Carolina Cardoso Guimarães Vasconcelos ◽  
Daniel Fernando Pereira Vasconcelos ◽  
...  
Keyword(s):  
Systematic Review ◽  
Helicobacter Pylori ◽  
Meta Analysis ◽  
Current Systematic Review ◽  
Increased Risk ◽  
Statistical Program ◽  
H Pylori ◽  
Ci Calculations ◽  
Review Manager

Aim: Helicobacter pylori (H. pylori) infection and periodontitis have considerable worldwide prevalence once they both present systemic alterations with a possible association between them. Therefore, we have performed this meta-analysis to assess the possible association between H. pylori infection and periodontitis. Material and Methods: A systematic search in the literature was performed for studies published before December 2, 2019 in diverse scientific and educational databases. The data was extracted by two investigators and the statistical analysis was performed by Review Manager statistical program with heterogeneity and Odds Ratio (OR) with 95% of Confidence Intervals (CI) calculations as well as a sensitive analysis to assess the accuracy of the results. The value of P<0.05 was considered as significant. In addition, we performed the analysis of the quality of included studies as well as the evaluation for risk of bias. Results: In overall analysis, H. pylori infection was associated with the risk of periodontitis development (OR = 1.72, CI: 1.47, 2.02, P<0.00001) and the periodontitis was considered as a risk factor for H. pylori infection (OR = 3.21, CI: 2.31, 4.47, P<0.00001). Moreover, the evaluation of dental plaque from patients with periodontitis reveled increased risk of H. pylori infection (OR = 3.46, CI: 2.39, 5.01, P<0.00001). Conclusions: This current systematic review and meta-analysis composed by 12 studies in 7,059 participants showed that H. pylori infection increased significantly the risk of the development of periodontitis and the periodontitis may be a risk for this bacterial infection.

scholarly journals Association of Helicobacter pylori Infection with the Risk of Metabolic Syndrome and Insulin Resistance: An Updated Systematic Review and Meta-Analysis

2021 ◽  
Author(s):  
Mobin Azami ◽  
Hamid Reza Baradaran ◽  
Parisa Kohnepoushi ◽  
Lotfolah Saed ◽  
Asra Moradkhani ◽  
...  
Keyword(s):  
Systematic Review ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Helicobacter Pylori ◽  
Cohort Studies ◽  
Odds Ratio ◽  
Meta Analysis ◽  
Case Control ◽  
Case Control Studies ◽  
H Pylori

Abstract Background Conflicting results of recent studies on the association between Helicobacter pylori (H. pylori) infection and the risk of insulin resistance and metabolic syndrome explored the need for updated meta-analysis on this issue. Therefore, this systematic review aimed to estimate the pooled effect of H. pylori infection on the risk of insulin resistance and metabolic syndrome. Methods To identify case-control studies and cohort studies evaluating the association of H. pylori infection with insulin resistance and metabolic syndrome, a comprehensive literature search was performed from international databases including Medline (PubMed), Web of Sciences, Scopus, EMBASE, and CINHAL from January 1990 until January 2021. We used odds ratio with its 95% confidence interval (95%CI) to quantify the effect of case-control studies and risk ratio with its 95%CI for the effect of cohort studies. Results 22 studies with 206911 participants were included for meta-analysis. The pooled estimate of odds ratio between H. pylori infection and metabolic syndrome in case-control studies was 1.19 (95%CI: 1.05, 1.35; I2 = 0%), and in cohort studies, the pooled risk ratio was 1.31 (95%CI: 1.13, 1.51; I2 = 0%). Besides, case-control studies showed the pooled odds ratio of 1.54 (95%CI: 1.19, 1.98; I2 = 6.88%) for the association between H. pylori infection and insulin resistance. Conclusion A positive association was found between H. pylori infection and insulin resistance as well as metabolic syndrome, so planning to eliminate or eradicate H. pylori infection could be an effective solution to improve metabolic syndrome or insulin resistance, and vice versa.

scholarly journals Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

2021 ◽  
Author(s):  
Ghorbanali Rahimian ◽  
Milad Shahini Shams Abadi ◽  
Reza Ahmadi ◽  
Mohammedhadi Shafigh ◽  
Fatemeh Azadegan-Dehkordi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Treg Cells ◽  
Infected Group ◽  
Ulcer Disease ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

scholarly journals Helicobacter pylori infection and inflammatory bowel diseases

2021 ◽  
Vol 11 (1) ◽  
pp. 68-78
Author(s):  
Yu. P. Uspenskiy ◽  
N. V. Baryshnikova ◽  
A. N. Suvorov ◽  
A. V. Svarval
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Inflammatory Bowel Diseases ◽  
Pathogenic Bacteria ◽  
T Cell Response ◽  
Aminosalicylic Acid ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
H Pylori

Helicobacter pylori is detected in the human intestine on average in 35% of clinical cases, but the question about its etiopathogenetic role in intestinal diseases has not been fully investigated. Many scientists study a relationship between the H. pylori persistence and development of various bowel diseases. Diverse viewpoints have been proposed regarding a potential link between H. pylori and inflammatory bowel diseases (IBD). Here we review the data from domestic and foreign studies aimed at examining potential role of H. pylori both as a trigger and protector resulting in the pathogenetic alterations leading to developing Crohn‘s disease and ulcerative colitis. The former is favored by the hypothesis wherein H. pylori may trigger IBD due to potential connection between extragastric infection and its direct damaging action as well as indirect effects contributing to the initiation of oxidative stress, autoimmune aggression and development of intestinal dysbiosis. In addition, the effects of enterohepatic Helicobacter spp. promoting IBD pathogenesis are discussed. The mechanisms underlying the protective role of H. pylori infection may be driven via differentially expressed acute and/or chronic local inflammatory mucosal response able to downmodulate systemic immune responses and suppress autoimmune reactions, as well as skewing host immune response from a pro-inflammatory Th1/Th17 cell-mediated towards regulatory T-cell response. Moreover, it was found that H. pylori may induce production of antibacterial peptides counteracting potentially pathogenic bacteria involved in IBD pathogenesis. In particular, it was found that IBD patients are dominated with moderate active antral gastritis coupled to atrophy, with the peak intensity observed in patients under 30 years of age. Intensity of intestinal metaplasia in the gastric mucosa of IBD patients accounted for by the duration of the disease course. Basal IBD therapy with 5-aminosalicylic acid lowers severity and activity of gastritis, degree of atrophy as well as magnitude H. pylori invasion in the gastric mucosa. There is evidence that 5-aminosalicylic acid-containing drugs may result in a so-called “spontaneous eradication” of H. pylori infection. Extended investigations are required to examine a role of H. pylori in IBD pathogenesis.

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