Pathology of non-Helicobacter pylori gastritis: extending the histopathologic horizons

Lauwers, Gregory Y.; Fujita, Hiroshi; Nagata, Koji; Shimizu, Michio

doi:10.1007/s00535-009-0146-3

Cited by 35 publications

(24 citation statements)

References 111 publications

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“…Previous reports suggest that non-H. pylori gastritis is primarily present in pediatric patients or others with underlying co-morbidities such as inflammatory bowel disease, autoimmune, and genetic diseases [51]. However, our studied population mainly constituted of adult patients with no known comorbidities; therefore, it may be plausible that other factors such as fungal and viral infections, excessive intake of NSAIDs or other drugs, and immunological disorders are responsible of inducing gastritis in these patients, as previously observed in other countries [52].…”

Section: Discussionmentioning

confidence: 89%

Prevalence, diversity and disease association of Helicobacter pylori in dyspeptic patients from Pakistan

Khan

Farooqui

Raza

et al. 2013

J Infect Dev Ctries

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Introduction: The etiological association of Helicobacter pylori with gastric ulcer (GU), gastric cancer (GC), and duodenal ulcer (DU) is well-known. Understanding the epidemiology of H. pylori facilitates the estimation of disease burden in a certain population. This study presents the diversity of H. pylori genotypes and their association with different clinical outcomes among dyspeptic patients in Pakistan over a period of four years. Methodology: Gastric biopsy samples from a total of 450 dyspeptic individualswere subjected to PCR, genotypingand histology. Results: A total of 201 (45%) cases were found positive for H. pylori. The detection rate was high in GU (91%), DU (86%) and GC (83%) cases compared with those cases who had intact gastric mucosa (18%). Histology revealed the presence of infection in 68% of cases of mild/chronic nonspecific gastritis with others belonging to the GU sequel. cagA gene carriage was observed in 104 (51%) cases or mostly from DU, GU and GC groups, of which 97 were Western type strains while 3 were East-Asian type strains that are rarely observed in South Asia. vacA allelic variant s1am1 was most commonly observed, followed by s1am2, and s1bm1, with direct correlation in diseased cases (gastritis, GU, DU and GC). Prevalent genotypic combinations were s1am1/cagA -in gastritis and s1am1/cagA + in DU, GU, and GC. Conclusions: Our study indicates the predominant circulation of Western type cagA and vacAs1am1 type H. pylori strains in Pakistan.

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Section: Discussionmentioning

confidence: 89%

Prevalence, diversity and disease association of Helicobacter pylori in dyspeptic patients from Pakistan

Khan

Farooqui

Raza

et al. 2013

J Infect Dev Ctries

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“…As a matter of fact, glandular atrophy as a result of chronic H. pylori ‐induced gastritis leads to reduced acid production and shifts in gastric pH value, which may facilitate the colonization of the gastric mucosa by other bacteria, viruses or even fungi . Further conditions leading to increased gastric pH are immunomodulated atrophic gastritis or acid suppressive therapy such as long‐term treatment with proton pump inhibitors (PPIs) . It has been hypothesized that bacterial N ‐nitrosation is increased and further contributes to carcinogenesis in the stomach .…”

Section: H Pylori and Its Pathophysiological Role In Upper Gastrointmentioning

confidence: 99%

H. pylori and its modulation of gastrointestinal microbiota

Schulz

Koch

Schütte

et al. 2015

J of Digest Diseases

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The discovery of Helicobacter pylori (H. pylori) changed the dogma of the stomach as a sterile organ. H. pylori is an obligate pathogen in the human stomach and recognized as a definite carcinogen. Extensive research on the interaction of this bacterium with the gastric mucosa has been performed over the past three decades. The development of new nucleotide sequencing techniques and new biocomputational tools has opened the field for studying the diversity and complexity of the microbiome in the gastrointestinal tract independently of cultural methods. These techniques allow to better characterize further gastric bacteria. However, the differentiation of alive resident and transient microbes requires an analysis beyond the pure detection of bacterial genomic material applying a combination with metabolomic analyses. Currently, the interaction of gastric microbiota with each other, with H. pylori and with the host is addressed by extensive research. This review gives a concise overview on current knowledge on this topic.

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“…Most importantly, studies with cohort design did not detect significant association between PGII and OSCC risk. In addition, cancer patients may develop gastritis due to non-steroidal anti-inflammatory drug (NSAID) use, opportunistic infections in stomach (cytomegalovirus, Epstein–Barr virus), malnutrition, anaemia, and consequent use of iron tablets (Abraham et al , 1999; Lauwers et al , 2010). Stage of tumours in most of our study population were III or IV at the time of diagnosis, and dysphagia was the presenting symptom, which led to high proportion of NSAID consumption among cases compared with controls (24.7% vs 15.8%, P =0.001).…”

Section: Discussionmentioning

confidence: 99%

Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

et al. 2012

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Background:Gastric fundal atrophy has been hypothesised to increase the risk of oesophageal squamous cell carcinoma (OSCC), but studies have shown inconsistent results.Methods:We measured serum pepsinogen I (PGI) and pepsinogen II (PGII) among 293 incident cases and 524 matched neighbourhood controls in a high-risk area of Northern Iran. Conditional logistic regression model was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs).Results:After controlling for age, sex, residence area and other potential confounders, gastric atrophy (defined by a validated criterion, PGI <55 μg dl−1) was associated with a two-fold increased risk (OR=2.01, 95% CI: 1.18, 3.45) of OSCC in the absence of nonatrophic pangastritis (defined as PGII <11.8 μg dl−1). Stratification by PGII decreased the misclassification errors due to cancer-induced gastritis. Presence of both poor dental health, indicated by higher than median sum of decayed, missing, and filled teeth (DMFT score), and gastric atrophy further increased the risk of OSCC (OR=4.15, 95% CI: 2.04, 8.42) with relative excess risk due to interaction (RERI) of 1.47 (95% CI: −1.15, 4.1). Coexistence of poor oral hygiene habit with gastric atrophy elevated OSCC risk eight times (OR=8.65, 95% CI: 3.65, 20.46) and the additive interaction index was marginally statistically significant (RERI=4.34, 95% CI: −1.07, 9.76).Conclusion:Gastric atrophy is a risk factor for OSCC, and poor dental health and oral hygiene habit may act synergistically in increasing the risk.

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Pathology of non-Helicobacter pylori gastritis: extending the histopathologic horizons

Cited by 35 publications

References 111 publications

Prevalence, diversity and disease association of Helicobacter pylori in dyspeptic patients from Pakistan

Prevalence, diversity and disease association of Helicobacter pylori in dyspeptic patients from Pakistan

H. pylori and its modulation of gastrointestinal microbiota

Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

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