scholarly journals Helicobacter Pylori as a Promoter of Accelerated Regeneration, Pathological Differentiation and Transformation of Normal Gastric Mucosa into Cancerous Type

2006 ◽  
Vol 6 (3) ◽  
pp. 57-60
Author(s):  
Zora Vukobrat-Bijedić ◽  
Svjetlana Radović ◽  
Azra Husić-Selimović ◽  
Srđan Gornjaković
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Gastric Carcinoma ◽  
Chronic Atrophic Gastritis ◽  
Epithelial Dysplasia ◽  
Control Group ◽  
Tumor Lesion ◽  
Pathological Differentiation ◽  
H Pylori ◽  
Lesser Curvature

The aim of the study was to ascertain presence of Helicobacter pylori in gastric carcinoma as a responsible promoter of inflammatory-regenerative changes, which lead to pathological differentiation and transformation of normal epithelial cells into intestinal type and, in progression, cause epithelial dysplasia that develops into early gastric carcinoma. The paper presents prospective study that includes clinical, pathohistological and microbiological aspects of carcinogenesis initiation in gastric mucosa. The subjects are patients treated at Gastroenterohepatology Clinic divided into two groups. One group included 50 patients with gastric carcinoma while the control group included 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to endoscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the region 1-2 cm removed from tumor lesion. We used HUT test to verify H. pylori presence in biopsy samples. We analyzed the samples for presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in gastric mucosa and evaluated their meaning for the prognosis. Our study confirmed Helicobaster pylori responsibility for inflammatory events in gastric mucosa in patients with gastric carcinoma. Slight and mild epithelial dysplasia with chronic atrophic gastritis grade I and II coupled with intestinal metaplasia may be considered an indicator for early detection of carcinoma. Such patients represent risk group for gastric carcinoma development.

scholarly journals Incomplete Intestinal Metaplasia as an Indicator for Early Detection of Gastric Carcinoma in The Events of Helicobacter Pylori Positive Chronic Atrophic Gastritis

2006 ◽  
Vol 6 (4) ◽  
pp. 48-53 ◽  
Author(s):  
Zora Vukobrat-Bijedić ◽  
Svjetlana Radović ◽  
Azra Husić-Selimović ◽  
Srđan Gornjaković
Keyword(s):  
Gastric Mucosa ◽  
Gastric Carcinoma ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Risk Group ◽  
Precancerous Lesion ◽  
Chronic Atrophic Gastritis ◽  
Tumor Lesion ◽  
H Pylori ◽  
Lesser Curvature

The aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. The paper presents prospective study that included 50 patients with gastric carcinoma and 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area 1-2 cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. This study confirmed responsibility of H. pylori for inflammatory events in gastric mucosa in patients with gastriccarcinoma. According to our findings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastriccarcinoma and is associated with chronic atrophic gastritis grade I and II (92% of subjects, p=0.0097, h=1, p=0.01). Thus, the finding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologically verified incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.

scholarly journals Association of Helicobacter pylori infection and stomach cancer: our experience

2018 ◽  
Vol 5 (8) ◽  
pp. 2794
Author(s):  
N. G. Javan ◽  
Wormi Sharon
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Carcinoma ◽  
Stomach Cancer ◽  
Histopathological Examination ◽  
Chronic Atrophic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Future Research ◽  
Gastric Cancer Prevention ◽  
H Pylori

Background: Infection with Helicobacter pylori (H. pylori) has been linked with chronic atrophic gastritis, an inflammatory precursor of gastric adenocarcinoma. There are data on the epidemiology, pathophysiology, and histology of this disease that show that Helicobacter pylori gastritis has an important role in gastric carcinogenesis. However, it has to be considered that only very few of those infected with Helicobacter pylori will develop gastric cancer. Hence, it will be a major target of future research to identify individuals who carry a greater risk for developing gastric cancer, and therefore may benefit from eradication of Helicobacter pylori in terms of gastric cancer prevention. Various studies revealed that approximately more than 50% of the world’s human population is infected by Helicobacter pylori. In underdeveloped countries, this association is shown to be much higher according to different studies.Methods: This study was conducted over a period of 36 months from 1st January 2014 till December 31st, 2016. All patients who underwent Gastrectomy during this period were taken. All specimens were investigated to see presence of helicobacter pylori by histological examination. A total of 50 Gastrectomy was performed by one surgical team over 36-month period.Results: Out of 50 patients, Helicobacter pylori positivity was seen in 33 (66%) cases by histopathological examination (HPE). Gastric cancer is more prevalent among males 31 (62%) as compared to 19 (38%) in females. It is more common among the older age group.Conclusions: Helicobacter pylori infection is higher in prevalence in cases of stomach cancer. Present study also showed that there is significant association of Helicobacter pylori infection with gastric carcinoma. Helicobacter pylori infection could be one of the etiological factors for gastric carcinoma.

scholarly journals Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

2016 ◽  
Vol 2 (3) ◽  
pp. 173
Author(s):  
Sergii Vernygorodskyi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Gastric Epithelium ◽  
Number Of Genes ◽  
Activating Transcription Factor ◽  
H Pylori ◽  
Gene Inhibition

<p class="BodyText1"><em>Helicobacter pylori</em> (<em>H. pylori</em>) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). <em>H. pylori</em> infection persistence leads to the formation of gastrointestinal phenotype of IM. <em>H. pylori</em> can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to <em>MUC5AC</em> gene inhibition and <em>MUC2</em> gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of <em>H. pylori</em> in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (<em>e.g.</em>, <em>SHH</em>, <em>SOX2</em>, and <em>RUNX3</em>) responsible for gastric differentiation, was identified to cause the appearance of IM. </p>

scholarly journals Protective Effect of Zuojin Pill on Helicobacter Pylori-Induced chronic atrophic gastritis in Rats and GES-1 Cells and Mechanisms of Action Exploration

2020 ◽  
Author(s):  
Shihua Wu ◽  
Chunmei Bao ◽  
Ruilin Wang ◽  
Jianzhong Zhang ◽  
Juling Zhang ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Protein Expression ◽  
Cell Viability ◽  
Atrophic Gastritis ◽  
Therapeutic Effect ◽  
Chronic Atrophic Gastritis ◽  
Expression Level ◽  
Cox 2 ◽  
H Pylori

Abstract Objective Zuojin Pill (ZJP) containing two Chinese herbal drugs: Coptidis Rhizoma and Euodiae Fructus is a classical formula and is widely accepted as a treatment of chronic atrophic gastritis (CAG) in China. This study aimed to explore the therapeutic effect and mechanism of ZJP which attenuated H. pylori -induced CAG in vivo and in vitro.Methods: H. pylori (Helicobacter pylori) was used to induce CAG rat model. 0.63, 1.26, and 2.52 g/kg of ZJP (was administered orally for four weeks. Therapeutic effect of ZJP was identified by H & E staining and serum indices. In addition, cell viability, morphology and proliferation were detected by cell counting kit-8 and high-content screening assay. Gene and protein expression related to JMJD2B/COX-2/VEGF axis were detected to further investigate the potential mechanism.Results Compared with the control group, the ZJP groups showed a significant protection effects on Gastric mucosa, as indicated by the reduced loss of glands and inflammatory cell infiltration. Meanwhile, ZJP could ameliorate cell viability, morphology changes, and proliferation in GES-1 cells. Moreover, the ZJP treatment decreased the amount of IL-8, and TNF-α, indicating that it could reduce the level of inflammation, and decrease stomach damage. The expression of JMJD2B/COX-2/VEGF axis related genes and proteins were measured by real-time quantitative PCR, western blot and immunohistochemistry methods. The ZJP groups were found to decrease relative genes and protein expression level compared with the model group. ZJP could improve gastric mucosa protection and reduce inflammation level by inhibiting the expression level of JMJD2B/COX-2/VEGF axis.Conclusion Our data confirmed the effective therapy of ZJP in H. pylori -induced CAG, which supports the role of ZJP as an anti-inflammatory and protection of gastric mucosa agent in CAG induced by H. pylori . These results may provide helpful tools for the treatment of CAG.

scholarly journals Influence of Helicobacter pylori on cytokine regulation in chronic atrophic gastritis

2020 ◽  
Vol 10 (1) ◽  
pp. 187-192
Author(s):  
O. V. Smirnova ◽  
A. A. Sinyakov
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Atrophic Gastritis ◽  
Chronic Atrophic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Cytokine Regulation ◽  
H Pylori ◽  
Cytokine Cascade

At present, the level of Helicobacter pylori infection is determined by geographic area, gender and age of the examined individuals, and can reach up to 95% of the total population. Environmental adaptation of H. pylori is exhibited in its ability to adhere to the gastric mucosal epithelium and modulated expression of its own virulent factors. Current concepts implicate that H. pylori can survive inside epithelial cells, evading host immune response. Cytokines are produced by immune cells and act to regulate its major stages. A cytokine cascade launched after Helicobacter pylori infection triggers immune reactions, progression of chronic inflammatory and destructive processes in the gastric mucosa. The role of cytokines in precancerous diseases of the stomach is ambiguous because, on the one hand, they activate immune response aimed at eliminating the pathogen, whereas on the other hand, they do contribute to the disease progression. The aim of our study was to examine profile of some cytokines and features of cytokine regulation in H. pylori-infected middle-aged males with chronic gastritis (CG) as well as chronic atrophic gastritis (CAG). In patients with CG with H. pylori, CAG and CAG with H. pylori, an increase in the cytokine IL-2 was observed that might contribute to augmented damaging effect of cytotoxic lymphocytes, as well as implementation of antitumor effect. CAG with H. pylori was featured with IL-8 hyperproduction, which resulted in increased absolute numbers of band neutrophils in peripheral blood and their decreased phagocytic activity evidencing about altered host defense mechanisms. There was increased amount of IFNy involved in recognition of malignantly transformed cells and upregulated expression of the major histocompatibility complex molecules on antigen-presenting cells. In patients with CG with H. pylori and CAG with H. pylori, production of IL-4 was increased, which might serve as a contributing factor to the chronicity of H. pylori-associated diseases. Overproduction of type 1 and type 2 cytokines indicates about activated Th1 and Th2 type immune reactions in H. pylori-associat-ed CG. A potent pro-inflammatory cytokine cascade triggers inflammatory changes in gastric mucosa with developing neutrophil infiltration and lymphocyte activation. Damage and death of epithelial cells upon inflammation form erosive and ulcerative defects, or changes manifested as gastric mucosal atrophy, metaplasia and neoplasia. The data obtained may be used as additional diagnostic criteria in early diagnostics of precancerous stomach diseases.

scholarly journals Prevalence of Erosive-ulcerative Lesions of the Stomach and Helicobacter Pylori Infection in Patients with Ulcerative Colitis

2019 ◽  
Vol 29 (3) ◽  
pp. 74-80
Author(s):  
N. A. Ponkratova ◽  
P. V. Pavlov ◽  
O. S. Shifrin
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Bowel Disease ◽  
Underlying Disease ◽  
Control Group ◽  
Inflammatory Bowel ◽  
Ulcerative Lesions ◽  
H Pylori

Aim. To assess the prevalence of erosive-ulcerative lesions of the gastric mucosa, as well as the frequency of Helicobacter pylori infection in patients with ulcerative colitis. Materials and methods. The study included 70 patients with ulcerative colitis. All patients, along with the standard examination using esophagogastroduodenoscopy, were diagnosed with regard to H. pylori infection: all 70 patients received a rapid urease test (RUT), 24 patients (34.3 %) had H. pylori DNA analyzed in feces, and 46 patients (65.7 %) had 13C labeled urea breath test. The study of H. pylori infection with RUT was carried out in 111 patients without inflammatory bowel disease, who formed the control group.Results. Endoscopic examination of patients with ulcerative colitis revealed inflammatory and erosive changes in the gastric mucosa. In 7.1 % of cases (5 out of 70 people), the erosion of the body stomach was detected, in 40.0 % of patients (28 out of 70) – erosion of the antrum. No effect of previous steroid therapy, as well as the high activity of ulcerative colitis on the frequency of the stomach erosive lesions (respectively, p = 0.433; p = 0.158) was detected. H. pylori infection was found in patients with ulcerative colitis significantly less frequently than in the control group (respectively, in 52.9 % (37 people out of 70) and 71.2 % of cases (79 people out of 111); p = 0.012). No relationship was found between H.pylori infection and the severity of the exacerbation of the underlying disease (p = 0.157).Conclusion. In patients with ulcerative colitis, erosive changes frequently found in the stomach do not correlate with the activity of the underlying disease. H. pylori infection is less common in patients with ulcerative colitis than in individuals not suffering from inflammatory bowel disease.

Helicobacter Pylori Infection in Sjögren’s Syndrome: Co-incidence or Causality?

2019 ◽  
Vol 15 (3) ◽  
pp. 238-241
Author(s):  
Massoud Saghafi ◽  
Nafiseh Abdolahi ◽  
Reza Orang ◽  
Mohammad Reza Hatef ◽  
Mohammad Hadi Molseghi
Keyword(s):  
Helicobacter Pylori ◽  
Serum Level ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Control Group ◽  
P Value ◽  
H Pylori ◽  
Sjögren‘S Syndrome

Background and Aim: Lymphoid cell infiltration and destruction of exocrine glands, specifically lacrimal and salivary glands are characteristics of Sjogren’s syndrome (SS). An etiological role has been proposed for Helicobacter pylori (H. pylori), interacting in the clinical course and complications of SS (including gastric cancer and lymphoma). The aim of this study was to identify the probable correlation between H. pylori infection and Sjogren’s syndrome (SS). Methods: In this case-control study, ELISA method was used to determine serum level of IgA and IgM anti H. pylori antibody in 43 subjects with SS according to the international criteria and 95 healthy subjects as control. SPSS-17 was used to analyze data with t-test. P value <.05 were considered significant. Results: Serum level of IgM (34.9% vs. 10.5%, p-value= 0.001) and IgA (67.4% vs. 46.3% p value= 0.021) anti H. pylori antibody were significantly higher in SS patients compared to the control group. There was a positive correlation between age and H. pylori infection (r=0.2, Pvalue= 0.05). Conclusion: Patients with SS had a higher prevalence of H. pylori infection compared to the normal population. Eradication of H. pylori is recommended particularly in older patients with SS.

The evaluation of nasal mucociliary clearance in patients with Helicobacter pylori infection

2019 ◽  
Vol 133 (03) ◽  
pp. 220-223
Author(s):  
S Üstün Bezgin ◽  
T Çakabay ◽  
K Irak ◽  
M Koçyiğit ◽  
B Serin Keskineğe ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Mucociliary Clearance ◽  
Endoscopic Examination ◽  
Control Group ◽  
Clearance Time ◽  
Saccharine Test ◽  
Significant Difference ◽  
And Gender ◽  
H Pylori ◽  
Nasal Mucociliary Clearance

AbstractObjectiveThis study aimed to examine nasal mucociliary clearance time in patients with Helicobacter pylori infection.MethodsFifty patients who were newly diagnosed with H pylori infection using gastric biopsy in the gastroenterology out-patient clinic, and 50 age- and gender-matched healthy adults who were admitted to the otorhinolaryngology out-patient clinic, were included in this study. After an otorhinolaryngological examination (anterior rhinoscopy and nasal endoscopic examination), the nasal mucociliary clearance time of each subject was calculated using the saccharine test.ResultsThe mean mucociliary clearance time was 06:29 ± 3:31 minutes (range, 00:55–15:19 minutes) in the control group and 10:12 ± 06:09 minutes (range, 01:28–32:00 minutes) in the study group. Comparisons of the two groups revealed a statistically significant difference (p = 0.002).ConclusionNasal mucociliary clearance time was significantly increased in patients with H pylori infection. The results suggest that H pylori infection may have an unfavourable effect on nasal mucociliary clearance.

scholarly journals Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 27
Author(s):  
Jacek Baj ◽  
Alicja Forma ◽  
Monika Sitarz ◽  
Piero Portincasa ◽  
Gabriella Garruti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Virulence Factors ◽  
Premalignant Lesions ◽  
Bacterial Pathogenicity ◽  
Current State ◽  
Genetic And Environmental Factors ◽  
H Pylori ◽  
Stimulation Of

Gastric cancer constitutes one of the most prevalent malignancies in both sexes; it is currently the fourth major cause of cancer-related deaths worldwide. The pathogenesis of gastric cancer is associated with the interaction between genetic and environmental factors, among which infection by Helicobacter pylori (H. pylori) is of major importance. The invasion, survival, colonization, and stimulation of further inflammation within the gastric mucosa are possible due to several evasive mechanisms induced by the virulence factors that are expressed by the bacterium. The knowledge concerning the mechanisms of H. pylori pathogenicity is crucial to ameliorate eradication strategies preventing the possible induction of carcinogenesis. This review highlights the current state of knowledge and the most recent findings regarding H. pylori virulence factors and their relationship with gastric premalignant lesions and further carcinogenesis.

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