scholarly journals Impact of alcohol on gastric mucosa in a population with high prevalence of Helicobacter pylori

2021 ◽  
Vol 8 (6) ◽  
pp. 764
Author(s):  
Sultan Nawahir ◽  
George Kurian ◽  
Thomas Alexander ◽  
Susy Kurian
Keyword(s):  
Gastric Mucosa ◽  
Alcohol Abuse ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Premalignant Lesions ◽  
Control Group ◽  
Chronic Alcohol ◽  
Chronic Alcohol Abuse ◽  
High Prevalence ◽  
H Pylori

Background: The purpose of the study was to see whether chronic alcohol abuse had any effect on the gastric mucosa in a population already affected by a high prevalence of Helicobacter pylori.Methods: 35 males with a history of chronic alcohol abuse were compared with 35 males who were abstinent or social drinkers. All subjects had complaints of dyspepsia. All subjects underwent endoscopy and targeted biopsies were taken from three specific sites in the stomach, namely body, antrum and incisura. Biopsies were studied to look for changes of atrophic gastritis and intestinal metaplasia. The presence or absences of H. pylori on the tissue biopsy were also recorded.Results: Atrophic gastritis were only assessable in 24 alcoholic patients and 21 non-alcoholic patients due to the inadequacy of the depth of the biopsy. AG were found to be equally distributed in both the groups. 23 (64.9%) patients in the alcoholic group and 19(54.5%) in the control group had AG (OR-1.54, p=0.47). Intestinal metaplasia was seen in 10 (28.5%) alcoholic group and 12 (34.2) in the control group (OR-0.65, p=0.45). Of the 42 subjects detected to have AG, 16 (38.1%) had IM. However, IM were always associated with AG. In addition, H. pylori were not seen to be different in the two groups. H. pylori were positive in 18 (51.4%) alcoholic and14 (40%) non-alcoholic patients (p=0.33).Conclusions: Chronic alcohol abuse doesn’t appear to have any major impact on the gastric mucosa in terms of producing premalignant lesions such as atrophic gastritis or intestinal metaplasia or enhancing the prevalence of H. pylori.

scholarly journals Alcohol abuse as a risk factor for developing thyroid cancer

2020 ◽  
pp. 113-113
Author(s):  
Nevena Kalezic ◽  
Milica Karadzic-Kocica ◽  
Nemanja Dimic ◽  
Mladen Kocica ◽  
Anka Toskovic ◽  
...  
Keyword(s):  
Risk Factor ◽  
Thyroid Cancer ◽  
Alcohol Abuse ◽  
Cancer Patients ◽  
Protective Factor ◽  
Control Group ◽  
Chronic Alcohol ◽  
Thyroid Cancers ◽  
Chronic Alcohol Abuse ◽  
Group I

Introduction/Objective. Alcohol abuse influence on developing thyroid cancer is controversial. While some studies consider it a protective factor, others deny any impact on thyroid cancer. The objective of the paper was to establish a possible link between alcohol abuse and certain types of thyroid cancers. Methods. The retrospective study included 502 patients with thyroid cancer and control group of 600 patients with benign forms of thyroid diseases (e.g. nodular, multinodular and toxic nodular goiter). Thyroid cancer patients were divided into 4 groups: I - papillary, II - medullary, III - anaplastic, and IV - follicular carcinoma, and grouped by sex, age (< 30 yrs.; > 30 yrs.) and alcohol abuse, as defined by WHO. Results. Thyroid cancer patients were predominantly male of younger age. This distribution difference was statistically significant in groups I and II (p < 0.001). Of total 10 (0.9%) patients with chronic alcohol abuse, 8 (1.6%) had thyroid cancer, while 2 (0.3%) belonged to the control group (p < 0.001). In thyroid cancer patients, chronic alcohol abuse was absent in group III and IV. Distribution in group I and II was 6 (1.6%) and 2 (2%) respectively (p < 0.001). Conclusion. Alcohol abuse deserves to be considered as a risk factor for papillary and medullary forms of thyroid cancer, while it does not stay the same for anaplastic and follicular thyroid cancers.

scholarly journals Endoscopic and histological evaluation of the mucous membrane of the stomach in relatives of people suffering from cancer of the stomach

2019 ◽  
Vol 16 (4) ◽  
pp. 391-403
Author(s):  
V. V. Karpenka ◽  
Ju. V. Gorgun ◽  
N. P. Mitkovskaya ◽  
V. V. Krasko
Keyword(s):  
Gastric Cancer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Main Group ◽  
Alcoholic Beverages ◽  
Histological Evaluation ◽  
Control Group ◽  
Cancer Of The Stomach ◽  
Younger Age ◽  
H Pylori

The condition of gastric mucosa was assessed in relatives of patients with gastric cancer (RPGC). The study included 108 RPGC (main group) and 102 patients with no family history of gastric cancer who were screened for dyspepsia. All study participants were subjected to clinical examination, questioning and esophagogastroduodenoscopy (EGDS) with a biopsy, in which the gastric mucosa state was assessed according to the modified Sydney system, the OLGA and OLGIM systems, and the definition of Helicobacter pylori (H. pylori) infection. It was established that the prevalence of H. pylori infection in the main group was 58.3 % (95 % CI 48.8–67.7), in the control group – 56.0 % (95 % CI 46.1–65.6). At RPGC, atrophy of any localization (46.3 % (95 % CI 39.4–53.2) versus 26.5 % (95 % CI 20.4–32.6), respectively, was found more often than in the control group, respectively, p = 0.002), antral atrophic gastritis (41.6 % (95 % CI 34.8–48.4) versus 26.5 % (95 % CI 20.4–32.6), respectively, p = 0.020), and isolated atrophy in the stomach body (4.6 % (95 % CI 1.7–7.4) versus 0 % ( p = 0.03). In RPGC, atrophy developed at a younger age (48.0 years (95 % CI 44.0–52.0) versus 53.0 years in the control group (95 % CI 48.3–57.8) p = 0.000). There were no significant differences between the groups in the incidence of metaplasia and dysplasia. The following risk factors for development of atrophy were identified in the factor analysis: age over 6f0 years (odd ratio (OR) 53.0; 95 % CI 12.2–390.1; p < 0.001), age over 40 years (OR 4.0; 95 % CI 2.0–8.2; p < 0.001), heredity burdened by gastric cancer (OR 2.7; 95 % CI 1.4–5.7; p = 0.006) and the use of strong alcoholic beverages (OR 5.5; 95 % CI 1.6–21.6; p = 0.009). The frequency of the atrophy development of the gastric mucosa is increased in RPGC, and atrophic gastritis develops at a younger age in comparison with individuals without a burdened hereditary history. In addition to the hereditary factor, the risk of atrophy is associated with age and alcohol use.

scholarly journals Review of Research on Routes of Helicobacter pylori Infection

2015 ◽  
Vol 4 (2) ◽  
pp. 45-49
Author(s):  
Hang Li
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Gastric Adenocarcinoma ◽  
Precancerous Lesions ◽  
Natural Environments ◽  
H Pylori

AbstractIn recent years, many scholars conducted in-depth research onHelicobacter pyloriand identified it as an important pathogen of chronic gastritis and peptic ulcer.H. pylorialso causes also and contributes to precancerous lesions (atrophic gastritis and intestinal metaplasia) and is closely related to occurrence and development of gastric adenocarcinoma and gastric mucosa-associated lymphoma. This study summarizes biological characteristics, epidemic status, and infection route ofH. pyloriand reviews research on roles of natural environments, especially drinking water, during infection.

Sa1728 Chronic Alcohol Abuse Induces Paneth Cell Antimicrobial Expression in Gastric Mucosa - A Consequence of Wnt Signaling Aberrations?

2015 ◽  
Vol 148 (4) ◽  
pp. S-316
Author(s):  
Maureen J. Ostaff ◽  
Christian Schäfer ◽  
Lioba F. Courth ◽  
Sabrina R. Stebe ◽  
German Ott ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Alcohol Abuse ◽  
Wnt Signaling ◽  
Paneth Cell ◽  
Chronic Alcohol ◽  
Chronic Alcohol Abuse

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 Natural Course of Atrophic Gastritis and Intestinal Metaplasia

2020 ◽  
Vol 20 (2) ◽  
pp. 101-106
Author(s):  
Beom Jin Kim
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Genetic Factors ◽  
Gastric Carcinogenesis ◽  
Natural Course ◽  
Precursor Lesions ◽  
High Prevalence

Atrophic gastritis (AG) and intestinal metaplasia (IM) are considered the main precursor lesions of gastric cancer, and the risk of gastric cancer in the gastric mucosa increases in the presence of AG and IM. The development of intestinal-type gastric adenocarcinoma represents the last step of an inflammation-metaplasia-dysplasia-carcinoma sequence, called the Correa cascade of multistep gastric carcinogenesis. The incidences of both AG and IM tend to increase with age. <i>Helicobacter pylori</i> is regarded the most important factor in the development of IM; the progression of AG to IM is also affected by numerous environmental factors and individual genetic factors. Therefore, understanding the natural course of AG and IM is very important, especially in areas with a high prevalence of gastric cancer such as Korea.

The impact of Helicobacter pylori on the presence of Barrett's esophagus in Azerbaijan, a high-prevalence area of infection

2019 ◽  
Vol 32 (11) ◽  
Author(s):  
S Aghayeva ◽  
K C Mara ◽  
D A Katzka
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Erosive Esophagitis ◽  
Control Group ◽  
Significant Difference ◽  
High Prevalence ◽  
H Pylori ◽  
The Impact

SUMMARY There is a strong evidence that Helicobacter pylori infection is inversely associated with Barrett's esophagus. In a high-prevalence region of H. pylori, low rates of esophageal cancer and its precursor BE may indicate its preventive effect. The aim of this study is to determine the impact of H. pylori on characteristics of Barrett's esophagus. A total of 3317 outpatient upper endoscopy reports from 2013 to 2015 from an urban center in Azerbaijan from all patients with dyspepsia were retrospectively analyzed for patients with Barrett's esophagus. This was matched in a 1:2 ratio to age and gender matched control patients without Barrett's esophagus. The prevalence of H. pylori on Barrett's esophagus and the randomly selected control group were compared. There were 83 patients with BE and 167 control group cases. Biopsy-proven BE was diagnosed in 83 patients: 39 (47%) females, with mean age 43.1 ± 13.3 years. Of these, 13 (15.7%) had long segment and 70 (84.3%) had short segment Barrett's esophagus. A control group included 167 patients: 78 (46.7%) females, with mean age (45.8 ± 13.9). All patients were Caucasians. The rates of gastric inflammation, the presence of atrophy, and intestinal metaplasia in gastric specimens did not differ in patients versus controls. The prevalence of H. pylori was determined as 63.2% in male and 61.5 in female groups (odd ratio (OR) = 0.99 95%CI 0.97, 1.01; P = 0.22). Inflammation of gastric mucosa was strongly associated with the infection (67% vs. 33%; OR = 4.46 95% CI: 2.01, 9.92, P &lt; 0.001). Atrophy was noted in majority of H. pylori-positive cases (OR = 1.43, 95% CI: 0.36, 5.65; P = 0.61). Gastric intestinal metaplasia was observed in 55.6% of H. pylori-positive patients and in 44.4% of negative individuals (OR = 0.74, 95% CI: 0.28, 1.94; P = 0.54). There was not a significant difference in the prevalence of HP in BE and control groups; 63.9% were positive for infection in BE cases and 61.7% of controls (OR = 1.10, 95% CI: 0.64, 1.90; P = 0.74). We found that neither presence of erosive esophagitis, length of BE nor dysplasia (45.5% of H. pylori-positive group, whereas 54.5%) was associated with the presence of the H. pylori infection (Table 1). In a predominantly Caucasian nation with a high prevalence of H. pylori gastritis, the presence of H. pylori was not inversely associated with the presence of Barrett's esophagus. These data challenge the mechanistic implications of this association.

TLR1 and PRKAA1 Gene Polymorphisms in the Development of Atrophic Gastritis and Gastric Cancer

2018 ◽  
Vol 27 (4) ◽  
pp. 363-369 ◽  
Author(s):  
Gintare Dargiene ◽  
Greta Streleckiene ◽  
Jurgita Skieceviciene ◽  
Marcis Leja ◽  
Alexander Link ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Genetic Polymorphisms ◽  
Association Studies ◽  
Control Group ◽  
Similar Distribution ◽  
Genome Wide Association Studies ◽  
Increased Risk ◽  
Infection Susceptibility ◽  
H Pylori

Background & Aims: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H.pylori infection, atrophic gastritis (AG) or GC in the European population.Methods: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time polymerase chain reaction. H. pylori status was determined by testing for anti-H. pylori IgG antibodies in the serum.Results: The study included 697 (59.2%) H. pylori positive and 481 (40.8%) H. pylori negative cases. We observed similar distribution of TLR1 and PRKAA1 alleles and genotypes in H. pylori positive and negative cases. TLR1 and PRKAA1 SNPs were not linked with the risk of AG. TC genotype of TLR1 gene was more prevalent in GC patients compared to the control group (29.7% and 22.3% respectively, p=0.002). Carriers of TC genotype had a higher risk of GC (aOR=1.89, 95% CI: 1.26–2.83, p=0.002). A similar association was observed in a dominant inheritance model for TLR1 gene SNP, where comparison of CC+TC vs. TT genotypes showed an increased risk of GC (aOR=1.86, 95% CI: 1.26–2.75, p=0.002). No association between genetic polymorphism in PRKAA1 gene and GC was observed.Conclusions: TLR1 rs4833095 SNP was associated with an increased risk of GC in a European population, while PRKAA1 rs13361707 genetic variant was not linked with GC. Both genetic polymorphisms were not associated with H. pylori infection susceptibility or the risk of AG.

Effect of Chronic Alcohol Abuse on the CNS Morbidity of HIV Disease

1998 ◽  
Vol 22 (s5) ◽  
pp. 196S-200S ◽  
Author(s):  
George Fein ◽  
Daniel J. Fletcher ◽  
Victoria Sclafani
Keyword(s):  
Alcohol Abuse ◽  
Hiv Disease ◽  
Chronic Alcohol ◽  
Chronic Alcohol Abuse

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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