Micronutrient antioxidants in gastric mucosa and serum in patients with gastritis and gastric ulcer: does Helicobacter pylori infection affect the mucosal levels?

Free radicals (FRs) play an important role in the pathogenesis of gastroduodenal mucosal inflammation, peptic ulcer disease, and probably even gastric cancer. Various micronutrients protect the gastric mucosa by scavenging FRs. Only limited data is available regarding the concentration of micronutrients in the gastric mucosa in patients with gastritis and peptic ulcer disease. Our aim was to analyze micronutrient antioxidant concentrations in the antral mucosa in patients with gastritis and gastric ulcer and to determine the influence of Helicobacter pylori infection on gastric mucosal antioxidants in patients with gastritis and gastric ulcer. Patients who underwent upper endoscopy for evaluation of dyspepsia were included in the study. Ascorbic acid, alpha-tocopherol, alpha-carotene, beta-carotene, total carotenoids, lutein, cryptoxanthin, and lycopene levels were measured in the sera and antral mucosal biopsies in these patients. The diagnosis of H. pylori was confirmed by histology, urease test (CLO) and serology. Patients with negative endoscopic findings and normal histology and no H. pylori infection served as controls. In patients with gastritis, alpha-tocopherol levels were reduced in serum and mucosa irrespective of H. pylori status, whereas carotenoids and ascorbic acid levels were similar to controls. However, in patients with gastric ulcer, serum and mucosal levels of all micronutrient antioxidants were markedly decreased compared with both controls and patients with gastritis. The degree of depletion of antioxidants was similar in patients with either H. pylori-induced or nonsteroidal antiinflammatory drug (NSAID)-induced ulcers. Patients with gastric ulcer have very low gastric antioxidant concentrations compared to patients with gastritis and normal mucosa. This depletion in antioxidants seems to be a nonspecific response and was not related to H. pylori infection.     

Does the method of Helicobacter pylori detection influence the association with gastric cancer risk?

BACKGROUND: The exact role of Helicobacter pylori as a causative agent of gastric cancer is still under debate. The aim of this study was to determine how the use of different diagnostic methods for detection of H. pylori influences the measures of prevalence of the infection and thus the association with risk of gastric adenocarcinoma. METHODS: We included 72 cases and 324 controls in an endoscopy clinic-based matched case-control study. Culture of H. pylori and immunohistochemical staining were performed on gastric biopsies. Serum samples were tested for H. pylori IgG by conventional ELISA and by immunoblotting. RESULTS: The overall prevalence of H. pylori was 68% based on all 4 diagnostic methods, 79% in the cases and 66% in the controls. Highest agreement, 91%, was observed between culture and immunohistochemistry with a Kappa value of 0.81. Immunoblotting detected the highest number of H. pylori-positive subjects in both cases and controls. The association of H. pylori positivity with gastric cancer was generally weaker and statistically non-significant using culture and immunohistochemistry compared with the serological tests, of which IgG ELISA yielded the higher odds ratio (OR 2.5, 95% confidence interval 1.4-4.4). CONCLUSION: The study shows that relative risk estimates for the association between H. pylori and gastric cancer risk are to some extent determined by the diagnostic method used to detect H. pylori infection.     

Is gastric nodularity a sign for gastric inflammation associated with Helicobacter pylori infection in children?

The aim of this study was to investigate the accuracy of using gastric nodularity (GN) as a marker for gastric inflammation associated with Helicobacter pylori infection in children. A retrospective analysis of 395 upper endoscopies done in children between 1990-1996 was performed. Demographics, clinical symptoms, endoscopic features, rapid urease test (RUT), and histological results were collected from each report. GN was found in 13 (3.5%) children. GN showed a significant correlation with age but not with gender. Multiple regression analysis showed a significant correlation between GN and gastritis with RUT but not with other histological determinants alone (gastritis, RUT, or H. pylori organisms). Nevertheless, GN had a poor accuracy rate to determine H. pylori-associated gastritis (sensitivity, 61%; positive predictive value, 12%). GN is a poor predictor for gastric inflammation associated with H. pylori infection in children. During endoscopy, gastric biopsies should always be obtained in children to establish the presence of mucosal inflammation.     

Is the presence of Helicobacter pylori in the dental plaque of patients with chronic periodontitis a risk factor for gastric infection?

BACKGROUND

Helicobacter pylori is considered to be a pathogen responsible for gastritis and peptic ulcers, and a risk factor for gastric cancer. A periodontal pocket in the teeth of individuals with chronic periodontitis may function as a reservoir for H pylori.

OBJECTIVE:

The present study was undertaken to evaluate whether the presence of H pylori in the dental plaque of patients with and without periodontitis correlates with gastric involvement.

METHODS:

A total of 101 patients with dyspepsia were included in the present study. Subjects were divided into periodontitis and non-periodontitis groups. For the detection of H pylori in dental plaque, samples were collected from two teeth using a periodontal curette. Subgingival plaque was obtained by inserting two sterile paper points into periodontal pockets for 20 s. This was followed by an upper gastrointestinal endoscopy and antral biopsies.

RESULTS:

Sixty-five per cent of patients had dental plaque positive for H pylori and more than 50% harboured the bacteria in their stomach. Periodontitis patients had a significantly higher percentage of H pylori in their dental plaque (79% versus 43%; P<0.05) and the stomach (60% versus 33%; P<0.05) than patients with no periodontitis. Additionally, 78% of patients from the periodontitis group versus only 30% from the nonperiodontitis group had a positive test result for the coexistence of H pylori in both dental plaque and the stomach.

CONCLUSION:

Patients with poor oral hygiene have a higher prevalence of H pylori in dental plaque and in the stomach. This finding suggests that the oral cavity may be a reservoir for H pylori, and potentially a source of transmission or reinfection.     

Helicobacter pylori and gastric cancer in the Middle East: A new enigma?

The Middle East is the home of ethnic groups from three main backgrounds: Semitic (Arabs and Jews), Indo-European (Persians and Kurdish) and Turkic (Turkish and Turkmens). Its geographic location, which has been under continuous influences from Asia, Europe and Africa, has made it an ideal site for epidemiological studies on Helicobacter pylori (H. pylori) infection and genotyping. The gastric cancer rate differs in this region from very high in Iran (26.1/105) to low in Israel (12.5/105) and very low in Eg...     

Association of the interleukin-1 β genetic polymorphism and gastric cancer risk in Japanese

Background. Helicobacter pylori infection is associated not only with gastroduodenal ulcers but with the development of gastric cancer. Interleukin-1 β (IL-1 β) is a potent inhibitor of gastric secretion. The −31 C-to-T base transition in the intron of this gene has been reported to be involved in carcinogenic changes within the stomach, especially in H. pylori-infected individuals. Methods. In this study, the −511 T-to-C polymorphism in the IL-1 β gene was investigated in 669 patients with gastric diseases. Results. The allelic frequencies of the C allele, which indicates low acid secretion and is a component of a supposedly high-risk genotype for gastric cancer, were 0.48 in H. pylori-negative noncancer controls, 0.52 in H. pylori-positive noncancer controls, 0.57 in subjects with chronic active gastritis (CAG) with H. pylori, 0.58 in subjects with intestinal metaplasia (IM) or CAG without H. pylori, and 0.52 in gastric cancer patients. Significant differences among the groups were observed between the IM or CAG without H. pylori group and the gastric cancer group and between the IM or CAG without H. pylori group and the H. pylori-negative noncancer control group (P < 0.05). Conclusions. The IL-1 β−511 genetic polymorphism was not associated with gastric cancer in a multistep carcinogenesis model. However, in view of the results for the IM or CAG without H. pylori group, the presence of the C allele may also indicate a risk of mucosal atrophy of the stomach in the Japanese population. Received: February 20, 2001 / Accepted: July 6, 2001     

Helicobacter pylori infection causes gastric cancer？ A review of the epidemiological, meta-analytic, and experimental evidence

Since the discovery of Campylobacter-like organisms {Helicobacter pylori) more than two decades ago the possibility of a relationship with gastric cancer has been postulated, tested and supposedly proven. There have been numerous human studies of various designs from many countries around the world. Several meta-analyses have been published and more recently a small number of experimental animal studies were reported looking at the association between Helicobacter pylori infection and gastric cancer. Over the years, the human epidemiologi-cal studies have produced conflicting results; the meta-analyses have as one would expect produced similar pooled estimates; while the early experimental animal studies require replication. The exact mechanisms by which H pylori might cause gastric cancer are still under investigation and remain to be elucidated.     

‘Serological biopsy’ in first‐degree relatives of patients with gastric cancer affected by Helicobacter pylori infection

Background: Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori‐related atrophic gastritis and hypochlorhydria are well‐documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a ‘Gastropanel’ blood test, including sPGI, sPGII, gastrin‐17 (G‐17) and antibodies anti‐H. pylori (IgG‐Hp), both functional and morphological features of gastric mucosa in Hp?+?ve subjects with a family history of gastric cancer. Materials and Methods: Twenty‐five Hp?+?ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first‐degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp?+?ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed. Results: No statistically significant differences were detected zbetween the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4?±?58.4 μg/L) were significantly lower than those in Group B (sPGI 159.5?±?80.6 μg/L; P?P?Conclusion: First‐degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPGI and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.     

Unique features and risk factors of Helicobacter pylori infection at the main children’s intermediate school in Rabigh,Saudi Arabia

Background

This study was conducted to determine characters and risk factors of Helicobacter pylori infection and its relationship with recurrent abdominal pain and other gastrointestinal symptoms at the main children’s intermediate school in Rabigh, Saudi Arabia.

Methods

A cross-sectional study was conducted at a boys’ intermediate school. A questionnaire for the gastrointestinal (GI) symptoms and relevant personal and socioeconomic risk factors related to H. pylori infection was distributed followed by H. pylori IgG antibody assay and 14C urea breath test to detect active infection.

Results

H. pylori was diagnosed by positive urea breath test in 51.5 % of students. H. pylori infection was symptomatic with at least one upper GI symptom in 89.7 % of infected students which was higher than symptomatic cases reported in any other study. H. pylori-infected students had significantly more association with the presence of any upper GI symptom (p?<?0.001), recurrent abdominal pain (p?<?0.001), anorexia (p?<?0.001), nausea (p?<?0.026), family history of peptic disease (p?<?0.001), drinking desalinated municipal water (p?<?0.001), lower income (p?=?0.02), and eating outside home (p?=?0.003) than uninfected students. Logistic regression analysis showed that the most significant predictors of H. pylori infection were presence of any upper GI symptom (OR 5.3, 95 % CI 2.32–15.71), family history of peptic disease (OR 2.2, 95 % CI 1.11–3.9), and drinking desalinated municipal water (OR 2.1, 95 % CI 1.09–3.2).

Conclusions

This study presented unique features and risk factors of H. pylori infection in 12–15-year-old Saudi boys in Rabigh, and mainly supported the role of H. pylori in causing recurrent abdominal pain.     

Helicobacter pylori infection and gastric cancer：evidence from a retrospectiv cohort study and nested case—control study in China

AIM: To explore the association between Helicobacter pylori (Hp) infection and risk of gastric cancer in China. METHODS: Utilizing gastroendoscopic biospsy tissue banks accumulated from 1980 to 1988 in Shandong, Zhejiang, and Jiangsu, where stomach cancer incidence was high, during stomach cancer screening conducted by Health Science Center of Peking University, School of Medicine of Zhejiang University, and Zhongshan Hospital of Fudan University. Warthin Starry silver staining method was applied to determine H. pylori infection status of biopsies collected during gastroendoscopic examination. In the retrospective study, the subjects were divided into two cohorts, the exposure cohort was positive H. pylori infection, and the non-exposure cohort was negative. Death from stomach cancer was determined as the outcome of the study. Logistic regression and Cox regression were applied to analyze the association between Helicobacter pylori infection and gastric cancer risk. In the nested case-control study, there were 28 deaths from gastric cancer in the fields of Muping, Shandong province, and Zhoushan, Zhejiang provinces. 4 controls were matched to each case on the basis of age (+/-5 years old), sex, residential place at the same time entered into the study. Conditional logistic regression analysis was used to analyze the data. RESULTS: There were a total of 2 719 subjects (male 1 399, female 1 320) with gastroendoscopic biopsies stored available treated as a cohort. H. pylori positive cohort included 1 671 subjects (61.5 %) and H. pylori negative cohort 1 048 subjects(38.5 %). These subjects were followed up for 1-19 years, averaged 10.88 years. The outcome of death from stomach cancer in the exposure cohort was 33, and in the non-exposure cohort 11. After adjustment for age and sex, RR=1.9850 (P=0.0491), 95 % CI was 1.0026, and 3.9301. The results of conditional logistic regression showed an OR of 4.467 and 95 % CI of 1.161, and 17.190 for the nested case control study. CONCLUSION: The results from the retrospective cohort study and the nested-case control study on the association of H. pylori infection and gastric cancer in China suggested that Helicobacter pylori infection might increase the risk of stomach cancer.     

H pylori infection and other risk factors associated with peptic ulcers in Turkish patients： A retrospective study

AIM: To identify and evaluate the relative impact of H pylori infection and other risk factors on the occurrence of gastric ulcer (GU), duodenal ulcer (DU) and gastritis in Turkish patients. METHODS: A total of 4471 patients (48.3% female) out of 4863 attended the Samatya hospital in Istanbul (June 1999 - October 2003) were included. The records of H pylori status (CLO-test), endoscopic f indings of GU, DU and gastritis, personal habits (smoking, alcohol intake) and medication [non-steroidal anti-inflammatory drugs (NSAIDs), aspirin intake] were analyzed using multi-way frequency analysis. RESULTS: We have found that GU in the presence of H pylori had significant association with aspirin (P = 0.0001), alcohol (P = 0.0090) and NSAIDs (P = 0.0372). DU on the other hand had significant association with aspirin/ smoking/NSAIDs (P = 0.0259), aspirin/alcohol (P = 0.0002) and aspirin/smoking (P = 0.0233), also in the presence of H pylori. In the absence of H pylori GU had significant association with alcohol/NSAIDs (P = 0.0431), and NSAIDs (P = 0.0436). While DU in the absence of H pylori had significant association with smoking/alcohol/ NSAIDs (P = 0.0013), aspirin/NSAIDs (P = 0.0334), aspirin/alcohol (P = 0.0360). CONCLUSION: In the presence of H pylori, aspirin, alcohol and NSAIDs intake act as an independent risk factors that had an augmenting impact on the occurrence of GU and only together on the occurrence of DU in Turkish patients.     

Relationship between IL-1β gene polymorphism and gastric mucosal IL-1β levels in patients with Helicobacter pylori infection

Background Interkeukin-1 (IL-1) gene cluster polymorphisms that are thought to enhance the production of IL-1β are associated with an increased risk of gastric cancer. To determine the role of host genetic factors in Helicobacter pylori infection, we examined the relationship between gastric mucosal IL-1β levels and IL-1B polymorphisms in patients with H. pylori infection.Methods Biopsy tissues obtained from 99 patients were homogenized and gastric mucosal IL-1β levels were measured by enzyme-linked immunosorbent assay (ELISA). Single-base polymorphisms at positions −511 and −31 in IL-1B were analyzed.Results The IL-1β level in the antrum was significantly higher in genotype IL-1B-511C/C than in H. pylori-negative patients (P < 0.05). The IL-1B polymorphism did not influence the degree of gastric neutrophil and mononuclear cell infiltration, or gastric atrophy. IL-1β levels in the corpus, but not those in the antrum, correlated to the severity of gastric atrophy.Conclusions These findings indicate that IL-1B polymorphisms enhance IL-1β production in the antrum; however, other factors might regulate the production of IL-1β in the corpus of the stomach, regardless of IL-1B polymorphisms, and high IL-1β production may be associated with the grade of gastric atrophy in the corpus mucosa in patients with H. pylori infection.     

Prevalence of H pylori associated 'high risk gastritis' for development of gastric cancer in patients with normal endoscopic findings

INTRODUCTION H pylori infection is an established risk factor for development of gastric cancer[1,2]. According to the model of carcinogenesis of the intestinal type adenocarcinoma proposed by Correa, the multi-step development starts from the condition o…     

What are the risk factors for aggravation of esophageal varices in patients with hepatocellular carcinoma?

BACKGROUND AND AIM: The risk factors for aggravation of esophageal varices (EV) in patients with hepatocellular carcinoma (HCC) are poorly understood. The aim of this study was to evaluate the effects of HCC on the appearance of the red color (RC) sign on EV and also investigate whether risk factors for the appearance of the RC sign differed between patients with and without HCC. METHODS: A total of 243 patients with cirrhosis (127 with HCC, 116 without HCC) without the RC sign, with no previous variceal hemorrhage, and not on prophylactic treatment for EV were enrolled. The endpoint was defined as being either when the RC sign was first noted, or when variceal bleeding occurred. In patients without HCC, follow-up was discontinued if HCC was discovered. The risk factors were analyzed by Cox proportional hazards regression. RESULTS: In patients with HCC, portal vein tumor thrombus was a statistically independent risk factor (risk ratio [RR] 4.58, 95% confidence interval [CI] 1.32-15.86), although the presence of HCC was not. A large HCC (> or =50 mm) tended to be a risk factor, but this was not statistically significant (RR 2.50, 95%CI 0.98-6.39). Child-Pugh classification and low platelet count were common risk factors regardless of whether HCC was present or not. CONCLUSIONS: Portal vein tumor thrombus, but not the presence of HCC, was a significant risk factor for aggravation of EV in patients with HCC. Cirrhotic patients with portal vein tumor thrombus should receive more aggressive management of portal hypertension to prevent aggravation of EV.     

What effect does Helicobacter pylori infection have on the risk of peptic ulceration in patients receiving NSAIDs for rheumatoid arthritis?

BACKGROUND: Patients with rheumatoid arthritis (RA) frequently develop dyspepsia which may be due to peptic ulceration. There have been conflicting published data on the possible interactive roles of nonsteroidal anti-inflammatory drugs (NSAIDs) and colonisation of the gastric antrum with Helicobacter pylori in the development of peptic ulceration. METHODS: We have prospectively assessed the prevalence of peptic ulcers in dyspeptic RA patients and investigated the factors responsible. We endoscoped 100 RA patients comparing the endoscopic findings to those in 100 age- and sex-matched dyspeptic control subjects. Data on NSAID consumption and Helicobacter colonisation were collected for each patient. RESULTS: Endoscopic evidence of peptic ulceration was found in 29 RA patients and in 16 of the control subjects (P=0.03). Multiple ulcers (>2) were found in significantly more RA patients than in controls (10 vs. 2). NSAIDs were being used by 60 RA patients and 22 controls (P<0.001). Helicobacter was found in 41 RA patients and in 33 controls (P=NS). The consumption of NSAIDs conferred a relative risk (RR) of ulceration of 8.67 (1.19-62.87), while the presence of Helicobacter gave a RR for ulcers of 3.71 (0.37-37.35) in RA patients. The RR for the combination of NSAID consumption and Helicobacter colonisation was 14.44 (2.05-101). The corresponding RRs for the dyspeptic controls were 2.13, 1.57 and 1.42 (all P=NS). CONCLUSIONS: Rheumatoid patients have more major and more multiple pathology than age-, sex- and symptom-matched controls. This is due mainly to their increased consumption of NSAIDs. The prevalence of Helicobacter was no greater in RA patients than in controls, but Helicobacter infection increased the risk of NSAID-induced ulceration.