beta-carotene and Helicobacter-Infections

Many micronutrients depend on a healthy stomach for absorption. Helicobacter pylori chronic gastritis may alter gastric physiology affecting homeostasis of vitamins and minerals.. Systematic review to assess whether H. pylori infection is associated with reduced micronutrient levels (other than iron) in the plasma or gastric juice and whether low micronutrient levels are modified by eradication treatment.. Medline was searched for relevant publications from inception to June 2010. Studies describing micronutrient levels in H. pylori-infected and not-infected adults and/or the effect of eradication treatment on micronutrient levels were included.. Fifty-two publications were selected: 46 investigated the association between H. pylori infection and reduced micronutrient levels and 14 the effect of eradication treatment on micronutrient levels. Sixty-four studies investigated vitamins (23 ascorbic acid, four ß-carotene, 21 cobalamin, 11 folate, and five α-tocopherol) and 10 addressed minerals (one calcium, one copper, one magnesium, one phosphorus, three selenium, and three zinc). Pooled standardized mean differences in micronutrient levels showed positive associations with H. pylori infection for ascorbic acid (gastric juice, -1.087) and cobalamin (-0.744), and a positive effect of eradication treatment, which increased ascorbic acid in the gastric juice (-1.408) and serum cobalamin (-1.910). No significant association between infection and low folate levels was observed. Meta-analyses for other micronutrients were not performed owing to insufficient data.. Meta-analyses indicate that H. pylori infection is associated with reduced levels of ascorbic acid and cobalamin, supported by the positive effect of eradication treatment. For other micronutrients, further studies are needed.

Topics: Ascorbic Acid; beta Carotene; Helicobacter Infections; Helicobacter pylori; Humans; Iron, Dietary; Micronutrients; Vitamin B 12

Gastric cancer (GC) is the result of a long multi-step and multifactorial process involving possible interactions between Helicobacter pylori infection, environmental exposures and host genetic susceptibility. Interactions between H. pylori infection, tobacco smoking and dietary antioxidants are biologically plausible. Positive interactions between risk factors imply that, in certain subgroups of the population, the risk of GC associated with simultaneous exposure to these factors is higher than that in the rest of the population, and these subgroups have to be the target for preventive measures. Using PubMed, we reviewed all studies published in English up to December 2008 carried out in humans on interactions between H. pylori infection and smoking exposure and between H. pylori infection and dietary factors in gastric carcinogenesis. Although relatively few epidemiological studies have evaluated the effect of the interaction between smoking and H. pylori infection on GC risk, there is a suggestion of a positive interaction between the two factors. In contrast, evidence suggests a negative interaction between dietary antioxidants and H. pylori infections on GC risk. The potential protective effect of dietary antioxidants such as vitamins C and E and beta-carotene seems to be stronger in those infected by H. pylori, even though results are inconsistent. In Asian populations, subjects infected by H. pylori and with high dietary salt intake may have a higher risk of GC than subjects without H. pylori infection and with a low salt intake. The risk of GC associated with red meat, processed meat or endogenous formation of nitrosamines appears to only be observed in subjects infected by H. pylori. More and larger epidemiological studies, mainly prospective studies, are necessary to reach a more definitive conclusion on these interactions.

Topics: Antioxidants; Ascorbic Acid; beta Carotene; Diet; Environmental Exposure; Helicobacter Infections; Humans; Risk Factors; Smoking; Stomach Neoplasms; Vitamin E

Antioxidants are substances capable of inhibiting oxidation. In chronic diseases, inflammatory response cells produce oxygen free radicals. Oxygen free radicals cause DNA damage, and this may lead to gene modifications that might be carcinogenic. Chronic Helicobacter pylori infection causes the production of DNA-damaging free radicals. In recent years, various groups have studied the effects of antioxidants, especially on H. pylori-associated gastric cancer. In most of the studies, it has been shown that H. pylori infection does affect the level of antioxidants measured in the gastric juice, but there are also controversial results. Recent experimental studies, both in vivo and in vitro, have shown that vitamin C and astaxanthin, a carotenoid, are not only free radical scavengers but also show antimicrobial activity against H. pylori. It has been shown that astaxanthin changes the immune response to H. pylori by shifting the Th1 response towards a Th2 T-cell response. Very few experimental studies support the epidemiologic studies, and further studies are needed to describe the effect and the mechanism of antioxidants in the H. pylori immune response.

Topics: Antioxidants; Ascorbic Acid; beta Carotene; DNA Damage; Helicobacter Infections; Helicobacter pylori; Humans; Risk Factors; Stomach Neoplasms; Th1 Cells; Th2 Cells; Xanthophylls

Gastric cancer is one of the most common malignancies worldwide. Histopathologic studies have identified a sequence of changes in the gastric mucosa that mark the slow progression from normal tissue to carcinoma. Epidemiologic evidence suggests that a diet rich in fresh fruit and vegetables could be a protective factor against this disease. This effect may be mediated through antioxidant vitamins.. A randomized, double-blind chemoprevention trial was conducted among 1980 subjects in Tachira State, Venezuela (whose population is at high risk for gastric cancer), to determine the effect of dietary supplementation with vitamin C, vitamin E, and beta-carotene on the progression and regression of precancerous gastric lesions. Subjects were randomly assigned to receive either a combination of vitamin C (750 mg/day), vitamin E (600 mg/day), and beta-carotene (18 mg/day) or placebo for 3 years. Changes in the gastric mucosa were determined by histologic diagnosis based on five biopsies taken from prespecified areas of the stomach at baseline and annually for 3 years. All biopsies were reviewed by a single expert pathologist. Progression rates (and regression rates) were calculated by comparing the first and last available gastroscopies for each subject and dividing the number of subjects whose diagnoses increased (decreased) in severity by the total follow-up time. Overall rate ratios were calculated by Poisson regression, controlling for baseline diagnosis. All statistical tests were two-sided.. Median plasma vitamin levels were increased in the treatment group between baseline and 1 year after randomization from 0.43 micromol/L (interquartile range [IQR] = 0.26-0.69) to 2.89 micromol/L (IQR = 1.76-4.22) for beta-carotene, from 26.7 micromol/L (IQR = 23.1-31.2) to 54.9 micromol/L (IQR = 42.8-67.6) for alpha-tocopherol, and from 47.70 micromol/L (IQR = 36.9-58.5) to 61.9 micromol/L (IQR = 52.2-72.7) for vitamin C. Overall progression rates per 100 person-years were 74.3 in the placebo group and 67.8 in the group randomly assigned to vitamins. Overall regression rates were 109.4 in the placebo group and 116.5 in the group randomly assigned to vitamins. There was no statistically significant difference in progression rate (rate ratio = 0.92, 95% confidence interval [CI] = 0.74 to 1.15) or regression rate (rate ratio = 1.09, 95% CI = 0.90 to 1.33) between vitamin and placebo groups.. Supplementation with antioxidant micronutrients is not an effective tool for gastric cancer control in this high-risk population. The results of this trial are consistent with previous findings on the lack of effect of nutritional supplementation on precancerous gastric lesions.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; beta Carotene; Cell Transformation, Neoplastic; Disease Progression; Double-Blind Method; Female; Gastric Mucosa; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Logistic Models; Male; Middle Aged; Patient Selection; Precancerous Conditions; Risk Assessment; Sample Size; Smoking; Stomach Neoplasms; Treatment Failure; Venezuela; Vitamin E; Vitamins

A randomized double blind placebo-controlled trial of the drug karinat was carried out in patients with chronic multifocal atrophic gastritis. Karinat contains beta-carotene 2.5 mg, alpha-tocopherol 5 mg, ascorbic acid 30 mg and garlic powder 150 mg per tablet. Out of 66 patients, 34 received karinat, 32--placebo. Both karinat and placebo were administered for 6 months, one tablet twice a day. Karinat therapy improved digestion, the fibrogastroscopic pattern of mucosa, inhibited Helicobacter pylori infection, stimulated stomach activity, mitigated intestinal metaplasia and interfered with the epithelial proliferation of gastric mucosa. These therapeutic effects were more pronounced in the study group. On the whole, the effectiveness of the drug was significantly higher (29%). Karinat should be recommended for the management of chronic atrophic gastritis, a precursor of stomach cancer.

Topics: alpha-Tocopherol; Anticarcinogenic Agents; Antioxidants; Ascorbic Acid; beta Carotene; Chronic Disease; Double-Blind Method; Drug Combinations; Female; Garlic; Gastritis, Atrophic; Helicobacter Infections; Humans; Male; Middle Aged; Plant Extracts; Stomach Neoplasms; Treatment Outcome

Background. Only a few reported studies focus on the natural history and course of advanced and severe chronic atrophic gastritis. Methods. In this study we followed 47 men (mean age 62 years) with advanced (moderate or severe) Helicobacter pylori-positive atrophic corpus gastritis. Duration of endoscopic follow-up was 6 years and follow-up based on serum levels of pepsinogen I and antibodies to H. pylori covered a period of 10 years. None of the patients was treated for H. pylori infection prior to end of follow-up. Results. The median H. pylori antibody titre declined (IgG from 4000 to 1300; IgA from 200 to 50) in the study population, and 11 men (23%) converted to seronegative (p=0.0005, Fisher's exact test). There was a small but significant (p=0.0004, Page's test) declining trend in mean atrophy score of the corpus during follow-up (from 2.5 to 2.2). However, no significant changes were observed in grade of atrophy or intestinal metaplasia of the antral mucosa or in grade of intestinal metaplasia in the corpus. The mean SPGI level remained at the initial low level during the entire follow-up. Conclusions. H. pylori antibodies disappear spontaneously within 10 years in almost one fourth of patients with advanced atrophic corpus gastritis. The disappearance of H. pylori antibodies is accompanied by no or more than a mild improvement of the gastric mucosa.

Topics: Aged; alpha-Tocopherol; Antibodies, Bacterial; beta Carotene; Diet; Gastric Mucosa; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin A; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Placebos

Gastric cancer is the second most frequent cause of death from cancer in the world and the leading cause of death from cancer in China. In September 1995, we launched a randomized multi-intervention trial to inhibit the progression of precancerous gastric lesions in Linqu County, Shandong Province, an area of China with one of the world's highest rates of gastric cancer. Treatment compliance was measured by pill counts and quarterly serum concentrations of vitamin C, vitamin E and S-allyl cysteine. In 1999, toxicity information was collected from each trial participant to evaluate treatment-related side-effects during the trial. Compliance rates were 93% and 92.9% for 39 months of treatment with the vitamins/mineral and garlic preparation, respectively. The means for serum concentrations of vitamins C and E were 7.2 microg/ml and 1695 microg/dl among subjects in the active treatment groups compared with 3.1 microg/ml and 752 microg/dl among subjects in the placebo treatment group, respectively. No significant differences in side-effects were observed between the placebo treatment group and the vitamins/mineral and garlic preparation treatment groups during the 39-month trial period.

Topics: Adult; Aged; Amoxicillin; Antioxidants; Ascorbic Acid; beta Carotene; China; Double-Blind Method; Drug Therapy, Combination; Female; Garlic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Patient Compliance; Penicillins; Phytotherapy; Plants, Medicinal; Precancerous Conditions; Prevalence; Selenium; Stomach Neoplasms; Treatment Outcome; Vitamin E

Our purpose was to find out if morphometric techniques can document long term changes in gastric antral atrophy after curing Helicobacter pylori infection with or without dietary supplementation with antioxidant micronutrients.. Study subjects were 132 adult volunteers from a Colombian region with high gastric cancer rates. Participants were randomly assigned to ascorbic acid, beta-carotene, and anti-H. pylori treatment, following a factorial design. Gastric biopsies were obtained at baseline and after 72 months of intervention. Atrophy was evaluated by a standard visual analog scale and by morphometry.. Statistically significant changes in antral atrophy were detected with morphometric techniques after intervention in subjects who received anti-H. pylori treatment. A nonsignificant trend was also observed with visual scores. This effect was greater among those who were free of infection at the end of the trial. After accounting for the effect of anti-H. pylori treatment, no significant effect was noted for dietary supplementation with ascorbic acid and/or beta-carotene.. We conclude that gastric atrophy improves significantly after long term control of H. pylori infection. This effect can be demonstrated both by conventional histological grading and by morphometry.

Topics: Adult; Aged; Anti-Bacterial Agents; Ascorbic Acid; Atrophy; beta Carotene; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Treatment Outcome

In this study, in vivo effectiveness of ascorbic acid (AA), beta carotene (BC) and allicin in HP eradication were evaluated. 210 patients who are HP positive in biopsy were involved in this study. The patients randomised to seven treatment groups (each group consisting of 30 patients). The first group was given standard eradication treatment (lansaprasol 30 mg bid, clarithromycin 500 mg bid, amoxicillin 1 g bid for 14 days). Second group received AA 1000 mg/day in addition to the standard treatment. Third group received only AA 1000 mg/day for 14 days. Fourth group was treated with standard regiment plus 120 mg/day BC. Fifth group was given only BC 120 mg/day for 14 days. Sixth group was given standard regiment and allicin 4200 micrograms/day. Seventh group received only Allicin 1200 micrograms/day for 14 days. The eradication was achieved in 20 (66.6%) in group I, 15 (50%) in group II, 3 (10%) in group III, 15 (50%) in group IV, 0 (0%) in group V, 27 (90%) in group VI and 7 (23.3%) in group VII. Allicin seemed to be potentially effective agent for HP eradication but ascorbic acid, beta caroten was found to be ineffective.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Antioxidants; Ascorbic Acid; beta Carotene; Clarithromycin; Disulfides; Drug Therapy, Combination; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Lansoprazole; Male; Omeprazole; Sulfinic Acids

Previous research has identified a high risk of gastric carcinoma as well as a high prevalence of cancer precursor lesions in rural populations living in the province of Nariño, Colombia, in the Andes Mountains.. A randomized, controlled chemoprevention trial was conducted in subjects with confirmed histologic diagnoses of multifocal nonmetaplastic atrophy and/or intestinal metaplasia, two precancerous lesions. Individuals were assigned to receive anti-Helicobacter pylori triple therapy and/or dietary supplementation with ascorbic acid, beta-carotene, or their corresponding placebos. Gastric biopsy specimens taken at baseline were compared with those taken at 72 months. Relative risks of progression, no change, and regression from multifocal nonmetaplastic atrophy and intestinal metaplasia were analyzed with multivariate polytomous logistic regression models to estimate treatment effects. All statistical tests were two-sided.. All three basic interventions resulted in statistically significant increases in the rates of regression: Relative risks were 4.8 (95% confidence interval [CI] = 1.6-14.2) for anti-H. pylori treatment, 5. 1 (95% CI = 1.7-15.0) for beta-carotene treatment, and 5.0 (95% CI = 1.7-14.4) for ascorbic acid treatment in subjects with atrophy. Corresponding relative risks of regression in subjects with intestinal metaplasia were 3.1 (95% CI = 1.0-9.3), 3.4 (95% CI = 1.1-9.8), and 3.3 (95% CI = 1.1-9.5). Combinations of treatments did not statistically significantly increase the regression rates. Curing the H. pylori infection (which occurred in 74% of the treated subjects) produced a marked and statistically significant increase in the rate of regression of the precursor lesions (relative risks = 8.7 [95% CI = 2.7-28.2] for subjects with atrophy and 5.4 [95% CI = 1.7-17.6] for subjects with intestinal metaplasia).. In the very high-risk population studied, effective anti-H. pylori treatment and dietary supplementation with antioxidant micronutrients may interfere with the precancerous process, mostly by increasing the rate of regression of cancer precursor lesions, and may be an effective strategy to prevent gastric carcinoma.

Topics: Adult; Aged; Anti-Bacterial Agents; Antioxidants; Ascorbic Acid; beta Carotene; Biopsy; Cell Transformation, Neoplastic; Disease Progression; Drug Therapy, Combination; Female; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Logistic Models; Male; Middle Aged; Precancerous Conditions; Remission, Spontaneous; Risk; Stomach; Stomach Neoplasms; Treatment Outcome

A randomized chemoprevention trial on precancerous lesions of the stomach is being conducted in Tachira State, Venezuela. The aims of the study are to evaluate the efficacy of vitamin supplementation in preventing the progression rate of precancerous lesions. Here we report on the pilot phase of the study in which two antioxidant preparations were evaluated on their ability to raise antioxidant levels in plasma and in gastric juice. The study aimed also to determine the antibiotic sensitivity profiles of Helicobacter pylori isolates prevalent in the area. Forty-three subjects with precancerous lesions (chronic gastritis, chronic atrophic gastritis, intestinal metaplasia and dysplasia) of the stomach were randomized to one of two antioxidant treatments. Treatment 1 (250 mg of standard vitamin C, 200 mg of vitamin E and 6 mg of beta-carotene three times a day) or treatment 2 (150 mg of standard vitamin C, 500 mg of slow release vitamin C, 75 mg of vitamin E and 15 mg of beta-carotene once a day) for 7 days. Blood levels of total vitamin C, beta-carotene and alpha-tocopherol and gastric juice levels of ascorbic acid and total vitamin C were measured before and after treatment on day 8. Both treatments increased the plasma levels of total vitamin C, beta-carotene and alpha-tocopherol/cholesterol but not those of ascorbic acid or total vitamin C in gastric juice. Treatment 1 was the best choice and resulted in a greater increase in the plasma levels of beta-carotene and alpha-tocopherol. H. pylori was cultured from 90% of the gastric biopsies; 35 isolates were identified which were highly resistant to metronidazole, a front-line antibiotic recommended against H. pylori in other settings.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; beta Carotene; Carotenoids; Chemoprevention; Chronic Disease; Disease Progression; Female; Gastric Juice; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Middle Aged; Pilot Projects; Precancerous Conditions; Stomach Neoplasms; Venezuela; Vitamin E; Vitamins

Matrix metalloproteinases (MMPs), key molecules of cancer invasion and metastasis, degrade the extracellular matrix and cell-cell adhesion molecules. MMP-10 plays a crucial role in

Topics: beta Carotene; Catalase; Cell Line; Epithelial Cells; Gastric Mucosa; Gene Expression Regulation, Enzymologic; Helicobacter Infections; Helicobacter pylori; Humans; MAP Kinase Signaling System; Matrix Metalloproteinase 10; Matrix Metalloproteinase Inhibitors; Neoplasm Invasiveness; PPAR gamma; Reactive Oxygen Species; RNA, Messenger; Stomach Neoplasms; Transcription Factor AP-1

Helicobacter have been detected in human bile and hepatobiliary tissue. Despite evidence that Helicobacter species promote gallstone formation and hepatobiliary tumors in laboratory studies, it remains unclear whether Helicobacter species contribute to these cancers in humans. We used a multiplex panel to assess whether seropositivity to 15 Helicobacter pylori proteins was associated with subsequent incidence of hepatobiliary cancers in the Finnish Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study. We included 64 biliary cancers, 122 liver cancers, and 224 age-matched controls which occurred over the course of 22 years. Helicobacter pylori seropositivity was defined as those positive to ≥ 4 antigens. Odds ratios (OR) and 95% confidence intervals were adjusted for major hepatobiliary cancer risk factors. Among the controls, 88% were seropositive to H. pylori at baseline. Among those who subsequently developed hepatobiliary cancer, the prevalence of seropositivity was higher: 100% for gallbladder cancer, 97% of extrahepatic bile duct cancer, 91% of ampula of Vater cancer, 96% of intrahepatic bile duct cancer, and 94% of hepatocellular carcinoma. Although the OR for gallbladder cancer could not be calculated, the OR for the other sites were 7.01 (95% confidence interval [CI]: 0.79-62.33), 2.21 (0.19-25.52), 10.67 (0.76-150.08), and 1.20 (0.42-3.45), respectively, with an OR of 5.47 (95% CI: 1.17-25.65) observed for the biliary tract cancers combined. ORs above 1 were observed for many of the investigated antigens, although most of these associations were not statistically significant.. Seropositivity to H. pylori proteins was associated with an increased risk of biliary tract cancers in ATBC. Further studies are needed to confirm our findings and to determine how H. pylori might influence the risk of biliary tract cancer.

Topics: alpha-Tocopherol; beta Carotene; Biliary Tract Neoplasms; Carcinoma, Hepatocellular; Case-Control Studies; Helicobacter Infections; Humans; Liver Neoplasms; Male; Middle Aged; Randomized Controlled Trials as Topic; Vitamins

The mean count of cells with chromosome aberrations increased in a 72-h culture of peripheral blood lymphocytes of children with Helicobacter pylori-associated gastroduodenal diseases. After eradication therapy, intensification of clastogenesis was observed in the majority of children. Addition of vetoron to the treatment protocols reduced manifestations of clastogenesis.

Topics: Adolescent; beta Carotene; Child; Child, Preschool; Chromosome Aberrations; Chromosome Disorders; Duodenitis; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male

Reactive oxygen species (ROS) play critical roles in Helicobacter pylori (H. pylori)-associated gastric ulceration and carcinogenesis. Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are involved in H. pylori-induced gastric diseases. Previously we demonstrated that H. pylori in Korean isolates induced the activation of mitogen-activated protein kinases (MAPK) and oxidant-sensitive transcription factors NF-kappaB and AP-1 which mediates the expression of iNOS and COX-2 in gastric epithelial AGS cells. beta-Carotene shows antioxidant activity and inhibits NF-kappaB-dependent gene expression in various cells. Present study aims to investigate whether beta-carotene inhibits H. pylori-induced expression of iNOS and COX-2 by suppressing the activation of MAPK, NF-kappaB, and AP-1 in gastric epithelial AGS cells. HP99 (H. pylori in Korean isolates) was added to AGS cells at the ratio of bacterium/cell, 300/1. beta-carotene inhibited H. pylori-induced increase in ROS level, the activation of MAPK (p38, the c-Jun NH2-terminal protein kinases, the extracellular signal-regulated kinases), NF-kappaB, and AP-1 and the expression of iNOS and COX-2 in AGS cells.. beta-carotene inhibits oxidant-mediated activation of inflammatory signaling and suppresses the expression of iNOS and COX-2 in gastric epithelial AGS cells infected with H. pylori.

Topics: beta Carotene; Cell Line; Cyclooxygenase 2; DNA-Binding Proteins; Enzyme Activation; Epithelial Cells; Extracellular Signal-Regulated MAP Kinases; Gastric Mucosa; Gene Expression Regulation, Enzymologic; Helicobacter Infections; Helicobacter pylori; Humans; I-kappa B Kinase; Inflammation Mediators; JNK Mitogen-Activated Protein Kinases; NF-kappa B; Nitric Oxide Synthase Type II; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Reactive Oxygen Species; RNA, Messenger; Stomach Ulcer; Transcription Factor AP-1

Colonization with Helicobacter pylori is a risk factor for gastric adenocarcinoma, but the magnitude of this association and its relationship to anatomic location of the cancer, duration of follow-up, age at diagnosis, histologic subtype, and H. pylori strain differences are less clear. We conducted a prospective nested case-control study of H. pylori serology to address these questions.. Case and control subjects were selected from the 29,133 50- to 69-year-old males recruited into the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. At baseline, detailed demographic data and a serum sample were collected. From 1985 to 1999, 243 incident cases of gastric adenocarcinoma were diagnosed in cohort members. Serum samples from 234 case subjects (173 with noncardia gastric cancers and 61 with gastric cardia cancers) and 234 age-matched control subjects were assayed for antibodies against H. pylori whole-cell and CagA antigens. We fit conditional logistic regression models to estimate the unadjusted and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for the association of H. pylori seropositivity, defined as seropositivity to either whole-cell or CagA antigens, with noncardia gastric and gastric cardia cancers. All statistical tests were two-sided.. H. pylori seropositivity was strongly associated with the risk of noncardia gastric cancer (adjusted OR = 7.9, 95% CI = 3.0 to 20.9) but was inversely associated with the risk of gastric cardia cancer (adjusted OR = 0.31, 95% CI = 0.11 to 0.89). H. pylori seropositivity rates did not vary statistically significantly by length of follow-up, age at diagnosis, or histologic subtype. A calculation of rates showed that the absolute risks of noncardia gastric and cardia gastric adenocarcinomas in the H. pylori-positive participants of this cohort would be 63 and 12 per 100,000 person-years, respectively, whereas corresponding rates in H. pylori-negative participants would be 8 and 37 per 100,000 person-years, respectively.. H. pylori is a strong risk factor for noncardia gastric cancer but is inversely associated with the risk of gastric cardia cancer. These findings bolster the hypothesis that decreasing H. pylori prevalence during the past century may have contributed to lower rates of noncardia cancer and higher rates of cardia cancer in Western countries.

Topics: Adenocarcinoma; Aged; alpha-Tocopherol; Antigens, Bacterial; Antioxidants; Bacterial Proteins; beta Carotene; Cardia; Case-Control Studies; Developed Countries; Dietary Supplements; Finland; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Neoplasms; Odds Ratio; Prevalence; Primary Prevention; Prospective Studies; Randomized Controlled Trials as Topic; Risk Assessment; Risk Factors; Seroepidemiologic Studies; Stomach Neoplasms; Time Factors

Topics: Anti-Bacterial Agents; Antioxidants; Ascorbic Acid; beta Carotene; Dietary Supplements; Disease Progression; Helicobacter Infections; Helicobacter pylori; Humans; Randomized Controlled Trials as Topic; Stomach; Stomach Neoplasms; Treatment Outcome

Topics: Achlorhydria; Ascorbic Acid; beta Carotene; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia; Phenotype; Precancerous Conditions; Remission Induction; Stomach Neoplasms; Treatment Outcome

Helicobacter pylori is a human gastroduodenal pathogen associated with type-B gastritis and gastric cancer. Low gastric tissue antioxidant levels are believed to increase the risk of developing gastric cancer. We investigated whether dietary antioxidant levels protect against infection and type-B gastritis in H. pylori-infected guinea pigs.. Dunkin-Hartley guinea pigs infected for 6 weeks with H. pylori were fed diets with various antioxidant levels. Stomach specimens were cultured, and gastritis was graded from 0 to 3.. Supplementation with vitamins A, C, and E and with selenium yielded H. pylori recovery from 17% of challenged animals, compared with 43% of those fed a control diet. Gastritis was scored at 0.33 and 0.93, respectively. Supplementation with only vitamin C or astaxanthin had less effect on gastritis and recovery rate. In a second experiment, gastritis score in a group given vitamins A, C, E, and selenium and beta-carotene was 2.25 and in a control group, it was 2.57. The H. pylori recovery rate was 75 and 100%, respectively, with fewer colonies from animals given antioxidant supplementation (P < 0.05).. A combination of antioxidants can protect against H. pylori infection in guinea pigs. In animal studies, antioxidant intake should be low to optimize development of H. pylori-associated disease. Furthermore we established that H. pylori causes severe gastritis in guinea pigs.

Topics: Animals; Antioxidants; Ascorbic Acid; beta Carotene; Diet; Gastritis; Guinea Pigs; Helicobacter Infections; Helicobacter pylori; Humans; Male; Selenium; Vitamin A; Vitamin E; Vitamins

The effects of Helicobacter pylori infection and its associated gastric histology on alpha-tocopherol and beta-carotene concentrations in serum, gastric juice and antral mucosa were investigated in patients undergoing routine gastroscopy for investigation of dyspepsia.. Eighty-six patients were studied. High-performance liquid chromatography was used to measure alpha-tocopherol and beta-carotene concentrations. H. pylori infection was assessed by histology, bacterial culture, rapid urease test and serology.. No obvious association was found between age, sex, smoking or endoscopic diagnosis and alpha-tocopherol or beta-carotene concentrations in serum, gastric juice and antral mucosa. However, alcohol drinkers had significantly lower antral mucosal and gastric juice beta-carotene concentrations compared to non-drinkers. Gastric juice beta-carotene concentration was markedly lower in patients infected with H. pylori than uninfected controls (2.9 nmol/l (interquartile range 0.3-4.3) versus 4.6 nmol/l (interquartile range 3.5-7.6), P = 0.01), but there was no significant difference in serum or gastric mucosal beta-carotene concentrations between the two patient groups. The presence of gastric atrophy and intestinal metaplasia was significantly associated with reduced mucosal alpha-tocopherol and beta-carotene concentrations. Furthermore, antral mucosal alpha-tocopherol concentrations decreased progressively as antral mucosal histology changed from normal to chronic gastritis alone and finally to atrophy and intestinal metaplasia.. Gastric alpha-tocopherol and beta-carotene concentrations are affected by H. pylori-associated gastric histological changes, and these findings suggest that H. pylori infection may not only impair the protective role of vitamin C, but also of alpha-tocopherol and beta-carotene in the stomach.

Topics: Adult; Aged; Aged, 80 and over; Alcohol Drinking; Analysis of Variance; beta Carotene; Chromatography, High Pressure Liquid; Female; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Statistics, Nonparametric; Vitamin E

Helicobacter pylori infection in humans is associated with chronic type B gastritis, peptic ulcer disease, and gastric carcinoma. A high intake of carotenoids and vitamin C has been proposed to prevent development of gastric malignancies. The aim of this study was to explore if the microalga Haematococcus pluvialis rich in the carotenoid astaxanthin and vitamin C can inhibit experimental H. pylori infection in a BALB/cA mouse model. Six-week-old BALB/cA mice were infected with the mouse-passaged H. pylori strain 119/95. At 2 weeks postinoculation mice were treated orally once daily for 10 days (i) with different doses of algal meal rich in astaxanthin (0.4, 2, and 4 g/kg of body weight, with the astaxanthin content at 10, 50, and 100 mg/kg, respectively), (ii) with a control meal (algal meal without astaxanthin, 4 g/kg), or (iii) with vitamin C (400 mg/kg). Five mice from each group were sacrificed 1 day after the cessation of treatment, and the other five animals were sacrificed 10 days after the cessation of treatment. Culture of H. pylori and determination of the inflammation score of the gastric mucosae were used to determine the outcome of the treatment. Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment. Lipid peroxidation was significantly decreased in mice treated with the astaxanthin-rich algal meal and vitamin C compared with that of animals not treated or treated with the control meal. Both astaxanthin-rich algal meal and vitamin C showed an inhibitory effect on H. pylori growth in vitro. In conclusion, antioxidants may be a new strategy for treating H. pylori infection in humans.

Topics: Agar; Animals; Ascorbic Acid; beta Carotene; Carotenoids; Disease Models, Animal; Helicobacter Infections; Helicobacter pylori; Lipid Peroxidation; Mice; Mice, Inbred BALB C; Xanthophylls

Topics: Animals; Anti-Bacterial Agents; Ascorbic Acid; beta Carotene; Disease Progression; Drug Therapy, Combination; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Precancerous Conditions; Randomized Controlled Trials as Topic; Risk; Stomach Neoplasms; Treatment Outcome

Helicobacter pylori is a gram-negative bacterium affecting about half of the world population, causing chronic gastritis type B dominated by activated phagocytes. In some patients the disease evolves into gastric ulcer, duodenal ulcer, gastric cancer or MALT lymphoma. The pathogenesis is in part caused by the immunological response. In mouse models and in human disease, the mucosal immune response is characterized by activated phagocytes. Mucosal T-lymphocytes are producing IFN-gamma thus increasing mucosal inflammation and mucosal damage. A low dietary intake of antioxidants such as carotenoids and vitamin C may be an important factor for acquisition of H. pylori by humans. Dietary antioxidants may also affect both acquisition of the infection and the bacterial load of H. pylori infected mice. Antioxidants, including carotenoids, have anti-inflammatory effects. The aim of the present study was to investigate whether dietary antoxidant induced modulation of H. pylori in mice affected the cytokines produced by H. pylori specific T-cells. We found that treatment of H. pylori infected mice with an algal cell extract containing the antioxidant astaxanthin reduces bacterial load and gastric inflammation. These changes are associated with a shift of the T-lymphocyte response from a predominant Th1-response dominated by IFN-gamma to a Th1/Th2-response with IFN-gamma and IL-4. To our knowledge, a switch from a Th1-response to a mixed Th1/Th2-response during an ongoing infection has not been reported previously.

Topics: Animals; Antioxidants; beta Carotene; Cytokines; Gastritis; Helicobacter Infections; Helicobacter pylori; Interferon-gamma; Interleukin-4; Mice; Mice, Inbred BALB C; Spleen; T-Lymphocytes, Helper-Inducer; Xanthophylls

In a cross-sectional study of 634 men aged 40 to 49 years, randomly selected from five areas of Japan with different rates of gastric cancer mortality, 121 men of 624 evaluated were diagnosed as having atrophic gastritis through serum pepsinogen I < 70 ng/ml and the pepsinogen I (PGI)/pepsinogen II (PGII) ratio < 3.0. We examined the relation of Helicobacter pylori (H. pylori) antibodies and dietary factors, including plasma level of antioxidant micronutrients, to the presence of atrophic gastritis. Presence of H. pylori IgG antibodies was associated with increased risk of atrophic gastritis (odds ratio [OR] = 1.9, 95 percent confidence interval [CI] = 1.1-3.3). As the level of plasma beta-carotene increased, we found a steady decrease in the risk of atrophic gastritis (OR for second quartile = 0.7, third quartile = 0.6, fourth quartile = 0.4, with CI = 0.2-0.8). Frequent intake of yellow vegetables also was associated with lower risk, while frequent intake of soybean products was related to increased risk. Although H. pylori antibodies, beta-carotene level, and intake of soybean products were all significant in the multivariate analysis, these factors did not explain the differences in atrophic gastritis prevalence among the five regions. The analysis of these risk factors in relation to each pepsinogen marker showed that although both H. pylori infection and low plasma beta-carotene were associated with the decreased level of serum PGI/II ratio, the former was derived from the increase of PGII, which is common in early stage of atrophic gastritis, and the latter from the decrease of PGI, which is specific to severe atrophic gastritis.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Antibodies, Bacterial; Antioxidants; beta Carotene; Carotenoids; Cross-Sectional Studies; Diet; Gastritis, Atrophic; Glycine max; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Japan; Life Style; Male; Middle Aged; Pepsinogens; Prevalence; Stomach Neoplasms; Vegetables