ascorbic-acid and Helicobacter-Infections

Topics: Animals; Antioxidants; Ascorbic Acid; Carcinogenesis; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Phytochemicals; Stomach Neoplasms

Helicobacter pylori infections affect almost 50% of the world population, constituting a risk factor for benign and malignant gastrointestinal diseases. The increased resistance to antibiotic treatment against this infection represents a dilemma in the search of other therapeutic alternatives.. To determine the efficacy of the use of vitaminC and E supplements concomitantly to antibiotic treatment against H. pylori infections.. We performed a systematic review on the MedLine (PubMed), Embase and Cochrane Central Register of Clinical Trials (CENTRAL) databases, searching for studies evaluating the efficacy of vitaminC and/or E supplements in the antibiotic treatment of H. pylori infections. The primary outcome was eradication of the infection. The secondary outcome was the adverse effects. The meta-analysis was conducted using the random effects method.. Ten studies were included and analyzed in two groups. The first group, which was comprised by 973patients, compared the use of supplementation with vitaminC and E, showing that, without discriminating the number of antibiotics used, there was no relationship with the eradication of the infection (OR: 1.98 [95%CI: 0.92-4.29] P=.08). The triple or quadruple antibiotic therapy had no effect on eradication rates either (OR 1.80 [95%CI: 0.64-5.08] P=.26 and OR: 2.84 [95%CI: 0.51-15.56] P=.22, respectively). No effect on the eradication rates was observed either in the group that only assessed the use of vitaminC, comprised by 702patients (OR: 1.17 [95%CI: 0.58-2.31] P=.65). Only four studies reported adverse effects, the most common one being nausea.. Supplementation with vitaminC and E in the antibiotic treatment against H. pylori has no effect. However, the reviewed studies had several biases and differences in the dosage of the supplements and antibiotics administered.

Topics: Anti-Bacterial Agents; Ascorbic Acid; Drug Therapy, Combination; Helicobacter Infections; Helicobacter pylori; Humans; Odds Ratio; Vitamin E; Vitamins

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

The discovery of Helicobacter pylori as the cause of gastritis and peptic ulcers ushered in the modern era of research into gastritis and into acid-peptic diseases and rekindled interest in the role of ascorbic acid in the pathophysiology and treatment of gastritis and peptic ulcer disease. Here, we review historic and modern studies on ascorbic acid and gastric diseases with an emphasis on H. pylori gastritis and its sequelae. The relationship of ascorbic acid and gastritis and peptic ulcer and its complications was extensively studied during the 1930s through the 1950s. Much of this extensive literature has been effectively "lost." Ascorbic acid deficiency was associated with all forms of gastritis (e.g., autoimmune, chemical, and infectious) due in varying degrees to insufficient intake, increased metabolic requirements, and destruction within the GI tract. Importantly, gastritis-associated abnormalities in gastric ascorbic acid metabolism are reversed by H. pylori-eradication and potentially worsened by proton pump inhibitor therapy. Diets rich in naturally occurring ascorbic acid are associated with protection of the gastric corpus from atrophy and a reduction in the incidence of gastric cancer possibly through the ability of ascorbic acid to reduce oxidative damage to the gastric mucosa by scavenging carcinogenic N-nitroso compounds and free radicals and attenuating the H. pylori-induced inflammatory cascade. Ascorbic acid supplementation was possibly associated with a decreased incidence of bleeding from peptic ulcer disease. Pharmacologic doses of ascorbic acid also may improve the effectiveness of H. pylori-eradication therapy. Occasionally, looking back can help plot the way forward.

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Helicobacter Infections; Helicobacter pylori; Humans; Stomach Diseases

Vitamins C and E can act as potent antioxidants to reduce the damage caused by reactive oxygen species in gastric mucosa. Whether vitamin supplements for Helicobacter pylori eradication regimen could improve the rate of eradication remains uncertain. Therefore, we performed a meta-analysis to evaluate the efficacy of vitamins C and E supplementation for the eradication of H. pylori. Searches were conducted in the databases PubMed, EMBASE and Cochrane Library. Randomised controlled trials (RCT) that fulfilled the inclusion criteria and addressed the clinical questions of this analysis were further assessed. Of the six RCT included, five had a low methodological quality. Of the six RCT, three compared the efficacy of the eradication regimen v. eradication regimen plus vitamins C and E. The result of the meta-analysis showed a non-significant difference in the eradication rate of H. pylori between the two groups (risk ratio (RR) 0·93, P = 0·76). Another three RCT compared the eradication regimen v. eradication regimen plus vitamin C only, and there too there was no significant difference in the eradication rate (RR 0·83, P = 0·32). In conclusion, vitamins C and/or E supplements to the H. pylori eradication regimen could not improve the eradication rate. However, currently available data do not draw a definitive conclusion about the effectiveness of antioxidant vitamins on H. pylori eradication, owing to the small sample size and low-to-moderate methodological quality.

Topics: Anti-Bacterial Agents; Ascorbic Acid; Helicobacter Infections; Helicobacter pylori; Humans; Randomized Controlled Trials as Topic; Vitamin E

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

A number of study have suggested a relationship between Helicobacter pylori infection and oxidative stress in the gastric epithelium. The oxidant- induced changes in zinc, iron, and vitamin C increase susceptibility to oxidative injury. Understanding of pathophysiologic mechanisms may provide new therapeutic strategies in treatment of oxidative injury of mucosa.

Topics: Antioxidants; Ascorbic Acid; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Iron; Oxidative Stress; Zinc

Vitamin C is actively secreted in human gastric juice. Proton pump inhibitor therapy lowers the concentration of vitamin C in gastric juice and the proportion of the vitamin in its active antioxidant form i.e., ascorbic acid. This has secondary effects on intragastric nitrite chemistry, resulting in a rise in gastric juice nitrite levels. There is also some evidence that proton pump inhibitors may reduce the bioavailability of ingested vitamin C. The effect of proton pump inhibitors on vitamin C and nitrite chemistry is more marked in Helicobacter pylori-infected subjects. Proton pump inhibitors also reduce the absorption of vitamin B(12) probably by inhibiting intragastric proteolysis and, thus, its release from food required prior to binding to R-proteins and gastric intrinsic factor. Under certain circumstances, the treatment may lower serum vitamin B(12) levels. Proton pump inhibitor therapy reduces the absorption of non-heme iron and this effect has been employed in the management of hemochromatosis. It may also retard clinical response to iron supplementation.

Topics: Absorption; Ascorbic Acid; Biological Availability; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Iron; Omeprazole; Proton Pump Inhibitors; Vitamin B 12; Vitamins

Ascorbic acid, as one of the important water-soluble vitamins, is essential for a range of physiological functions, including the syntheses of collagen, carnitine and neurotransmitters. It is also an important dietary antioxidant against oxidative stress. Current information suggests that vitamin C might be protective against the development of gastric cancer. Chronic infection with Helicobacter pylori is recognized to be a significant cause of gastric adenocarcinoma. Inflammation induced by H. pylori infection in the stomach not only causes significantly enhanced consumption of vitamin C, but also reduces secretion of the vitamin into the gastric lumen. Most of the evidence relating to vitamin C and H. pylori infection derives from clinical studies and experiments directly examining the effect of vitamin C on H. pylori-associated gastric carcinogenesis and remains limited. Furthermore, results from recent studies suggest that vitamin C might also increase the risk of cancer through its pro-oxidant activity and protect against oxidative stress in cancer cells through its antioxidant action. In this article we review recent publications on vitamin C research and assess the potential roles of vitamin C in H. pylori associated gastric carcinogenesis. The possible adverse effects of the vitamin C are also discussed.

Topics: Adenocarcinoma; Animals; Antioxidants; Ascorbic Acid; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Oxidative Stress; Risk Factors; Stomach Neoplasms; T-Lymphocytes

Topics: Anti-Bacterial Agents; Antioxidants; Ascorbic Acid; Gastritis, Atrophic; Helicobacter Infections; Humans; Precancerous Conditions; Stomach; Stomach Neoplasms

Intestinal metaplasia (IM) of the stomach is a risk factor in developing intestinal-type gastric cancer and hence the question of reversibility is vital. There is emerging epidemiological evidence that with long term follow up, IM may be reversible although a combination of antioxidant agents and eradication of H pylori may be necessary to achieve this. The pathogenesis of IM is currently being elucidated and it is likely that a combination of bacterial, host, and environmental factors will be shown to lead to IM. In assessing gastric cancer risk, histochemical typing of IM will most probably be replaced by molecular markers.

Topics: Alleles; Anti-Bacterial Agents; Ascorbic Acid; CDX2 Transcription Factor; Helicobacter Infections; Helicobacter pylori; Homeodomain Proteins; Humans; Intestines; Metaplasia; Microsatellite Repeats; Precancerous Conditions; Risk; Smoking; Stomach; Stomach Neoplasms; Trans-Activators

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

Recent studies have suggested a relationship between Helicobacter pylori infection and various important micronutrients, including iron and vitamin B12, suggesting likely biological factors in the association between Helicobacter pylori and microcytic or macrocytic anaemia. There is some evidence that direct or indirect consequences of Helicobacter pylori gastritis on acid secretion account for the role of the bacterium in the absorption process of iron and Vitamin B12. The plasma, intragastric and mucosal concentration of different antioxidant compounds such as ascorbic acid, a-tocopherol and beta-carotene is also affected by Helicobacter pylori gastritis supporting the possible role of Helicobacter pylori in the multistep cascade leading to gastric carcinogenesis. The relationship between Helicobacter pylori infection and micronutrients is, therefore, a promising and, until now, poorly investigated field of research.

Topics: Antioxidants; Ascorbic Acid; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Absorption; Iron; Micronutrients; Selenium; Vitamin A; Vitamin B 12; Vitamin E

Vitamin C's role in the prevention of disease and malignancy has been studied over the last several decades. Vitamin C intake has been shown to have an inverse relationship with gastric cancer. Recent follow-up studies on high-risk populations suggest that ascorbic acid, the reduced form of vitamin C, protects against gastric cancer, for which H. pylori is a significant risk factor. In populations infected with H. pylori, there is a reduction in gastric juice ascorbic acid concentration. This article reviews the risk factors for gastric cancer and the role of vitamin C in prevention of the disease.

Topics: Ascorbic Acid; Disease Progression; Free Radical Scavengers; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Risk Factors; Stomach Neoplasms

Topics: Antioxidants; Ascorbic Acid; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Lymphocytes; Stomach Neoplasms

Topics: Anticarcinogenic Agents; Ascorbic Acid; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Stomach Neoplasms

A review of the literature reveals a very consistent association between gastric cancer risk and low intake of fruits and vegetables. This observation has been documented in many countries with different epidemiological techniques: interpopulation correlations, case-control studies and follow up of several cohorts. Low serum levels of beta-carotene and alpha-tocopherol, but not vitamin C, have been reported in patients with gastric dysplasia. Helicobacter pylori infection has been associated with lower concentrations of vitamin C in the gastric juice. Detailed studies in Colombia and New Orleans have shown a gradient towards lower concentration in the gastric juice and lower ratios of gastric juice to serum concentration of vitamin C in the following comparisons: i) lower vs. higher gastric cancer risk; ii) mild vs. advanced gastric precancerous histopathologic lesions; iii) mild vs. advanced degree of atrophy; iv) mild vs. advanced damage to the surface gastric epithelium; v) lower vs. higher gastric pH. Such a gradient is not observed for serum levels of vitamin C. The role of infection with H. pylori in the metabolism of ascorbic acid is discussed, as well as the possible role of ascorbic acid in inhibiting cell damage by reactive oxygen species.

Topics: Antioxidants; Ascorbic Acid; Diet; Fruit; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Incidence; Stomach Neoplasms; Vegetables

Helicobacter pylori infection is now recognized to be an important acquired factor in the pathogenesis of duodenal ulcer disease. There is also an association between H pylori and the subsequent development of gastric cancer. The mechanism of the association between the infection and those disorders is incompletely understood but there is increasing evidence that H pylori-induced disturbances of gastric function play a pivotal role. In this article we review the role of H pylori infection in the pathophysiology of these important upper gastrointestinal diseases.

Topics: Ascorbic Acid; Duodenal Ulcer; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Stomach Neoplasms

Topics: Ascorbic Acid; Cell Division; Cell Transformation, Neoplastic; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Stomach; Stomach Neoplasms

In many Western developed countries, the incidence of stomach cancer has declined dramatically. This decrease was an extraordinary, "unplanned triumph", especially when compared to other cancers. Stomach cancer is still the most prevalent malignant tumor in Korea. Most Koreans carry Helicobacter pylori in their stomach. Thus, a new hypothesis, based on the relationship between the host and Helicobacter pylori, is presented as the carcinogenesis of human stomach cancer. The reasons for why the N-nitrosamide hypothesis should be dismissed as the etiology of stomach cancer, and why the contemporarily available principles and practice of intervention strategies to rapidly decrease the surprisingly high prevalence rate of Helicobacter pylori infection are impractical at this moment, are explained. In order to introduce an alternative provisional strategy of the "planned triumph" for the population vulnerable to stomach cancer, vitamin C is defined as an anti-inflammatory agent on the basis of the pathogenesis of Helicobacter pylori infection.

Topics: Animals; Ascorbic Acid; Helicobacter Infections; Helicobacter pylori; Humans; Nitroso Compounds; Stomach Neoplasms

Topics: Ascorbic Acid; Duodenal Ulcer; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Stomach Neoplasms; Virulence

Topics: Antacids; Anti-Ulcer Agents; Ascorbic Acid; Gastric Acid; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Intestine, Small; Risk Factors; Stomach; Stomach Neoplasms

Evidence has shown that both C-reactive protein (CRP) and serum amyloid component A (SAA) are increased in individuals with gastritis and stomach cancer. Controlling the level of these biomarkers by inhibiting the gastric infection with high doses of ascorbic acid may reduce the risk of carcinogenesis. A population-based double-blind randomised controlled trial in a Japanese population with atrophic gastritis in an area of high stomach cancer incidence was conducted between 1995 and 2000. Daily doses of 50 or 500 mg vitamin C were given, and 120 and 124 participants completed the 5-year study, respectively. Although serum ascorbic acid was higher in the high-dosage group (1.73 (SD 0.46) μg/l) than in the low-dosage group (1.49 (SD 0.29) μg/l, P< 0.001), at the end of the study, no significant difference was observed for CRP between the low- and high-dosage groups (0.39 (95 % CI 0.04, 4.19) mg/l and 0.38 (95 % CI 0.03, 4.31) mg/l, respectively; P= 0.63) or for SAA between the low- and high-dosage groups (3.94 (95 % CI 1.04, 14.84) μg/ml and 3.85 (95 % CI 0.99, 14.92) μg/ml, respectively; P= 0.61). Vitamin C supplementation may not have a strong effect on reducing infections in individuals with atrophic gastritis.

Topics: Adult; Aged; Ascorbic Acid; C-Reactive Protein; Dietary Supplements; Double-Blind Method; Female; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Japan; Male; Middle Aged; Serum Amyloid A Protein; Stomach Neoplasms

Helicobacter pylori eradication rates of currently accepted triple therapy regimens vary between geographic locations and do not exceed 70-80%. Eradication rates are much lower in locations where uncontrolled antibiotic use is common such as Turkey. In the present study, we aimed to test whether supplementing vitamins C and E to standard triple therapy, including a proton pump inhibitor plus amoxicillin plus clarithromycin, increased the H. pylori eradication rate.. Two hundred patients infected with H. pylori were randomized into two groups in an open-label trial. In group A, patients (n = 160) were given standard triple therapy, including lansoprazole 30 mg BID plus amoxicillin 1000 mg BID plus clarithromycin 500 mg BID for 14 days, plus vitamin C 500 mg BID plus vitamin E 200 IU BID for 30 days. In group B, patients (n = 40) were given standard triple therapy for 14 days. The success of H. pylori eradication was defined as a negative ¹⁴C-urea breath test result, 4-6 weeks after the completion of therapy. Comaprisons were by both intention-to-treat (ITT) and per-protocol (PP) analysis.. Two hundred patients (137 women, 63 men) were analysed using ITT analysis and 195 patients completed the study. In group A, H. pylori eradication was achieved in 132 of the 160 patients (82·5%) included in ITT analysis and 132 of the 157 patients (84%) included in PP analysis. In group B, H. pylori eradication was achieved in 18 of the 40 patients (45%) included in ITT analysis and 18 of the 38 patients (47·4%) included in PP analysis. Eradication rates were significantly higher in group A than in group B (P < 0·005). Eradication rates were not statistically significant between men and women in both groups.. Adding vitamins C and E to standard triple therapy increases the eradication rate of H. pylori. Vitamins C and E may increase the eradication rate via increasing the effectiveness of the antibiotics by decreasing oxidative stress in the gastric mucosa and strengthening the immune system.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Amoxicillin; Anti-Bacterial Agents; Ascorbic Acid; Clarithromycin; Combined Modality Therapy; Dietary Supplements; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Intention to Treat Analysis; Lansoprazole; Male; Middle Aged; Outpatient Clinics, Hospital; Proton Pump Inhibitors; Turkey; Vitamin E

In the Shandong Intervention Trial, 2 weeks of antibiotic treatment for Helicobacter pylori reduced the prevalence of precancerous gastric lesions, whereas 7.3 years of oral supplementation with garlic extract and oil (garlic treatment) or vitamin C, vitamin E, and selenium (vitamin treatment) did not. Here we report 14.7-year follow-up for gastric cancer incidence and cause-specific mortality among 3365 randomly assigned subjects in this masked factorial placebo-controlled trial. Conditional logistic regression was used to estimate the odds of gastric cancer incidence, and the Cox proportional hazards model was used to estimate the relative hazard of cause-specific mortality. All statistical tests were two-sided. Gastric cancer was diagnosed in 3.0% of subjects who received H pylori treatment and in 4.6% of those who received placebo (odds ratio = 0.61, 95% confidence interval = 0.38 to 0.96, P = .032). Gastric cancer deaths occurred among 1.5% of subjects assigned H pylori treatment and among 2.1% of those assigned placebo (hazard ratio [HR] of death = 0.67, 95% CI = 0.36 to 1.28). Garlic and vitamin treatments were associated with non-statistically significant reductions in gastric cancer incidence and mortality. Vitamin treatment was associated with statistically significantly fewer deaths from gastric or esophageal cancer, a secondary endpoint (HR = 0.51, 95% CI = 0.30 to 0.87; P = .014).

Topics: Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Ascorbic Acid; China; Confounding Factors, Epidemiologic; Dietary Supplements; Factor Analysis, Statistical; Female; Follow-Up Studies; Garlic; Gastrointestinal Agents; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Logistic Models; Male; Middle Aged; Odds Ratio; Omeprazole; Precancerous Conditions; Proportional Hazards Models; Stomach Neoplasms; Vitamin E; Vitamins

We aimed to evaluate the changes in histopathologic features, concentrations of vitamins C and E in gastric mucosa, and total antioxidant capacity of the body after ingestion of ascorbic acid and alpha tocopherol in patients with Helicobacter pylori.. Patients with H. pylori-positive nonulcer dyspepsia were included in this study. Tissue samples were taken from the lesser and greater curvature in both prepyloric antrum and corpus for histopathologic examination and measurement of vitamins C and E concentrations. Blood samples were obtained for measurement of the total antioxidant capacity of the body. The patients were given vitamin C 500 mg BID and vitamin E 200 IU BID for 4 weeks orally. At the end of the 4th week, the initial procedures were repeated. Histopathologic examination of the tissue samples were carried out by two pathologists.. The mean vitamins C and E concentrations in gastric mucosa at the 4th week were higher than those at the beginning (p = .000 and p = .006, respectively). Mean total antioxidant capacity of the body at the beginning and that at the 4th week were similar (p = .689). H. pylori intensity in the antrum at the beginning was higher than that at the 4th week for both pathologists (p = .007 and p = .039). Neutrophilic activity in the antrum at the beginning was higher than that at the 4th week for both pathologists (p = .000 and p = .025). Neutrophilic activity in the corpus at the beginning was higher than that at the 4th week for pathologist 1 (p = .033), and they were similar for pathologist 2 (p = .763).. The findings that H. pylori intensity and neutrophilic activity decrease through increasing gastric ascorbic acid and alpha tocopherol concentrations suggest that supplementation with vitamins C and E increases the eradication rates via impairing the microenvironment created by the bacteria and facilitating the diffusion of antibiotics into gastric mucosa.

Topics: Adult; alpha-Tocopherol; Ascorbic Acid; Dietary Supplements; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Young Adult

It was shown that supplementation of vitamins C and E to therapy increased Helicobacter pylori eradication rate. In the present study, we aimed to evaluate whether supplementation of antioxidant vitamins to therapy increases H. pylori eradication rates in patients with chronic stress and low antioxidant capacity.. This study included 120 patients who presented to gastroenterology outpatient clinic with H. pylori-positive nonulcer dyspepsia and low total antioxidant capacity. Patients in group A (n=80) were given lansoprazole (30 mg, BID), amoxicillin (1000 mg, BID), and clarithromycin (500 mg, BID) for 14 days, as well as vitamin C (500 mg, BID) and vitamin E (200 IU, BID) for 30 days. Patients in group B (n=40) were given lansoprazole (30 mg, BID), amoxicillin (1000 mg, BID), and clarithromycin (500 mg, BID) for 14 days.. Total antioxidant capacity were lower than normal levels in all patients. One hundred and fifteen patients (77 in group A, 38 in group B) were analyzed with per protocol analysis. In group A, H. pylori eradication was achieved in 63.8% of the patients included in the intention to treat analysis and in 66.2% of the patients included in the per protocol analysis. In group B, H. pylori eradication was achieved in 42.5% of the patients included in the intention to treat analysis and in 44.7% of the patients included in the per protocol analysis. Eradication rates were significantly higher in group A than in group B (P<0.005).. Supplementation with vitamins C and E increased H. pylori eradication rate of standard triple therapy.

Topics: Adult; Antioxidants; Ascorbic Acid; Dietary Supplements; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Vitamin E

Manganese superoxide dismutase is the primary antioxidant enzyme in the mitochondria and is involved in carcinogenesis. To investigate the association between MnSOD Val(16)Ala polymorphism and risk of advanced gastric lesions, and its effects on chemoprevention, a population-based study was conducted in Linqu, a high-risk area of gastric cancer in China.. Genotypes were determined by PCR-RFLP analysis in 3,355 subjects with the baseline histopathologic diagnosis in 1994, and 2,758 of these subjects received subsequent three interventions including vitamin supplementation for 7.3 years. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by unconditional logistic regression model.. We found an increased risk of dysplasia in subjects with the Val/Ala+Ala/Ala genotype (OR, 1.31; 95% CI, 1.02-1.68) compared with the Val/Val genotype. Stratified analysis indicated that a significantly elevated risk of intestinal metaplasia (OR, 3.40; 95% CI, 2.64-4.38) or dysplasia (OR, 4.01; 95% CI, 2.79-5.74) was found in subjects carrying the Val/Ala+Ala/Ala genotype and Helicobacter pylori infection, and an interaction between this genotype and a high serum H. pylori IgG titer (>2.94) on the risk of dysplasia was observed (P(interaction) = 0.01). Furthermore, an elevated chance for regression of gastric lesions was observed in subjects with the Val/Ala+Ala/Ala genotype and high IgG titer in an intervention trial with vitamin supplementation (OR, 2.45; 95% CI, 1.37-4.38).. These findings suggest that Val(16)Ala polymorphism may play an important role in development of advanced gastric lesions and modify the effect of vitamin supplementation on the evolution of gastric lesions.. Val(16)Ala polymorphism is related to gastric cancer development.

Topics: Adult; Ascorbic Acid; Asian People; Dietary Supplements; Female; Garlic; Genetic Predisposition to Disease; Helicobacter Infections; Humans; Male; Middle Aged; Polymerase Chain Reaction; Polymorphism, Restriction Fragment Length; Polymorphism, Single Nucleotide; Precancerous Conditions; Selenium; Stomach Neoplasms; Superoxide Dismutase; Vitamin E; Vitamins

Vitamin C in gastric juice and in vitro has been shown to inhibit the growth of Helicobacter pylori (H. pylori).. The purpose of this study was to investigate the effect of addition of vitamin C to eradication regimen on H. pylori eradication rate.. This randomised controlled clinical trial was conducted on 312 patients with H. pylori infection who had referred to the Taleghani Research Center of Gastroenterology and Liver Disease.. Patients were randomly divided into two groups. Group A patients (162 patients) received amoxicillin 1g and metronidazole 500 mg b.i.d., bismuth 240 mg b.i.d. and omeprazole 40 mg q.i.d. in two divided doses. Patients in group B (150 patients) received the same regimen plus 500 mg vitamin C per day. All patients received therapy for 2 weeks. Four weeks later all patients underwent urea breath test and results were compared.. A total of 140 patients in group A and 141 in group B completed the study. On intention-to-treat analysis 48.8% of patients in group A in comparison to 78% in group B responded to eradication therapy and had negative urea breath test (p<0.0001).. Addition of vitamin C to H. pylori treatment regimen of amoxicillin, metronidazole and bismuth can significantly increases H. pylori eradication rate.

Topics: Adolescent; Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Anti-Infective Agents; Anti-Ulcer Agents; Ascorbic Acid; Bismuth; Dietary Supplements; Drug Therapy, Combination; Endoscopy, Gastrointestinal; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Omeprazole; Young Adult

This study aims to assess the antioxidant property of vitamins E and C in Helicobacter pylori infection, and to determine if adding them to standard triple therapy plus bismuth subcitrate increases the H. pylori eradication rate.. This study included 160 patients infected with H. pylori, who were randomized into one of two groups. Patients in group A (n = 80) received lansoprazole (30 mg, b.i.d.), amoxicillin (1000 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and bismuth subcitrate (300 mg, q.i.d.) for 14 days, while patients in group B (n = 80) received vitamin C (500 mg, b.i.d.) and vitamin E (200 IU, b.i.d.) for 30 days, in addition to lansoprazole (30 mg, b.i.d.), amoxicillin (1000 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and bismuth subcitrate (300 mg, q.i.d.) for 14 days. Total antioxidant capacity (TAC) was evaluated with a Randox kit. Success rate was calculated using both intention-to-treat (ITT) and per-protocol (PP) analyses.. One hundred and sixty patients were analyzed using ITT analysis. One hundred and fifty-three patients completed the study. In group A, H. pylori eradication was achieved in 48 (60%) of the 80 patients included in the ITT analysis, and in 48 (64%) of the 75 patients included in the PP analysis. In group B, H. pylori eradication was achieved in 73 (91.25%) of the 80 included in the ITT analysis and in 73 (93.5%) of the 78 patients included in the PP analysis. The eradication rate was significantly higher in group B than in group A (p < .005). TAC was at the lower limit of normal in both groups and the difference between them was not statistically significant (p > .05).. In group B, H. pylori eradication rate was 91.25%, which is higher than the ideal 80% eradication rate. The results of the present study show that adding the prescribed doses of vitamins E and C to antimicrobial therapy is effective in eradicating H. pylori infection.

Topics: Adult; Antioxidants; Ascorbic Acid; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Organometallic Compounds; Oxidative Stress; Treatment Outcome; Vitamin E

Although a number of reports regarding the role of reactive oxygen species (ROS) as the first step in cancer induction exist, few studies have investigated how vitamin C influences ROS in human plasma.. Using the ROS assay system, a method recently established by one of the authors, we aimed to evaluate the effect of vitamin C supplementation on serum ROS among subjects diagnosed with chronic gastritis.. A total of 244 Japanese subjects with atrophic gastritis were randomized to take 5-year supplementation of either 50 mg or 500 mg of vitamin C.. The adjusted difference in the changes of total ROS between baseline and after 5-year supplementation was statistically significant between the intervention groups: 2.70 decrease (corresponds to 1.26% decrease) in the high-dose group and 4.16 increase (corresponds to 3.79% increase) in the low-dose group, p for difference = 0.01.. Vitamin C was suggested to reduce oxidative stress among subjects with atrophic gastritis.

Topics: Adult; Aged; Analysis of Variance; Antioxidants; Ascorbic Acid; Chronic Disease; Dietary Supplements; Dose-Response Relationship, Drug; Female; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Oxidative Stress; Reactive Oxygen Species

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

Randomized trials have yielded mixed results on the effects of treatment for Helicobacter pylori and little information on the effects of vitamins or garlic supplements on precancerous gastric lesions. We conducted a randomized trial to test the effects of one-time H. pylori treatment and long-term vitamin or garlic supplements in reducing the prevalence of advanced precancerous gastric lesions.. Most of the adults aged 35-64 years in 13 randomly selected villages in Linqu County, Shandong Province, China, were identified and given baseline endoscopies in 1994. In 1995, 3365 eligible subjects were randomly assigned in a factorial design to three interventions or placebos: amoxicillin and omeprazole for 2 weeks in 1995 (H. pylori treatment); vitamin C, vitamin E, and selenium for 7.3 years (vitamin supplement); and aged garlic extract and steam-distilled garlic oil for 7.3 years (garlic supplement). Subjects underwent endoscopies with biopsies in 1999 and 2003, and the prevalence of precancerous gastric lesions was determined by histopathologic examination of seven standard biopsy sites. The 3365 eligible randomized subjects represented 93.5% of those with baseline endoscopy and included all baseline histologic categories except gastric cancer. Only 0.18% had normal gastric mucosa. Logistic regression was used to estimate the intervention effects on the odds of advanced precancerous gastric lesions, and t-tests were used to assess effects on histologic severity. All statistical tests were two-sided.. H. pylori treatment resulted in statistically significant decreases in the combined prevalence of severe chronic atrophic gastritis, intestinal metaplasia, dysplasia, or gastric cancer in 1999 (odds ratio [OR] = 0.77; 95% confidence interval [CI] = 0.62 to 0.95) and in 2003 (OR = 0.60; 95% CI = 0.47 to 0.75), and had favorable effects on the average histopathologic severity and on progression and regression of precancerous gastric lesions in 2003. H. pylori treatment did not reduce the combined prevalence of dysplasia or gastric cancer. However, fewer subjects receiving H. pylori treatment (19/1130; 1.7%) than receiving placebo (27/1128; 2.4%) developed gastric cancer (adjusted P = .14). No statistically significant favorable effects were seen for garlic or vitamin supplements.. H. pylori treatment reduces the prevalence of precancerous gastric lesions and may reduce gastric cancer incidence, but further data are needed to prove the latter point. Long-term vitamin or garlic supplementation had no beneficial effects on the prevalence of precancerous gastric lesions or on gastric cancer incidence.

Topics: Adult; Amoxicillin; Ascorbic Acid; China; Disease Progression; Double-Blind Method; Drug Therapy, Combination; Factor Analysis, Statistical; Female; Garlic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Logistic Models; Male; Middle Aged; Omeprazole; Phytotherapy; Precancerous Conditions; Prevalence; Selenium; Severity of Illness Index; Stomach Neoplasms; Vitamin E

In the 1-year double-blind placebo-controlled intervention trial, it was shown that daily supplementation of patients with gastric premalignant lesions (intestinal metaplasia, IM) with a complex, containing Ester-C with antioxidantsand (2100 mg of Ca-ascorbate + 340 mg of bioflavonoids), produced a sharp decrease of abnormally high ornithine decarboxylase activity in IM gastric mucosa that was accom panied by practically total IM regression in 11 of 18 (61%) patients.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; Chronic Disease; Double-Blind Method; Female; Gastric Mucosa; Gastritis, Atrophic; Helicobacter Infections; Humans; Intestines; Male; Metaplasia; Middle Aged; Ornithine Decarboxylase

Aspirin (ASA) represents an important risk factor for gastric mucosal injury. Recently, vitamin C releasing aspirin (ASA-VitC) has been shown to reduce gastric toxicity of ASA in animal model of gastric injury. The aim of the present study was to compare the effect of ASA and ASA-VitC on the gastric mucosal damage before and after Helicobacter pylori (Hp) eradication in 10 young healthy Hp-positive volunteers. All subjects underwent endoscopy at day 0 (before ASA or ASA-VitC treatment) and at day 3 following treatment (1.6 g ASA/day or 1.6 g ASA + 0.96 g Vit C/day). In addition, in vitro experiments were performed in which gastric mucosal cell line (MKN-45 cells) was incubated with ASA or ASA-VitC alone or in combination with H.pylori. Expression of constitutive and inducible NO synthase (cNOS, iNOS) was analyzed by Western blot. Moreover, COX-2 expression was analyzed in gastric biopsies at mRNA and protein level by RT-PCR and Western blot, respectively. In humans, treatment with ASA-VitC induced significantly less gastric mucosal lesions than plain ASA. Furthermore, in comparison to plain ASA, ASA-VitC caused stronger inhibition of cNOS and increase in iNOS expression in the gastric mucosa. In vitro studies demonstrated a significant increase in iNOS expression in MKN-45 cells incubated with Hp. This effect was aggravated by the addition of ASA, but not ASA-VitC, to MKN-45 cells incubated with H.pylori. Both ASA and ASA-VitC stimulated the COX-2 expression in the gastric mucosa. We conclude that ASA-VitC in comparison with ASA induces less gastric mucosal damage and this protective effect may be due to its inhibitory effect on iNOS expression.

Topics: Adolescent; Adult; Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; Aspirin; Cells, Cultured; Cyclooxygenase 2; Drug Interactions; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Male; Nitric Oxide Synthase Type II; RNA, Messenger

The gastric juice concentration of vitamin C is reduced in subjects with elevated intragastric pH. This is probably because of the fact that the vitamin is unstable at non-acidic pH and undergoes irreversible denaturation.. To determine whether elevation of intragastric pH reduces the bioavailability of dietary vitamin C.. Plasma vitamin C was measured before and after a course of omeprazole 40 mg/day for 4 weeks in 14 Helicobacter pylori positive and 15 H. pylori negative subjects. Dietary intake of vitamin C was measured and intragastric pH monitored.. Compared with the H. pylori negative subjects, H. pylori positive subjects had a lower mean daily vitamin C intake (141.7 mg vs. 41.5 mg, P < 0.01) and also lower plasma vitamin C concentration (25.1 microg/mL vs. 17.4 microg/mL, P < 0.0001). After 28 days of 40 mg/day of omeprazole the mean plasma vitamin C level had fallen by 12.3% (P = 0.04). This fall affected both the H. pylori positive and negative subjects.. We have shown that a short course of omeprazole will cause a reduction in the plasma vitamin C level of healthy volunteers. This decrease in plasma vitamin C is independent of dietary intake of the vitamin and indicates reduced bioavailability. The clinical significance of this is unclear but any adverse effects will be most apparent in H. pylori infected subjects who have a low pre-treatment vitamin C status.

Topics: Ascorbic Acid; Biological Availability; Enzyme Inhibitors; Female; Gastric Acid; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Omeprazole; Proton Pump Inhibitors

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

We conducted a population-based, double-blind, randomized controlled trial to examine the effect of vitamin C supplementation on serum pepsinogen (PG) level, Helicobacter pylori (H. pylori ) infection, and cytotoxin-associated gene A (Cag A) status. Subjects aged 40 to 69 years living in one village in Akita prefecture, a high-risk area for gastric cancer in Japan, were recruited through annual health check-up programs. Among 635 subjects diagnosed as having chronic gastritis on the basis of serum PG levels, after excluding ineligible cases, 439 subjects were assigned to one of four groups using a 2 x 2 factorial design (0 or 15 mg/day beta-carotene and 50 or 500 mg/day vitamin C). However, based on the results from two beta-carotene trials in the United States, we discontinued beta-carotene (vitamin C supplementation was continued). Finally, 120 subjects in the low-dose group (vitamin C 50 mg), and 124 subjects in the high-dose group (vitamin C 500 mg) completed the 5-year supplementation. The difference in the change of PGI/II ratio between baseline and after 5-year follow up was statistically significant between the intervention groups among those who completed the supplementation: - 0.25 for the low-dose group and - 0.13 for the high-dose group (P = 0.046). To conclude, vitamin C supplementation may protect against progression of gastric mucosal atrophy.

Topics: Administration, Oral; Adult; Aged; Antigens, Bacterial; Ascorbic Acid; Bacterial Proteins; Chronic Disease; Dietary Supplements; Double-Blind Method; Female; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Time Factors

To test whether vitamin C and E supplements to triple therapy can improve the Helicobacter pylori eradication rate and gastric inflammation.. A total of 104 H. pylori-infected patients were randomized to receive: either lansoprazole, amoxicillin, and metronidazole twice daily for 1 week (triple-only group) or lansoprazole, amoxicillin, metronidazole plus vitamin C (250 mg) and vitamin E (200 mg) twice daily for 1 week, followed immediately by vitamin C and E once daily for 6 consecutive weeks (triple-plus-vitamin group). Eight weeks after the completion of triple therapy, patients were assessed for the effectiveness of H. pylori eradication. The severity of gastric inflammation in histology was assessed for the acute and chronic inflammation scores.. Intention-to-treat and per-protocol eradication rates were 59.1% and 64.4% in the triple-only group, and 40% and 44% in the triple-plus-vitamin group. In the patients infected with metronidazole susceptible isolates, the triple-only group had a higher intention-to-treat eradication rate than those in the triple-plus-vitamin group (80% vs. 53.1%, p <.01). However, for the metronidazole resistance isolates, the intention-to-treat eradication rates between the two groups were not different (26.3% vs. 21.7%, p = NS). The improvements of both acute and chronic inflammation scores in histology were not different between the two groups.. Adding vitamin C and E to triple therapy cannot improve the H. pylori eradication rate and gastric inflammation. For patients with metronidazole susceptible strain infection, adding these vitamins may even reduce the eradication rate of triple therapy.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Amoxicillin; Anti-Bacterial Agents; Ascorbic Acid; Dietary Supplements; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Lansoprazole; Male; Metronidazole; Omeprazole; Severity of Illness Index; Stomach Diseases; Treatment Outcome; Vitamin E

Reactive oxygen species have been implicated in Helicobacter pylori-mediated gastric carcinogenesis, whereas diets high in antioxidant vitamins C and E are protective. We have examined the effect of vitamin C and E supplements in combination with H. pylori eradication on reactive oxygen species activity in H. pylori gastritis. H. pylori-positive patients were randomized into four groups: triple therapy alone (Bismuth chelate, tetracycline, and metronidazole for 2 weeks), vitamins alone (200mg vitamin C and 50mg vitamin E, both twice per day for 4 weeks), both treatments or neither. Plasma and mucosal ascorbic acid, malondialdehyde and reactive oxygen species were determined before and after treatment. Compared with normal controls (n 61), H. pylori-positive patients (n 117) had higher mucosal reactive oxygen species and malondialdehyde levels and lower plasma ascorbic acid. Plasma ascorbic acid doubled in both groups of patients receiving vitamins and mucosal levels also increased. Malondialdehyde and reactive oxygen species fell in patients in whom H. pylori was eradicated but vitamin supplements were not effective either alone or in combination with H. pylori eradication. Supplements of vitamins C and E do not significantly reduce mucosal reactive oxygen species damage in H. pylori gastritis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; Double-Blind Method; Drug Therapy, Combination; Follow-Up Studies; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Malondialdehyde; Middle Aged; Reactive Oxygen Species; Vitamin E; Vitamins

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

Intestinal type metaplasia plays a role in intestinal type gastric carcinoma development. Ascorbic acid demonstrates a protective effect against gastric carcinogenesis, due to its ability to inactivate oxygen free-radicals as well as its nitrite-scavenging effects.. To assess whether long-term ascorbic acid administration following Helicobacter pylori eradication could affect intestinal metaplasia regression in the stomach.. Sixty-five patients were included in the study. The inclusion criterion was the presence of intestinal metaplasia on the gastric mucosa after H. pylori eradication. An upper gastrointestinal endoscopy was performed and 3 biopsy specimens were taken in the antrum, 3 in the gastric body, and 2 in the incisura angularis. Patients were randomized to receive 500 mg of ascorbic acid o.d., after lunch (32 patients) for 6 months or no treatment (33 patients). All patients underwent to endoscopic control at the end of the 6 months.. H. pylori infection recurrence was detected in 6 (9.4%) patients (three from each group), and these patients were excluded from further analysis. We were unable to find evidence of intestinal metaplasia in any biopsied site of the gastric mucosa in 9/29 (31%) patients from the ascorbic acid group and in 1/29 (3.4%) of the patients from the control group (P=0.006). Moreover, a further six (20.7%) patients from the ascorbic acid group presenting chronic inactive pangastritis with widespread intestinal metaplasia at entry, showed less extensive antritis with intestinal metaplasia at control, whilst a similar finding was only seen in one patient from the control group (P=0.051).. The administration of ascorbic acid significantly helps to resolve intestinal metaplasia of the gastric mucosa following H. pylori eradication, and its use as a chemoprevention treatment should be considered.

Topics: Adult; Aged; Ascorbic Acid; Female; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Diseases; Male; Metaplasia; Middle Aged; Prospective Studies; Recurrence; Stomach Diseases

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

Low gastric juice total vitamin C concentration in the presence of Helicobacter pylori infection probably plays a role in gastric carcinogenesis. Vitamin C plays a role in the neutralization of various pathogenic factors connected with H. pylori infection, including the destruction of free radicals, which damage tissues and cell DNA, and inhibition of the formation of N-nitroso compounds, which have a strong carcinogenic activity. The aim of the study was to determine whether tobacco smoking had any effect on gastric juice vitamin C concentration in healthy subjects and in patients infected with H. pylori. Eighty-six patients with dyspeptic symptoms undergoing routine endoscopy entered the study after giving informed consent. In all patients plasma and gastric juice total vitamin C levels were measured by a spectrophotometric method. They were entered into four groups: group I (controls) - H. pylori-negative non-smokers (n = 17), group II - H. pylori-negative smokers (n = 16), group III - non-smokers with H. pylori infection (n = 21), and group IV - H. pylori-infected smokers (n = 32). In the control group (I) the mean gastric juice total vitamin C concentration was 17.1 microg/ml (range 5.3-40.0 microg/ml), which was significantly higher (P < 0.05) than in group II (12.6 microg/ml, range 5.1-21.0 microg/ml), group III (5.8 microg/ml range 2.1-13.7 microg/ml) and group IV (3.9 microg/ml, range 1.1-10.6 microg/ml) (P < 0.001). Statistically significant differences also were noted between groups II and III (P < 0.01) and groups II and IV (P < 0.001) and between groups III and IV (P < 0.05). These results demonstrate that the concentration of vitamin C in gastric juice is significantly lower in smokers than in non-smokers. This was observed in healthy subjects as well as H. pylori-infected patients. This phenomenon may be one of the mechanisms whereby smoking contributes to the production of gastric lesions, impairs healing of peptic ulcers and also increases the recurrence rate of peptic ulcers in cases with H. pylori infection.

Topics: Adult; Ascorbic Acid; Female; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Nicotiana; Plants, Toxic; Smoking

In the fall of 1995, 3411 subjects in 13 rural villages in Linqu County, Shandong Province, China, began participating in a blinded, randomized 23 factorial trial to determine whether interventions can reduce the prevalence of dysplasia and other precancerous gastric lesions. One intervention is treatment for infection by Helicobacter pylori with amoxicillin and omeprazole. A second is dietary supplementation with capsules containing vitamin C, vitamin E, and selenium. A third is dietary supplementation with capsules containing steam-distilled garlic oil and Kyolic aged garlic extract. Investigators will evaluate histopathologic endpoints after gastroscopies with biopsies from seven standard sites in 1999. Initial data from pill counts and sampled blood levels of vitamin E, vitamin C, and S-allylcysteine indicate excellent compliance. Subjects have tolerated all interventions well, although 3.1% of those assigned to amoxicillin and omeprazole developed rashes, compared to 0.3% to those in the control group. Preliminary breath tests demonstrate substantial reductions in gastric urease activity, an indication of infection by Helicobacter pylori, among those assigned to amoxicillin and omeprazole.

Topics: Adult; Amoxicillin; Anti-Ulcer Agents; Ascorbic Acid; China; Double-Blind Method; Drug Therapy, Combination; Garlic; Helicobacter Infections; Helicobacter pylori; Humans; Middle Aged; Omeprazole; Penicillins; Phytotherapy; Plant Extracts; Plants, Medicinal; Precancerous Conditions; Selenium; Stomach Neoplasms; Vitamin E

Low gastric juice total vitamin C concentration in the presence of Helicobacter pylori (H. pylori) infection probably plays a role in gastric carcinogenesis. In vitro vitamin C has been shown to inhibit the growth of H. pylori. The aims of this study were to determine the effect of high dose vitamin C administration on H. pylori infection and on gastric juice total vitamin C concentration in patients with H. pylori related chronic gastritis. Sixty patients with dyspeptic symptoms and proven chronic gastritis and H. pylori infection, who were undergoing routine endoscopy, entered the study after giving informed consent. They were randomly coded into two treatment groups. Group 1 (controls, n = 28) were treated with antacids for 4 weeks and Group 2 (n = 32) received vitamin C 5g daily also for 4 weeks. Nine patients did not complete the study and were excluded. Plasma and gastric juice total vitamin C levels were measured at baseline, at the end of 4 weeks treatment and again 4 weeks after treatment cessation. In the control group H. pylori infection remained unchanged in all 24 patients throughout as did the mean gastric juice total vitamin C concentration. However, in the vitamin C treated group eight of 27 patients (30%) who completed the treatment course the H. pylori infection was eradicated (P = 0.01). In these patients the mean gastric juice total vitamin C concentration rose significantly from 7.2 +/- 1.6 micrograms/ml after 4 weeks treatment (P < M 0.001) and 19.8 micrograms/ml 4 weeks after treatment was discontinued (P < 0.001). In the remaining 19 patients with persistent H. pylori infection, the mean gastric juice total vitamin C concentration rose less than in those with successful H. pylori eradication; 6.3 +/- 1.7 micrograms/ml before treatment, 10.8 +/- 1.5 micrograms/ml after 4 weeks treatment (P < 0.05) and a return to pre-treatment levels (7.1 +/- 2.7 micrograms/ml) 4 weeks after vitamin C intake stopped. There were no side effects of vitamin C treatment. This study has shown that 4 weeks daily high dose vitamin C treatment in H. pylori infected patients with chronic gastritis resulted in apparent H. pylori eradication in 30% of those treated. In those patients there was also a highly significant rise in gastric juice total vitamin C concentration which persisted for at least 4 weeks after the treatment ceased. A significant, though less marked, gastric juice total vitamin C concentration increase was observed during vitamin C treatment

Topics: Adolescent; Adult; Aluminum Hydroxide; Antacids; Ascorbic Acid; Carbonates; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged

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

Topics: Ascorbic Acid; Clarithromycin; Double-Blind Method; Drug Combinations; Europe; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Omeprazole; Placebos; Stomach Neoplasms

Ascorbic acid, the reduced form of vitamin C, may protect against gastric cancer and is secreted by the normal stomach. Secretion is impaired in Helicobacter pylori (H pylori) associated chronic gastritis. This study examined if eradication of H pylori improves gastric juice ascorbate values. Fasting gastric juice and plasma samples were collected at endoscopy from patients participating in trials of H pylori eradication for duodenal ulcer disease and intestinal metaplasia before and up to 15 months after attempted eradication. Ascorbic acid and total vitamin C concentrations were determined by high performance liquid chromatography. In 12 patients in whom H pylori was successfully eradicated gastric juice ascorbate and total vitamin C concentrations and the ratio of juice to plasma vitamin C rose after treatment. Analysis after treatment suggested that the rise was greatest in patients with high final plasma vitamin C concentrations, even though these did not change with treatment. By contrast, in 22 patients in whom H pylori eradication was unsuccessful there were no significant changes in juice or plasma concentrations after treatment. It is concluded that successful eradication of H pylori improves secretion of vitamin C into gastric juice. It is speculated that this increases protection against gastric cancer.

Topics: Aged; Ampicillin; Anti-Ulcer Agents; Ascorbic Acid; Drug Therapy, Combination; Duodenal Ulcer; Fasting; Follow-Up Studies; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Intestines; Male; Metaplasia; Metronidazole; Organometallic Compounds; Oxytetracycline; Treatment Outcome

Helicobacter pylori gastritis affects gastric pH and concentrations of ascorbic acid, hydrogen peroxide, hypochlorite, ammonia and urea, pepsin, and mucin. First, the separate effects of each of these altered factors on oxidation of pork were investigated during in vitro gastrointestinal digestion. Lipid and protein oxidation increased (range 23-48%) in duodenal digests of pork previously exposed to elevated (6.1) versus normal acidic stomach pH (2.3 to 3.5) conditions. Salivary nitrite reduced the formation of lipid and protein oxidation products (range 14-20%) under normal acidic but not elevated stomach pH conditions. Higher amounts of hydrogen peroxide and lower amounts of ascorbic acid decreased concentrations of lipid oxidation products in duodenal pork digests, whereas ammonia slightly stimulated protein oxidation during digestion. Second, two H. pylori gastritis-duodenal digestion models were installed using a set of altered compound concentrations at normal acidic or elevated stomach pH. The elevated pH-gastritis-duodenal digestion model increased pork protein oxidation compared with the normal pH-gastritis and the normal digestion model (14.3 ± 2.1 vs 8.2 ± 1.0 nmol DNPH/mg protein, P < 0.001). Compared with the other models, protein oxidation was also increased when nitrite-cured pork was exposed to the elevated pH-gastritis-duodenal digestion model (10.8 ± 1.4 vs 5.9 ± 0.8 nmol DNPH/mg protein, P < 0.001), but no significant effect of the model was observed when the pork was seasoned with herbs. Lipid oxidation was not or was marginally affected by the installed model.

Topics: Ammonia; Animals; Ascorbic Acid; Digestion; Duodenum; Gastric Acid; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen Peroxide; Hydrogen-Ion Concentration; Lipids; Models, Biological; Oxidation-Reduction; Proteins; Red Meat; Sus scrofa

Topics: Amoxicillin; Anti-Bacterial Agents; Ascorbic Acid; Drug Therapy, Combination; Helicobacter Infections; Helicobacter pylori; Humans; Proton Pump Inhibitors; Treatment Outcome

To investigate the effects of dietary vitamin C and foods containing vitamin C on gastric cancer risk.. Our study included 830 control subjects and 415 patients. Data regarding demographics, medical history, and lifestyle, including dietary and nutrient intake, were collected using reliable self-administered questionnaires. Dietary intake information was collected from the participants using a food frequency questionnaire that has been previously reported as reliable and valid. A rapid urease test and a histological evaluation were used to determine the presence of Helicobacter pylori (H. pylori) infection. Twenty-three vitamin C-contributing foods were selected, representing over 80% of the cumulative vitamin C contribution.. In analyses adjusted for first-degree family history of gastric cancer, education level, job, household income, smoking status, and regular exercise, an inverse association between vitamin C intake and gastric cancer risk was observed for the highest (≥ 120.67 mg/d) vs the lowest (< 80.14 mg/d) intake category [OR (95%CI): 0.64 (0.46-0.88)], with a significant trend across the three intake categories (P = 0.007). No protective effect of vitamin C was detected after stratification by gender. No effect of vitamin C intake on the gastric cancer incidence was found in either men or women infected with H. pylori. Vitamin C-contributing foods, including cabbage [0.45 (0.32-0.63), 0.50 (0.34-0.75), 0.45 (0.25-0.81)], strawberries [0.56 (0.40-0.78), 0.49 (0.32-0.74), 0.52 (0.29-0.93)], and bananas [0.40 (0.29-0.57), 0.41 (0.27-0.62), 0.34 (0.19-0.63)], were protective factors against the risk of gastric cancer based on the results of the overall adjusted analyses and the results for men and women, respectively.. A protective effect of vitamin C and vitamin C-contributing foods against gastric cancer was observed. Further studies using larger sample sizes are required to replicate our results.

Topics: Adult; Ascorbic Acid; Carcinoma; Case-Control Studies; Diet; Dietary Carbohydrates; Energy Intake; Female; Fruit; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Male; Middle Aged; Protective Factors; Republic of Korea; Risk Factors; Solanum tuberosum; Stomach Neoplasms; Surveys and Questionnaires

In our study, we aimed to assess the effect of vitamin E and C supplementation to triple and quadruple Helicobacter pylori eradication regimens.. Four hundred patients with H. pylori infection were classified into four groups. Patients in group A (n=100) received amoxicillin, clarithromycin, and lansoprazole for 2 weeks. In group B, patients (n=100) received vitamins C and E for a month, in addition to amoxicillin, clarithromycin, and lansoprazole for 2 weeks. Patients in group C (n=100) received amoxicillin, clarithromycin, lansoprazole, and bismuth subcitrate for 2 weeks, whereas those in group D (n=100) received vitamins C and E for a month, in addition to amoxicillin, clarithromycin, lansoprazole, and bismuth subcitrate for 2 weeks. H. pylori eradication was assessed with the C14 urea breath test 2 months after the end of the therapy. The eradication rate was assessed using per-protocol (PP) and intention-to-treat (ITT) analyses.. Three hundred forty-eight patients finished the study. The eradication of H. pylori was achieved in 63 of 84 patients (75%) by PP and 63 of 100 (63%) by ITT analysis in group A, 60 of 84 (71.4%) by PP and 60 of 100 (60%) by ITT analysis in group B, 72 of 89 (80.9 %) by PP and 72 of 100 (72%) by ITT analysis in group C, and 76 of 91 (83.5%) by PP and 76 of 100 (76%) by ITT analysis in group D. There was no remarkable change between groups A and B (p>0.05). Similar results were also found between groups D and C (p>0.05).. This study revealed that supplementing vitamins C and E to either the triple or quadruple therapies did not provide an additional advantage for achieving significantly higher eradication rates for H. pylori.

Topics: Adult; Aged; Amoxicillin; Anti-Infective Agents; Anti-Ulcer Agents; Ascorbic Acid; Breath Tests; Clarithromycin; Dietary Supplements; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lansoprazole; Male; Middle Aged; Organometallic Compounds; Retrospective Studies; Treatment Outcome; Vitamin E; Vitamins; Young Adult

Since its discovery in 1982, the global importance of Helicobacter pylori-induced disease, particularly in developing countries, remains high. The use of rodent models, particularly mice, and the unanticipated usefulness of the gerbil to study H. pylori pathogenesis have been used extensively to study the interactions of the host, the pathogen, and the environmental conditions influencing the outcome of persistent H. pylori infection. Dietary factors in humans are increasingly recognized as being important factors in modulating progression and severity of H. pylori-induced gastric cancer. Studies using rodent models to verify and help explain mechanisms whereby various dietary ingredients impact disease outcome should continue to be extremely productive.

Topics: Animals; Ascorbic Acid; Developing Countries; Diet; Dietary Fats; Disease Models, Animal; Folic Acid; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Humans; Mice; Salts; Stomach Neoplasms

Helicobacter pylori (H. pylori) infection plays an important role in gastric carcinogenesis. This bacterium may induce cancer transformation and change the susceptibility of gastric mucosa cells to various exogenous dietary irritants. The aim of the study was to evaluate the influence of H. pylori infection on the reaction of the stomach cells to a genotoxic effect of heterocyclic amines (HCAs). These well-known mutagens are formed during cooking of protein-rich foods, primarily meat. Taking into account that persons consuming a mixed-western diet are exposed to these compound nearly an entire lifetime and more than half of human population is infected with H. pylori, it is important to assess the combined effect of H. pylori infection and HCAs in the context of DNA damage in gastric mucosa cells, which is a prerequisite to cancer transformation. We employed 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,8-dimethyl-imidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) because these substances are present in a great amount in cooked and fried meat. Using alkaline comet assay, we showed that the extent of the DNA damage induced by HCAs was significantly higher in H. pylori infected gastric mucosa cells than in non-infected counterparts. We did not observed any difference in the efficiency of repair of DNA lesions induced by HCAs in both type of cells. Vitamin C reduced the genotoxic effects of HCAs in H. pylori infected and non-infected gastric mucosa cells. Melatonin more effectively decreased DNA damage caused by HCAs in H. pylori infected gastric mucosa cells as compared with control. Our results suggest that H. pylori infection may influence the susceptibility of gastric mucosa cells to HCAs and dietary antioxidative substances, including vitamin C and melatonin may inhibit the genotoxic effects of HCAs on gastric mucosa cells and may reduce the risk of carcinogenesis caused by food borne mutagens and H. pylori infection.

Topics: Adult; Ascorbic Acid; Breath Tests; Carbon Isotopes; Comet Assay; DNA Damage; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Imidazoles; Male; Melatonin; Middle Aged; Poland; Quinoxalines; Statistics, Nonparametric

Topics: Ascorbic Acid; Helicobacter Infections; Helicobacter pylori; Humans

While the association between bioavailability of vitamins E and C and Helicobacter pylori infection has been extensively researched in gastritis and gastric cancer patients, little is known about this relationship in asymptomatic adults.. To investigate the effect of H. pylori infection on bioavailability of vitamins E and C in asymptomatic adults.. Volunteers from the University of Toronto, aged 18-45 years, were screened, for their H. pylori infection status. H. pylori-negative (n = 32) and asymptomatic H. pylori-positive (n = 27) participants received vitamin C (500 mg) and vitamin E (400 IU) supplements daily for 28 days. Plasma vitamins C, E and thiols concentrations were assessed before (baseline) and after supplementation.. Postsupplementation plasma levels of vitamin C and E were significantly higher than presupplementation levels in both groups. Yet, changes in plasma vitamins E and C were not significantly different between the two groups [vitamin C (mumol/l): 13.97 +/- 16.86 vs. 20.87 +/- 27.66, p > 0.05; vitamin E (mumol/l): 15.52 +/- 9.4 vs. 14.47 +/- 15.77; p > 0.05 for H. pylori-negative and H. pylori-positive groups, respectively]. In addition, no significant difference was found in plasma thiols levels between groups (p > 0.05).. These findings suggest that H. pylori does not influence antioxidants bioavailability in its asymptomatic stages of infection until a factor or combination of factors triggers the inflammation cascade which may lead to increased oxidative stress and possibly reduced bioavailability of vitamins E and C.

Topics: Adolescent; Adult; Antioxidants; Ascorbic Acid; Biological Availability; Diet; Dietary Supplements; Energy Intake; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Oxidative Stress; Sulfhydryl Compounds; Vitamin E; Young Adult

Anti-Helicobacter pylori (H. pylori) effects of aminoreductone (AR), a Maillard reaction product, were evaluated in this study. AR effectively inhibited the growth of all 24 strains (19 clinical isolates and 5 isogenic mutants) irrespective of susceptibility to antibiotics and clinical manifestation. The minimum inhibitory concentration (MIC) of AR ranged from 0.5 to 5 mM. A killing assay with multiples of MIC was performed, demonstrating that the killing activity of AR was significantly higher than that of its derived melanoidin, an inhibitor of H. pylori urease-gastric mucin adherence, formed in the final stage of the Maillard reaction. These significant effects of AR on H. pylori were observed even in acidic conditions (pH 3). At most, 25 mM AR effectively exhibited bactericidal activity in all strains. These results rise up the possibility that foods containing AR, such as milk and dairy products, are valuable sources for preventing colonization of H. pylori in the stomach and its associated tissue damages.

Topics: Anti-Bacterial Agents; Ascorbic Acid; Helicobacter Infections; Helicobacter pylori; Humans; Microbial Sensitivity Tests

In human studies, low vitamin C intake has been associated with more severe Helicobacter pylori gastritis and a higher incidence of gastric cancer. However, vitamin C supplementation has not been definitively shown to protect against gastric cancer. Using vitamin C-deficient B6.129P2-Gulo(tm1Umc/mmcd) (gulo(-/-)) mice lacking L-gulono-gamma-lactone oxidase, we compared gastric lesions and Th1 immune responses in H. pylori-infected gulo(-/-) mice supplemented with low (33 mg/L) or high (3,300 mg/L) vitamin C in drinking water for 16 or 32 weeks. Vitamin C levels in plasma and gastric tissue correlated with the vitamin C supplementation levels in gulo(-/-) mice. H. pylori infection resulted in comparable gastritis and premalignant lesions in wildtype C57BL/6 and gulo(-/-) mice supplemented with high vitamin C, but lesions were less severe in gulo(-/-) mice supplemented with low vitamin C at 32 weeks post infection. The reduced gastric lesions in infected gulo(-/-) mice supplemented with low vitamin C correlated with reduced Th1-associated IgG2c, gastric IFN-gamma and TNF-alpha mRNA and higher H. pylori colonization levels. These results in the H. pylori-infected gulo(-/-) mouse model suggest that although supplementation with a high level of vitamin C achieved physiologically normal vitamin C levels in plasma and gastric tissue, this dose of vitamin C did not protect gulo(-/-) mice from H. pylori-induced premalignant gastric lesions. In addition, less severe gastric lesions in H.pylori infected gulo(-/-) mice supplemented with low vitamin C correlated with an attenuated Th1 inflammatory response.

Topics: Animals; Ascorbic Acid; Chromatography, High Pressure Liquid; Dietary Supplements; Female; Gastritis; Helicobacter Infections; Interferon-gamma; L-Gulonolactone Oxidase; Male; Mice; Mice, Inbred C57BL; Polymerase Chain Reaction; Precancerous Conditions; Receptors, IgG; Sex Factors; Stomach Neoplasms; Th1 Cells; Tumor Necrosis Factor-alpha

Gastric cancer is a major health burden in the Asia-Pacific region but consensus on prevention strategies has been lacking. We aimed to critically evaluate strategies for preventing gastric cancer.. A multidisciplinary group developed consensus statements using a Delphi approach. Relevant data were presented, and the quality of evidence, strength of recommendation, and level of consensus were graded.. Helicobacter pylori infection is a necessary but not sufficient causal factor for non-cardia gastric adenocarcinoma. A high intake of salt is strongly associated with gastric cancer. Fresh fruits and vegetables are protective but the use of vitamins and other dietary supplements does not prevent gastric cancer. Host-bacterial interaction in H. pylori infection results in different patterns of gastritis and differences in gastric acid secretion which determine disease outcome. A positive family history of gastric cancer is an important risk factor. Low serum pepsinogens reflect gastric atrophy and may be useful as a marker to identify populations at high risk for gastric cancer. H. pylori screening and treatment is a recommended gastric cancer risk reduction strategy in high-risk populations. H. pylori screening and treatment is most effective before atrophic gastritis has developed. It does not exclude the existing practice of gastric cancer surveillance in high-risk populations. In populations at low risk for gastric cancer, H. pylori screening is not recommended. First-line treatment of H. pylori infection should be in accordance with national treatment guidelines.. A strategy of H. pylori screening and eradication in high-risk populations will probably reduce gastric cancer incidence, and based on current evidence is recommended by consensus.

Topics: Adenocarcinoma; Anti-Bacterial Agents; Anticarcinogenic Agents; Ascorbic Acid; Asia; Biomarkers, Tumor; Dietary Supplements; Evidence-Based Medicine; Fruit; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Mass Screening; Pacific Islands; Pedigree; Pepsinogens; Prevalence; Risk Assessment; Risk Factors; Sodium Chloride, Dietary; Stomach Neoplasms; Vegetables; Vitamins

Helicobacter pylori infection induces chronic gastritis and lowers gastric juice ascorbic acid concentrations. We investigated how H. pylori eradication affected multiple variables that could prevent or delay development of new or occult gastric cancer in patients with early gastric cancer treated by endoscopic mucosal resection. Gastric juice pH, nitrite concentrations, and total vitamin C concentrations, serum concentrations of vitamin C and specific H. pylori antibody, and intensity of neutrophil infiltration in gastric mucosa were determined before and after successful H. pylori eradication. Successful eradication increased acid output and ascorbic acid secretion into gastric juice, accompanied by disappearance of polymorphonuclear infiltration from the surface epithelium and decreased gastric juice nitrite concentrations. Our data suggest that H. pylori eradication decreases the nitrosation rate as the ratio of vitamin C to nitrite increases. This decreases reactive oxygen species and nitric oxide, eliminating their damaging effect on DNA and reducing cell turnover.

Topics: Aged; Aged, 80 and over; Ascorbic Acid; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Nitrites; Stomach Neoplasms

The objective of this study was to determine whether the intake of nitrate relative to antioxidant vitamin rather than absolute intake of nitrate affects the risk of gastric cancer (GC). In a case-control study in Korea using a food frequency questionnaire, trained dietitians interviewed 136 GC cases and an equal number of controls matched by sex and age. As an index of nitrate intake relative to antioxidant vitamins intake, we calculated the nitrate:antioxidant vitamin consumption ratio. The mean daily nitrate intake from foods was very high in our subjects. Higher absolute intake of nitrate was not associated with GC risk [odds ratios (OR) = 1.13; 95% confidence interval (CI) = 0.42-3.06]. However, the GC risk distinctly increased as the nitrate:antioxidant vitamin consumption ratio increased, particularly with higher nitrate:vitamin E (OR = 2.78; 95% CI = 1.01-7.67) and nitrate:folate ratios (OR = 3.37; 95% CI = 1.28-8.87). Therefore, GC risk was influenced by the intake of nitrate relative to antioxidant vitamins. Our results suggest that a decrease in the intake of nitrate relative to antioxidant vitamins is considerably more effective in reducing GC risk than either a lower absolute intake of nitrate or a higher intake of antioxidant vitamins alone.

Topics: Antioxidants; Ascorbic Acid; Case-Control Studies; Confidence Intervals; Diet; Feeding Behavior; Female; Helicobacter Infections; Helicobacter pylori; Humans; Korea; Male; Middle Aged; Nitrates; Odds Ratio; Risk Factors; Stomach Neoplasms; Surveys and Questionnaires; Vitamin E; Vitamins

The risk of gastric cancer (GC) associated with dietary intake of nitrosodimethylamine (NDMA) and endogenous formation of nitroso compounds (NOCs) was investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC). The study included 521,457 individuals and 314 incident cases of GC that had occurred after 6.6 average years of follow-up. An index of endogenous NOC (ENOC) formation was estimated using data of the iron content from meat intake and faecal apparent total NOC formation according to previous published studies. Antibodies to Helicobacter pylori and vitamin C levels were measured in a sub-sample of cases and matched controls included in a nested case-control within the cohort. Exposure to NDMA was < 1 microg on average compared with 93 mug on average from ENOC. There was no association between NDMA intake and GC risk (HR, 1.00; 95% CI, 0.7-1.43). ENOC was significantly associated with non-cardia cancer risk (HR, 1.42; 95% CI, 1.14-1.78 for an increase of 40 microg/day) but not with cardia cancer (HR, 0.96; 95% CI, 0.69-1.33). Although the number of not infected cases is low, our data suggest a possible interaction between ENOC and H.pylori infection (P for interaction = 0.09). Moreover, we observed an interaction between plasma vitamin C and ENOC (P < 0.02). ENOC formation may account for our previously reported association between red and processed meat consumption and gastric cancer risk.

Topics: Adenocarcinoma; Animals; Ascorbic Acid; Case-Control Studies; Cattle; Diet; Dimethylnitrosamine; Europe; Female; Helicobacter Infections; Helicobacter pylori; Humans; Iron; Male; Meat; Middle Aged; Nitrosamines; Prospective Studies; Risk Factors; Stomach Neoplasms

Vitamin C is present as ascorbic acid (Asc) with antioxidative properties and as its oxidation product dehydroascorbic acid (dAsc). Asc is actively transported from blood to gastric juice where it prevents formation of carcinogenic nitrosamines and protects mucosa from reactive oxygen species. Another important function of gastric mucosa is proton pump-dependent secretion of hydrochloric acid. The pump maintains high pH gradient between gastric juice and plasma. The aim of the work was to analyse relations between gastric juice pH and concentrations of Asc and dAsc in plasma, gastric mucosa and juice as well as other factors modifying metabolism of vitamin C and function of gastric mucosa.. 31 patients were subjected to diagnostic endoscopy due to dyspepsia. Concentrations of Asc and dAsc were measured in plasma, gastric mucosa and juice with HPLC method. pH of gastric juice was determined. Histopathology examination of mucosa and urease test for Helicobacter pylori were performed. Data concerning dyspeptic symptoms and used drugs, including vitamin C preparations, were collected.. Patients taking vitamin C preparations had significantly lower gastric juice pH values than the others (median 2.2 vs 5.4; p < 0.01). Treatment with vitamin C preparations was also associated with higher Asc concentrations in gastric juice (median 16.6 vs. 1.8 micromol/L; p < 0.09); the difference was statistically significant in the subgroup of patients with gastritis (median 16.6 vs. 0.1 micromol/L; p < 0.04). Strong negative correlations of pH with Asc (Rs = -0.67; p < 0.001) and dAsc (Rs = -0.48; p < 0.01) concentrations were observed in gastric juice. Positive correlation of pH and relative dAsc content expressed as percent of total vitamin C concentration in gastric juice was also statistically significant (Rs = +0.48; p < 0.05).. Performance of the proton pump and vitamin C metabolism in the stomach are closely mutually connected. Modification of hydrochloric acid secretion may affect gastric juice vitamin C concentration. Potentially disadvantageous influence of antisecretory drugs on the mechanisms of antioxidative protection in the stomach needs further investigation.

Topics: Ascorbic Acid; Chlorates; Chromatography, High Pressure Liquid; Female; Gastric Juice; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged

The direct effect of intact Helicobacter pylori on gastric epithelial cells SGC-7901 and the protection given by the antioxidants vitamin C and sodium selenite were studied. Incubation of SGC-7901 cells with H. pylori simultaneously caused a significant increase of DNA damage (DNA strand breakage and DNA fragmentation) and ROS formation, as well as a significant decrease of intracellular GSH content in a H. pylori multiplicity of infection (MOI) dependent manner in gastric cells. ROS formation was strongly positively correlated while GSH content was negatively correlated with DNA strand breakage and fragmentation, indicating that DNA damage may be mainly caused by H. pylori-induced oxidative stress in gastric cells. The antioxidants, vitamin C and sodium selenite, directly increased GSH content while diminishing ROS formation and DNA damage in H. pylori-infected SGC-7901 cells, indicating that vitamin C and sodium selenite can protect gastric cells against H. pylori damage. The protections by vitamin C and sodium selenite further demonstrated that DNA damage may be derived from oxidative stress in H. pylori-infected gastric cells. The results suggested that DNA damage caused by H. pylori-induced oxidative stress may be one important factor in the pathogenesis of H. pylori, and that vitamin C and sodium selenite may have a preventive or therapeutic role against H. pylori-associated gastric diseases.

Topics: Antioxidants; Ascorbic Acid; Cell Line; Comet Assay; DNA Damage; DNA Fragmentation; Epithelial Cells; Gastric Mucosa; Glutathione; Helicobacter Infections; Helicobacter pylori; Humans; Indicators and Reagents; Oxidative Stress; Reactive Oxygen Species; Sodium Selenite

We quantified the effect of antioxidant vitamins in gastric cancer risk, taking into account Helicobacter pylori seropositivity and overall fruit and vegetable intake. Incident cases were identified in two large hospitals in Porto, Portugal, and controls were randomly sampled among city dwellers. Food intake was assessed with a previously validated semiquantitative food-frequency questionnaire. A commercially available chromatographic immunoassay was used for the detection of immunoglobulin G antibodies. Complete questionnaire information and serum samples were available for 233 cases and 311 controls. Compared with subjects in the lowest tertile of dietary intake, the odds ratios (ORs) for those in the highest were 0.85 (95% confidence interval, CI = 0.45-1.60) for vitamin C, 1.04 (95% CI = 0.60-1.80) for vitamin E, and 1.33 (95% CI = 0.77-2.30) for provitamin A carotenoids after further adjusting for fruit and vegetable consumption. Fruit and vegetables remained an independent protective factor (OR = 0.45; 95% CI = 0.23-0.89) after further adjustment for the intake of antioxidant vitamins. H. pylori status had no significant interaction with dietary items. Factors other than H. pylori infection and intake of vitamin C and provitamin A carotenoids seem to account for the inverse association between fruit and vegetable consumption and gastric cancer.

Topics: Aged; Antioxidants; Ascorbic Acid; Case-Control Studies; Confidence Intervals; Diet; Diet Surveys; Female; Fruit; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Odds Ratio; Portugal; Risk Factors; Stomach Neoplasms; Surveys and Questionnaires; Vegetables; Vitamin E; Vitamins

Epidemiological studies show that high intake of food-bound vitamin C and E reduces the risk of gastric cancer. Whether dietary supplementation with antioxidant micronutrients interferes with Helicobacter pylori infection and associated diseases is unclear. The aim of this study was to investigate if dietary vitamin C or E supplementation influences the progression of gastritis, gastric mucosal nitrosative and oxidative protein damage, gastric mucosal lipid peroxidation, or gastric mucosal oxidative DNA damage in H. pylori-infected Mongolian gerbils.. Gerbils were divided into four groups: H. pylori-infected animals fed with vitamin C- or vitamin E-supplemented food, and infected and uninfected animals given standard rodent food. Subgroups of animals were killed at different time-points until 52 weeks postinfection. Concentrations of 3-nitrotyrosine and thiobarbituric acid-reactive substances (TBARS) in the gastric mucosa were determined with an immunodot blot and a fluorometric method, respectively. Mucosal concentrations of carbonyl carbons on proteins and 8-hydroxydeoxyguanosine were determined by enzyme-linked immunosorbent assay. Gastritis was scored semiquantitatively.. Vitamin supplements had no effect on the colonization with H. pylori. Vitamin C as well as vitamin E supplements reduced mucosal 3-nitrotyrosine concentrations to normal levels in infected animals. Vitamin E supplements decreased mucosal protein carbonyls and TBARS in short-term gastritis. In addition, vitamin C supplements caused attenuated mucosal oxidative DNA damage and milder mucosal inflammation in short-term gastritis.. Vitamin C or vitamin E supplementation leads to some short-term protective effects on H. pylori-induced gastritis in Mongolian gerbils. These effects seem to subside over time when the infection persists.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Antioxidants; Ascorbic Acid; Deoxyguanosine; Dietary Supplements; Disease Models, Animal; Gastric Mucosa; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Male; Stomach Neoplasms; Thiobarbituric Acid Reactive Substances; Tyrosine; Vitamin E; Vitamins

Increasing resistance to currently used antimicrobials has resulted in the evaluation of other agents that have antimicrobial activity against Helicobacter pylori. H. pylori American Type Culture Collection (ATCC) strain 49503 (a toxin-producing strain known to be associated with gastric cancer) was grown, a cell suspension prepared in 2 mL PBS and diluted 10-fold. One hundred microL of this cell suspension was added to vitamin C 0.5%, vitamin E 0.5%, garcinol 100 microg/mL, Protykin (containing 50% trans-resveratrol) 100 microg/mL and garcinol + Protykin 100 microg/mL in Lennox broth, and incubated for 16 h under microaerophilic conditions. Three replicates of 10 microL from each 10(-7) dilution tube were plated, colonies were counted after 16 h, and growth of H. pylori was confirmed by the CLO test. These colony counts were compared to control cultures without the addition of any antioxidants. The experiments were then repeated with the addition of 15 microg/mL of clarithromycin to experimental and control samples. Enhanced killing of H. pylori by 37.6% was noted when vitamin C was added, which increased to 66% when clarithromycin was added, compared to controls (p < 0.05). With garcinol and Protykin alone there was 91.4 and 87% killing of H. pylori, respectively, while a combination of garcinol + Protykin resulted in 90.8% killing compared to controls (p < 0.05). When clarithromycin was added, there was 76.3% increased killing with garcinol alone, 55.3% with Protykin alone, and 73.7% with garcinol + Protykin compared to controls (containing clarithromycin) (p < 0.05). Vitamin E had no effect on H. pylori growth compared to controls. We conclude from this study that some antioxidants such as vitamin C, garcinol and Protykin, but not vitamin E, may have potential as antimicrobial agents against H. pylori.

Topics: Anti-Bacterial Agents; Anti-Infective Agents; Antioxidants; Ascorbic Acid; Clarithromycin; Helicobacter Infections; Helicobacter pylori; Microbial Sensitivity Tests; Stilbenes; Time Factors; Urease; Vitamin E

The mechanism of citric acid-enhanced Helicobacter pylori urease activity remains unclear.. To compare ascorbic, citric and malic acid given at the same concentration and pH on intragastric urease activity.. Volunteers received 40 mg of famotidine the evening prior to breath testing. After an overnight fast volunteers were randomized to receive 100 mL of water or 100 mm citric, malic, or ascorbic acid, pH 2.3 containing 75 mg of 13C-urea. At 15 min a second 100 mL solution of one of the test solutions was taken without added urea.. Twelve volunteers were studied (eight men, four women, age 19-57, median 50.7) in a randomized-crossover study. The mean breath test result at 30 min with ascorbic (17.5 +/- 5), malic (25.8 +/- 5) and citric acid (29.5 +/- 5) were all significantly greater than with water (9.5 +/- 3). Citric and malic acid were similar (P = 0.699) and significantly greater than ascorbic acid (P < 0.02). When the ascorbic acid was followed by citric acid, the result was similar to that with citrate alone (25.8 +/- 4) and greater than with ascorbic then ascorbic (P = 0.026).. Enhancement of H. pylori urease activity is not strictly a function of the pH. We propose the effect is related to differential effects of the availability of nickel, which is required for urease activity. Citric acid and malic acid were essentially equivalent such that malic acid could substitute for citric acid in the UBT; ascorbic acid would be a poor choice.

Topics: Adult; Ascorbic Acid; Citric Acid; Female; Helicobacter Infections; Helicobacter pylori; Humans; Malates; Male; Middle Aged; Prospective Studies; Stomach Diseases; Urease

Researches show that epidemiologic factors of gastric cancer include living habit, eating moldy food and pickles, dystrophy, lack of microelements, and inherit, etc. This study was to explore universalities of these factors in Wuwei, a city in northwest China with high incidence of gastric cancer, and provide evidences for the first-prevention of gastric cancer.. Family histories of the residents in Wuwei City were investigated with case-control method. Separating ratio and heredity degree of gastric cancer were calculated with Li-Mantel-Cart method and Falconer's regression method. Chronic gastritis patients were followed-up by home-visit, gastroscopy, and pathology. Cancerigenic fungi and volatility N-nitrosate compounds in residents' meal, Helicobacter pylori (Hp) in gastric mucosa, and total content of vitamin C in 293 healthy adults' serum were detected by culture, authentication, and laboratory examinations.. In Wuwei City, the separating ratio of gastric cancer was 0.077; the heredity degree of first-degree relatives was 22.91%u cancerization rate of year in person of atrophic gastritis crowd was 1.09%. Eight kinds of nitrosamine and 14 kinds of cancerigenic fungi were detected from residents' meal. Total content of vitamin C in serum of the 293 healthy adults in summer was (5.74+2.79) mg/L. Positive rate of Hp in gastric mucosa of the residents was 67%.. The major extrinsic factors of gastric cancer in Wuwei City include various strong carcinogens existing in residents' meal and lack of vitamin Cu its intrinsic factors include infection of Hp, atrophic gastritis (especially atypical hyperplasia), and heritage susceptibility.

Topics: Adult; Ascorbic Acid; China; Disease Progression; Female; Follow-Up Studies; Food Analysis; Food Microbiology; Gastric Mucosa; Gastritis, Atrophic; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Nitrosamines; Precancerous Conditions; Risk Factors; Stomach Neoplasms

This study, carried out on 51 patients with multifocal atrophic gastritis (MAG) and 92 age and sex-matched dyspeptic controls, was designed to examine both exocrine (gastric acid) and endocrine (gastrin) gastric secretion before and after therapeutic intervention including Helicobacter pylori eradication and vitamin C treatment.. Fasting and gastrin-releasing peptide-induced gastric acid secretion, serum levels of gastrin and proinflammatory (IL-1beta, IL-8, TNF-alpha) as well as gastric mucosal gene expression of ornithine decarboxylase (ODC), cyclooxygenase 2 (COX-2) and growth factors (epidermal growth factor and transforming growth factor alpha) were determined before and after the eradication of Helicobacter pylori and therapy with large doses (1 g/d) of vitamin C for 3 months.. The H. pylori eradication, assessed by C-urea breath test, and vitamin C therapy failed to reverse the histological atrophy of the gastric mucosa but improved significantly the functional status of the atrophied mucosa, especially its exocrine and endocrine secretory activities, attenuated the expression of premalignant markers such as ODC and COX-2, raised the production of growth factors and diminished the release of proinflammatory cytokines.. These results indicate that MAG may be considered as an environmental disease of the gastric mucosa, whose functional status can be improved by the eradication of H. pylori combined with antioxidant therapy with large doses of vitamin C.

Topics: Adult; Aged; Anti-Bacterial Agents; Antioxidants; Ascorbic Acid; Case-Control Studies; Cyclooxygenase 2; Cytokines; Epidermal Growth Factor; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Ornithine Decarboxylase; RNA, Messenger; Transforming Growth Factor alpha

To examine the effects of dietary factor and Helicobacter pylori (H. pylori) infection with emphasis on vitamin intake on the risk of gastric cancer (GC), we conducted a case-control study in South Korea, a high-risk area for GC. Trained dietitians interviewed 136 cases histologically diagnosed with GC. An equal number of hospital controls was selected by matching sex and age. High dietary intakes of vegetable fat [odds ratio (OR) = 0.35; 95% confidence interval (CI) = 0.15-0.83], folate (OR = 0.35; 95% CI = 0.13-0.96), and antioxidants, such as vitamin A (OR = 0.34; 95% CI = 0.13-0.83), beta-carotene (OR = 0.33; 95% CI = 0.13-0.82), vitamin C (OR = 0.26; 95% CI = 0.09-0.72), and vitamin E (OR = 0.41; 95% CI = 0.17-1.01), were shown to have a protective effect on GC risk using a multivariate model adjusting for foods significantly related to GC in our previous study (charcoal grilled beef, spinach, garlic, mushroom, and a number of types of kimchi) and supplement use. When stratified according to H. pylori infection, high intakes of vitamin C (OR = 0.10; 95% CI = 0.02-0.63) and vitamin E (OR = 0.16; 95% CI = 0.03-0.83) exhibited highly significant inverse associations with GC among the H. pylori-infected subjects compared with noninfected individuals. GC risk was significantly decreased only when consumption levels for two of these vitamins were high. Our findings suggest that high intake of antioxidant vitamins contribute to the reduction of GC risk and that GC risk in Korea may be decreased by encouraging those with H. pylori infection to increase their intake of antioxidant vitamins.

Topics: Antioxidants; Ascorbic Acid; Case-Control Studies; Feeding Behavior; Female; Helicobacter Infections; Helicobacter pylori; Humans; Korea; Male; Middle Aged; Multivariate Analysis; Stomach Neoplasms; Surveys and Questionnaires; Vegetables; Vitamin E

Helicobacter pylori has been established as a major cause of gastritis and peptic ulcer disease in adults and children. H. pylori infection may also have a role in the development of some extra-gastrointestinal diseases, including iron deficiency anemia. The aim of this study is to investigate H. pylori-related changes in gastric physiology and histology and the relationship of these changes to iron deficiency anemia in children.. Fifty-two patients with gastrointestinal complaints were studied. Hematologic parameters, 3-day vitamin C and iron consumption, serum gastrin levels, and gastric juice ascorbic acid levels were compared in patients with and without H. pylori infection. Dietary intake of vitamin C and iron, serum gastrin, gastric juice ascorbic acid content, and gastric histology were compared in patients with H. pylori infection and anemia and in patients with H pylori infection and no anemia. The CagA status of the H. pylori organisms was evaluated.. Twenty-eight of 52 patients had H. pylori. Thirty-one patients had iron deficiency anemia. H. pylori infection was associated with low serum iron levels. H. pylori gastritis was associated with a decrease in the gastric juice ascorbic acid level. Infection with CagA-positive strains was associated with a greater decrease in gastric juice ascorbic acid than infection with CagA-negative strains. However, the gastric juice ascorbic acid levels of patients with H. pylori and anemia were not different from those of non-anemic patients with H. pylori. Among patients with H. pylori infection, pangastritis was twice as common in those with anemia than in those without anemia.. H. pylori infection was associated with a decrease in gastric juice ascorbic acid concentration, and this effect was more pronounced in patients with the CagA-positive strain. Pangastritis was more common in patients whose H. pylori.infection was accompanied by anemia.

Topics: Anemia, Iron-Deficiency; Antigens, Bacterial; Ascorbic Acid; Bacterial Proteins; Child; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Absorption; Iron; Iron, Dietary; Male; Stomach; Virulence

A hospital-based case-control study was carried out between 1994 and 1996 to evaluate the risk of gastric cancer (GC) according to Helicobacter pylori-CagA (+) seropositivity, nitrite and ascorbic acid intake. Three geographical areas of Mexico were selected on the basis of their contrasting dietary patterns and H. pylori seroprevalence. Nitrite and ascorbic acid consumption were estimated by interview among 211 cases and 454 matched controls. Serum antibodies against IgG H. pylori and CagA were detected by immunosorbent assays. The adjusted risk for GC was significantly higher among CagA+ subjects compared with those that were CagA negative (Odds Ratio (OR)=2.04 95% Confidence Interval (CI) 1.37-3.02 P for trend P < 0.001), this effect remained significant among diffuse GC cases (OR 2.05 95% CI 1.25-3-36). No significant effects due to nitrite and ascorbic consumption or interactions of these nutrients with CagA seropositivity were detected. Seropositivity to H. pylori CagA+ strains may be an independent factor for diffuse GC in Mexico.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Bacterial; Ascorbic Acid; Bacterial Proteins; Biomarkers, Tumor; Case-Control Studies; Diet; Enzyme-Linked Immunosorbent Assay; Female; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Nitrites; Risk Factors; Stomach Neoplasms

The interaction between Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid is still controversial. This study was designed to compare the effect of acetylsalicylic acid and vitamin C-releasing acetylsalicylic acid on the gastric mucosal damage and microbleeding before and after eradication of H. pylori in 10 young healthy volunteers. Acetylsalicylic acid induced significantly more gastric lesions and higher microbleeding than acetylsalicylic acid-vitamin C. After successful H. pylori eradication therapy, acetylsalicylic acid induced significantly higher mucosal lesions and microbleeding than before eradication. In contrast, after acetylsalicylic acid-vitamin C, gastric lesion index was significantly lower and eradication therapy failed to aggravate it. All H. pylori-positive subjects showed significant up-regulation of antioxidant enzyme (superoxide dismutase, catalase, glutathione peroxidase). Plain acetylsalicylic acid stronger than acetylsalicylic acid-vitamin C reduced gastric gene expression of these antioxidant enzymes. H. pylori eradication significantly decreased expression of these enzymes and this was further enhanced by plain acetylsalicylic acid, but not acetylsalicylic acid-vitamin C. Under plain acetylsalicylic acid therapy, the expression of proinflammatory cytokines was increased before and after eradication of H. pylori. We conclude that vitamin C combined with acetylsalicylic acid, unlike plain acetylsalicylic acid without vitamin C, protects gastric mucosa in man probably due the attenuation of oxidative stress and proinflammatory cytokines.

Topics: Adolescent; Adult; Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; Aspirin; Blotting, Western; Catalase; Cytokines; Female; Gastric Mucosa; Gastrointestinal Hemorrhage; Gene Expression Regulation, Enzymologic; Glutathione Peroxidase; Helicobacter Infections; Humans; Male; NF-kappa B; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Reverse Transcriptase Polymerase Chain Reaction; Stomach Ulcer; Superoxide Dismutase

Topics: Ascorbic Acid; Case-Control Studies; Dose-Response Relationship, Drug; Helicobacter Infections; Humans; Risk Factors; Stomach Neoplasms

Seroepidemiological and clinical studies suggest that Helicobacter pylori may cause iron deficiency anaemia (IDA) in the absence of peptic lesions by undefined mechanisms, which still remain to be fully elucidated. Gastric acidity and ascorbic acid (AA) promote iron absorption. AA is lowered in the presence of H pylori infection. H pylori can cause atrophic body gastritis with achlorhydria, decreased iron absorption, and consequent IDA. Whether alterations in intragastric acidity and AA concentrations play a role in IDA developing in patients with H pylori gastritis remains to be determined.. To evaluate gastric juice pH and gastric juice and plasma AA in patients with H pylori infection and unexplained IDA, compared with controls with IDA and a healthy stomach or with controls with H pylori infection and no IDA.. Patients with IDA and H pylori gastritis were characterised by concomitant increased intragastric pH (median value 7) and decreased intragastric AA (median value 4.4 micro g/ml) compared with controls with a healthy stomach (median pH 2; median intragastric AA 17.5 micro g/ml) and with H pylori positive controls without IDA (median pH 2.1; median intragastric AA 7.06 micro g/ml). Intragastric AA was inversely related to pH (r=-0.40, p=0.0059) and corporal degree of gastritis (r=-0.53, p=0.0039). Plasma AA concentrations were lower in all infected groups than in healthy controls.. Patients with unexplained IDA and H pylori gastritis present concomitant changes in intragastric pH and AA that may justify impaired alimentary iron absorption and consequent IDA.

Topics: Adult; Aged; Anemia, Iron-Deficiency; Ascorbic Acid; Female; Gastric Acidity Determination; Gastric Juice; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged

Serum superoxide dismutase, plasma ascorbic acid and lipid peroxidation in H. pylori gastritis and gastric cancer patients were compared with values for age matched healthy subjects. Serum superoxide dismutase and serum malondialdehyde were analyzed spectrophotometrically whereas plasma ascorbic acid was determined by colorimetric method. Significant increase in serum superoxide dismutase and serum malondialdehyde and significant decrease in plasma ascorbic acid were observed in H. pylori gastritis and gastric cancer patients compared to control subjects. The concentration of serum superoxide dismutase and serum malondialdehyde was significantly higher and plasma ascorbic acid was significantly lower in gastric cancer as compared to H. pylori gastritis patients. Our results demonstrate that a correlation existed between the concentration of serum superoxide dismutase, plasma ascorbic acid and lipid peroxidation in H. pylori gastritis and gastric cancer patients.

Topics: Adult; Antioxidants; Ascorbic Acid; Female; Gastritis; Helicobacter Infections; Humans; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Oxidants; Oxidative Stress; Stomach Neoplasms; Superoxide Dismutase

It is well known that chronic gastritis induced by Helicobacter pylori may be associated with hypochlorhydria and may also be accompanied by low levels of vitamin C in plasma and gastric juice in adults. This study investigates the relationship between H. pylori infection and vitamin C levels in the blood, plasma and gastric juice and the gastric juice pH of Korean children.. During a 5-year period, multiple gastric antral biopsies were taken from 452 children who underwent gastroduodenoscopy. The biopsy specimen was inoculated into phenol red buffered urea broth and incubated for 48 hours to detect color changes. The histopathologic findings were evaluated using the Sydney System. Concentrations of vitamin C in whole blood, plasma, and gastric juice aspirate were measured using the 2,4-dinitrophenylhydrazine method.. Four hundred fifty-two patients (228 boys, 224 girls) aged 1 to 15 years were enrolled in this study. H. pylori was detected in 112 patients (24.8%) using histology, whereas it was found in 204 patients (45.1%) using the urease test. One hundred seven patients (23.7%) had active gastritis, and 421 patients (93.1%) had chronic gastritis. Vitamin C levels in whole blood, plasma, and gastric juice exhibited significant negative correlation with the age of patients, the histologic density of H. pylori, the degree of active and chronic gastritis, and the severity of H. pylori infection (based on urease positivity and histologic density of H. pylori). Gastric juice pH was correlated with the degree of chronic gastritis and was significantly higher in urease-positive patients.. The data demonstrate that vitamin C levels in whole blood, plasma, and gastric juice and the gastric juice pH in Korean children are closely related to the severity of H. pylori infection and the histologic changes in the stomach. These data suggest that vitamin C may play a role in determining infection and progression, and vitamin C supplementation may be an important axis for the management of H. pylori infection in children.

Topics: Adolescent; Age Distribution; Analysis of Variance; Ascorbic Acid; Child; Child, Preschool; Endoscopy; Female; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Korea; Male; Pyloric Antrum; Urease

To examine the relation between serum ascorbic acid and Helicobacter pylori serology from a probability sample of US adults.. Data from 6,746 adults (ages 20 to 90 years) enrolled in the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994 were analyzed. Multiple logistic regression models were examined taking into account sample weights and the complex survey design of NHANES III, and controlling for the effects of potential confounders. Because race appeared to modify the association between serum ascorbic acid and seropositivity to H. pylori, we conducted the analyses stratified by race.. A total of 2,189 adults (32%) had a positive serology for H. pylori, and, of these, 1,175 (54%) were positive for the CagA antigen. Among whites, a 0.50 mg/dL increase in serum ascorbic acid level was associated with decreased seroprevalence of H. pylori (Odds Ratio (OR) = 0.89, 95% confidence interval (CI) CI 0.82-0.96, p < 0.01). In analyses that controlled for seroprevalence of H. pylori, a 0.50 mg/dL increase in serum ascorbic acid level among whites was independently associated with a decreased seroprevalence of the pathogenic cagA-positive strain of H. pylori (OR = 0.31, 95% CI 0.12-0.79, p < 0.05). Serum ascorbic acid levels were not significantly associated with H. pylori serology among non-whites (all p > 0.05).. Higher serum levels of ascorbic acid were associated with a decreased seroprevalence of H. pylori and of the pathogenic cagA-positive strain of H. pylori among whites. If these associations are related causally and are not the result of residual confounding by factors such as socioeconomic status, ascorbic acid may affect the risk of H. pylori infection and in turn, the risk for peptic ulcer disease and gastric cancer among white Americans.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Antigens, Bacterial; Antioxidants; Ascorbic Acid; Bacterial Proteins; Female; Helicobacter Infections; Helicobacter pylori; Humans; Logistic Models; Male; Middle Aged; Nutrition Surveys; Odds Ratio; Seroepidemiologic Studies; United States

N-nitroso compounds are carcinogens formed from nitrite, a process that is inhibited by vitamin C in gastric juice. Helicobacter pylori infection has been reported to increase nitrite and decrease vitamin C in gastric juice. Therefore, susceptibility to gastric cancer in H. pylori-infected patients may be derived from increased N-nitroso compounds in gastric juice. However, most H. pylori-infected patients do not develop gastric cancer.. To investigate additional factors that may affect susceptibility to gastric cancer, we compared nitrite and vitamin C levels in gastric juice from H. pylori-infected patients with and without gastric cancer.. Serum and gastric juice were obtained from 95 patients undergoing diagnostic endoscopy, including those with normal findings, duodenal ulcer, gastric ulcer, atrophic gastritis and gastric cancer. Serum was analysed for H. pylori antibody, nitrate and nitrite, gastrin and pepsinogens; gastric juice was analysed for pH, nitrite and vitamin C.. pH and nitrite levels were increased and vitamin C levels decreased in the gastric juice of patients with atrophic gastritis and gastric cancer compared with other patients. However, in patients with a similar gastric acidity (pH 5-8), nitrite concentrations in the gastric juice were significantly higher and vitamin C levels significantly lower in patients with gastric cancer than in those with atrophic gastritis.. Although hypochlorhydria increases intraluminal nitrite and decreases intraluminal vitamin C, which increases the intraluminal formation of N-nitroso compounds, our results indicate that patients with gastric cancer may have additional factors that emphasize these changes.

Topics: Aged; Ascorbic Acid; Female; Gastric Juice; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Nitrites; Risk Factors; Stomach Neoplasms

Helicobacter pylori gastritis induces reversible lowering of Ascorbic Acid (AA) intragastric concentrations. No studies have been aimed at determining the gastric juice AA concentration of atrophic body gastritis (ABG) patients. Uric Acid (UA), is another potent hydro-soluble scavenger of ROS and its possible modification in the gastric juice of patients with H. pylori gastritis have never been investigated. This study was aimed at investigating the levels of AA and UA in the plasma and gastric juice of ABG patients, compared with H. pylori positive patients without corporal atrophy, and with healthy individuals.. Thirteen ABG patients (Group 1); 32 Chronic non-atrophic H. pylori gastritis patients (Group 2); and 13 healthy stomach controls (Group 3) attending gastroscopy with gastric biopsies (antrum=3, corpus=3) had plasma and intragastric levels of AA and UA measured.. Intragastric AA concentration was significantly lower in group 1 (median 0.21 microg/ml, range 0.1-24) compared both with groups 2 (median 5.5 microg/ml, range 0.1-33.2) (p=0.043) and 3 (median 14.9 microg/ml, range 0.34-44.8) (p=0.0028). Intragastric UA was not different between the three groups. Intragastric AA concentration resulted negatively correlated with the intragastric pH (Spearman r=-0.47, p=0.0003). In patients with gastritis (groups 1 and 2) there was a significant negative correlation between the sum of the Sydney Score variables in the body mucosa, and AA in the gastric juice (Spearman r=-0.55; p=0.0001).. The study shows that intragastric pH is the key factor for the depletion of gastric juice AA observed in patients with corporal atrophy and to a lower extent with nonatrophic H. pylori gastritis.

Topics: Adolescent; Adult; Aged; Antioxidants; Ascorbic Acid; Female; Gastric Acid; Gastric Juice; Gastritis; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Stomach; Uric Acid

Gastric juice vitamin C may be protective against gastric carcinogenesis but concentrations are significantly reduced by Helicobacter pylori infection. We investigated the in vitro effects of vitamin C at concentrations comparable with those found in gastric juice on gastric cancer cells and H pylori.. Gastric cancer cell lines and various H pylori strains were treated with L-ascorbic acid for up to 72 hours. Cell viability, and protein and DNA synthesis were determined. Flow cytometry was used for assessment of H pylori adherence, cell cycle distribution, and apoptosis. H pylori growth and its haemagglutination activity were determined using viability count and microtitration assay.. Vitamin C induced a significant dose dependent growth inhibition of gastric AGS and MKN45 cells but this effect was significantly reduced at levels similar to those in gastric juice of H pylori infected patients (<50 microM). Although vitamin C had no obvious effect on H pylori growth, haemagglutination activity, or adherence ability to gastric AGS cells compared with untreated controls, it significantly enhanced H pylori associated apoptosis and induced cell cycle arrest in these cells.. Vitamin C may inhibit gastric cancer cell growth and alter H pylori induced cell cycle events at concentrations comparable with those in gastric juice, but has no effect on H pylori growth or pathogenicity. However, the inhibitory effect on gastric cancer cells was lost at vitamin C concentrations found in patients with H pylori infection.

Topics: Adenocarcinoma; Ascorbic Acid; Bacterial Adhesion; Cell Division; Flow Cytometry; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Hemagglutination; Hemagglutination Tests; Humans; Hydrogen-Ion Concentration; Intestinal Mucosa; Stomach Neoplasms; Tumor Cells, Cultured

The aim of the study was to elucidate what are the concentrations of vitamin C in gastric juice in patients with gastric cancer in comparison to patients with metaplasia.. In patients aged 20 to 75 years with H. pylori infection and chronic gastritis, metaplasia and gastric cancer the concentration of vitamin C was determined by spectrofotometry of gastric juice during gastroscopy. On the basis of the results of histological examination the following four groups were isolated. Group I (control)--12 patients with normal gastric mucosa, group II--15 patients with chronic gastritis, group III--17 patients with metaplasia and group IV--16 patients with gastric cancer H. pylori infection was confirmed by urease test and histological examination (Giemsa stainning) in all patients.. In controls the mean concentration of vitamin C in gastric juice was 18.2 mg/ml (5.7-31.2 mg/ml), in group II--6.3 mg/ml (2.9-13.1 mg/ml) in group III--3.9 mg/ml (2.6-10.1 mg/ml) and group IV--3.2 mg/ml (1.7-9.2 mg/ml). Statistically significant differences of vitamin C concentration were found among group I and group II, III and IV (p<0.001) and among groups II and III and IV (p < 0.01).. There are not differences of vitamin C concentration in gastric juice between patients with metaplasia and patients with gastric cancer. This points out that low levels of this vitamin in gastric juice might play the role in the earlier stages of carcinogenesis.

Topics: Adult; Ascorbic Acid; Female; Gastric Juice; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Precancerous Conditions; Stomach Neoplasms

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

Helicobacter pylori infection is recognized to lower the concentration of vitamin C in gastric juice. The objective of this study was to assess the effect of the infection on the systemic availability of dietary vitamin C.. The study involved 1,106 men and women aged 25-74 randomly recruited from the population of north Glasgow. Their H. pylori status, dietary vitamin C intake calculated from a food frequency questionnaire and plasma vitamin C concentration were measured. Correction was made for potential confounding factors such as age, sex, smoking and social status.. The mean plasma vitamin C concentration in those who were H. pylori-positive was only 65% of that in those classified negative. Although partly explained by differences in age, sex, social class, smoking and vitamin C intake, the systemic reduction was observed across almost all sub-groups after stratification. Correction for all these factors still gave a plasma vitamin C level for H. pylori positives which was only 80% of that for negatives (P < 0.0001).. H. pylori substantially impairs the bio-availability of vitamin C. This, together with the reduced vitamin C intake of H. pylori-positive subjects, markedly reduces the plasma vitamin C level of infected subjects. The reduced circulating levels of vitamin C in H. pylori-infected subjects may contribute to the aetiology of gastric cancer, as well as other diseases associated with anti-oxidant deficiency.

Topics: Adult; Aged; Antioxidants; Ascorbic Acid; Biological Availability; Diet; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged

Helicobacter pylori infection is associated with elevated gastric mucosal concentrations of the lipid peroxidation product malondialdehyde and reduced gastric juice vitamin C concentrations. Malondialdehyde can react with DNA bases to form the mutagenic adduct malondialdehyde-deoxyguanosine (M(1)-dG). We aimed to determine gastric mucosal levels of M(1)-dG in relation to H. pylori infection and malondialdehyde and vitamin C concentrations. Patients (n = 124) attending for endoscopy were studied. Levels of antral mucosal M(1)-dG were determined using a sensitive immunoslot-blot technique; antral mucosal malondialdehyde was determined by thiobarbituric acid extraction, and gastric juice and antral mucosal ascorbic acid and total vitamin C were determined by high-performance liquid chromatography. Sixty-four H. pylori-positive patients received eradication therapy, and endoscopy was repeated at 6 and 12 months. Levels of M(1)-dG did not differ between subjects with H. pylori gastritis (n = 85) and those with normal mucosa without H. pylori infection (n = 39; 56.6 versus 60.1 adducts/10(8) bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 micromol/ml; P < 0.001), and antral mucosal ascorbic acid was unchanged (48.0 versus 42.7 micromol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M(1)-dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M(1)-dG levels were unchanged 6 months (63.3 versus 87.0 adducts/10(8) bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/10(8) bases; P = 0.8; n = 13) after successful eradication of H. pylori. M(1)-dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori.

Topics: Adult; Aged; Ascorbic Acid; Chromatography, High Pressure Liquid; Deoxyguanosine; Endoscopy; Female; Gastric Juice; Gastric Mucosa; Helicobacter Infections; Humans; Immunoassay; Lipid Peroxidation; Male; Middle Aged

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

Vitamin C (Asc) as a reactive oxygen species scavenger inhibits detrimental oxidation reactions and counteracts formation of mutagenic compounds which damage DNA in the gastric and duodenal mucosa. It has been considered as an important factor in reducing risk of gastric carcinoma. However, the role of uric acid (UA) as an antioxidant factor and its influence on gastric mucosa has not been so well investigated. The aim of the study was to evaluate the relationship between vegetable, fruit and fruit juices intake and water soluble antioxidant (Asc and UA) concentrations in plasma and gastric mucosa. The study also assessed the prevalence and intensity of inflammatory changes in mucosa and Helicobacter pylori infection. 34 patients participated in the study. Asc and UA concentrations in plasma and gastric mucosa samples were examined with the use of liquid chromatography (HPLC) method. Histopathological examinations of gastric mucosa were also performed. Higher concentrations of Asc and UA in plasma and less frequent inflammatory changes of gastric mucosa were found in patients regularly consuming vegetables and fruits. It may suggest the protective effect of these compounds on mucosa. No significant relationship was found between H. pylori infection and antioxidant concentrations in plasma and gastric tissue in patients with chronic gastritis.. Diet rich in fruits, vegetables and fruit juices helps in reducing prevalence of inflammatory changes in gastric mucosa. It can be associated with higher Asc and UA concentrations in plasma and higher UA concentrations in gastric mucosa. Lower Asc and UA concentrations in patients with gastritis have no significant relationship with H. pylori infection.

Topics: Adult; Analysis of Variance; Antioxidants; Ascorbic Acid; Beverages; Chromatography, High Pressure Liquid; Feeding Behavior; Female; Fruit; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Uric Acid; Vegetables

Previous studies have shown that gastric acid suppression worsens corpus gastritis in Helicobacter pylori (H. pylori)-positive patients. We evaluated the effect of acid-suppressive therapy and vitamin C on H. pylori-associated gastritis.. Forty patients with reflux esophagitis were divided into three groups by the status of H. pylori and therapy: group A (n=15), H. pylori (+) and omeprazole 20 mg; group B (n=15), H. pylori (+) and omeprazole 20 mg + vitamin C 1200 mg; and group C (n=10), H. pylori (-) and omeprazole 20 mg. In all three groups, the mucosal interleukin (IL)-8 contents, H. pylori colonization density, neutrophil infiltration in the corpus, and serum gastrin were evaluated at entry and 2 weeks after starting therapy; in group B, serum vitamin C levels were also measured.. In group A, the IL-8 contents and the degree of neutrophil infiltration during therapy exceeded those at entry, whereas in groups B and C, these values did not change significantly with treatment. Helicobacter pylori colonization density during therapy was similar to that at entry in all three groups. The serum gastrin (in all groups) and vitamin C levels (in group B) during therapy exceeded those at entry.. Potent acid suppression worsens H. pylori-associated corpus gastritis, although such worsening gastritis may be inhibited by vitamin C.

Topics: Acids; Anti-Ulcer Agents; Ascorbic Acid; Drug Therapy, Combination; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole

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

Omeprazole produces greater acid inhibition in Helicobacter pylori-positive than -negative subjects. We investigated whether this is accompanied by more profound changes in the intragastric milieu that facilitates bacterial synthesis of N-nitroso compounds.. Gastric juice pH; nitrite, ascorbic acid, and total vitamin C concentrations; and colonization by other bacteria were examined before and during omeprazole treatment in subjects with and without H. pylori infection. Studies were performed in the fasting state and after consumption of 2 mmol nitrate (equivalent to a salad meal).. Before omeprazole, H. pylori-positive and -negative subjects were similar for all parameters. During omeprazole, H. pylori-positive subjects had a higher intragastric pH (7.8 vs. 3.0; P < 0.00001) and greater colonization with non-H. pylori species (5 x 10(7) vs. 5 x 10(5) CFU/mL; P < 0.05). These bacteria included nitrosating species. During omeprazole treatment, H. pylori-positive subjects had higher intragastric nitrite levels after the nitrate meal (median area under the concentration/time curve, 12,450 vs. 4708 micromol/L. min; P = 0.04). Omeprazole lowered intragastric vitamin C levels in H. pylori-positive but not -negative subjects (1.8 vs. 3.4 microg/mL, respectively; P = 0.02).. In H. pylori-positive subjects, omeprazole produces disturbances in intragastric nitrite, vitamin C, and bacterial colonization that facilitate bacterial N-nitrosation. This may place them at increased risk of mutagenesis and carcinogenesis.

Topics: Adult; Anti-Ulcer Agents; Ascorbic Acid; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Microbiological Techniques; Middle Aged; Nitrites; Nitrosation; Omeprazole; Saliva

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

Gastric cancer is generally thought to arise through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. To identify such determinants, we launched a follow-up study in 1989-1990 among 3433 adults in Linqu County, China, a region with very high rates of gastric cancer.. Data on cigarette smoking, alcohol consumption, and other characteristics of the participants were obtained by interview in 1989-1990, when an initial endoscopy was taken. At study entry, antibodies to Helicobacter pylori were assayed in 2646 adults (77% of people screened), and levels of serum micronutrients were measured in approximately 450 adults. Follow-up endoscopic and histopathologic examinations were conducted in 1994. Antibodies to H. pylori, levels of serum micronutrients, and other baseline characteristics were compared between subjects whose condition showed progression to dysplasia or gastric cancer from study entry to 1994 and subjects with no change or with regression of their lesions over the same time frame. All P: values are two-sided.. The presence of H. pylori at baseline was associated with an increased risk of progression to dysplasia or gastric cancer (odds ratio [OR] = 1.8; 95% confidence interval [CI] = 1.2-2.6). The risk of progression to dysplasia or gastric cancer also was moderately increased with the number of years of cigarette smoking. In contrast, the risk of progression was decreased by 80% (OR = 0.2; 95% CI = 0.1-0.7) among subjects with baseline ascorbic acid levels in the highest tertile compared with those in the lowest tertile, and there was a slightly elevated risk in those individuals with higher levels of alpha-tocopherol.. H. pylori infection, cigarette smoking, and low levels of dietary vitamin C may contribute to the progression of precancerous lesions to gastric cancer in this high-risk population.

Topics: Adult; Ascorbic Acid; China; Disease Progression; Female; Follow-Up Studies; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Odds Ratio; Precancerous Conditions; Risk; Risk Factors; Smoking; Stomach; Stomach Neoplasms

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

To date it is not known whether gastric juice vitamin C levels are influenced by Helicobacter pylori CagA(+) strains. The aim of the present study, therefore, was to study the impact of H. pylori CagA status on gastric juice vitamin C levels.. We studied 30 H. pylori(+) patients, and the results were compared with 10 endoscopically and histologically normal H. pylori(-) subjects (control group) who were similar to the H. pylori(+) group in terms of age and sex. In all patients, gastric juice vitamin C levels were determined and the severity of gastritis was graded on a scale of 0 (absent) to 3 (severe). CagA was determined by immunoblotting the sera from patients against H. pylori antigens.. Among 30 H. pylori(+) patients, 20 were CagA(+) and 10 CagA(-). In the entire group of H. pylori(+) patients, the median gastric juice vitamin C levels (mg L-1) were 16.35 (range 3.5-33.6) and were significantly lower (P < 0.001) than in the control group of H. pylori(-) patients [35.5 (23.1-50.2)]. In addition, in the entire group of H. pylori(+) patients there was a highly significant (P < 0.0001) inverse correlation between the gastritis activity score and the gastric juice vitamin C levels. In the group of H. pylori CagA(+) patients, the median levels of gastric juice vitamin C were 13.8 (3.5-31.2) and were significantly lower than the corresponding levels in both the H. pylori CagA(-) group [24.8 (22-33.6), P < 0.01] and the H. pylori(-) control group [35.5 (23.1-50.2), P < 0.001], the last groups being similar. Furthermore, the gastritis activity median score in the H. pylori CagA(+) group [2 (1-3)] was significantly higher (P < 0.05) than in the H. pylori CagA(-) group [1 (1-2)].. These data indicate that infection with CagA(+) H. pylori strains significantly lowers the gastric juice vitamin C levels in comparison with CagA(-) H. pylori strains, which might have a significant impact on gastric carcinogenesis.

Topics: Adolescent; Adult; Antibodies, Bacterial; Antigens, Bacterial; Ascorbic Acid; Bacterial Proteins; Blotting, Western; Chronic Disease; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Prospective Studies

Test meals are used in the urea breath test to slow gastric emptying and to increase the area of contact with the substrate. Recently, citric acid has been suggested as an improved liquid test meal. The mechanism is unknown and could act by delaying gastric emptying, decreasing the pH at the site of the bacteria, or both. Our aim was to evaluate the effects of citric acid test meals on urea hydrolysis in vivo, to identify the possible mechanism for enhanced urea hydrolysis, and to identify the minimum effective dose.. We compared the U.S. commercial 13C-urea breath test with four liquid test meals (200 ml of water) consisting of citric acid, ascorbic acid, sodium citrate, and glucose polymer and also after the subcutaneous administration of pentagastrin. We studied healthy volunteers with and without proven H. pylori infection (by serology and histology). 13C-urea was administered orally simultaneously with the liquid test meals or immediately after the pudding had been ingested. Breath samples were taken before and after oral administration of the 13C-urea.. A dose response in urease activity was evident as the amount of citric acid was increased from 1 to 4 g. Citric acid at 1, 2, or 4 g produced significant increases in breath 13CO2 activity, compared with the commercial pudding (p < 0.05). Ascorbic acid (p = 0.053), subcutaneous pentagastrin (to lower pH) (p = 0.199), and glucose polymer (p = 0.03) (to delay gastric emptying) all approximately doubled breath 13CO2, compared with the commercial kit. Nevertheless, the increases were all significantly less than with the 4 g citric acid test meal.. The data are consistent with the marked effect of citric acid on gastric emptying and, possibly, distribution of the urea within the stomach being largely responsible for the enhanced urease activity with citric acid test meals. It should be possible to use a low dose of citric acid (e.g., 1 g per 200 ml) to enhance the simplicity and palatability of the test.

Topics: Ascorbic Acid; Breath Tests; Carbon Dioxide; Carbon Isotopes; Citrates; Citric Acid; Dose-Response Relationship, Drug; Gastric Acidity Determination; Gastric Emptying; Glucans; Helicobacter Infections; Helicobacter pylori; Humans; Pentagastrin; Sodium Citrate; Urea; Urease

Vitamin C is an important endogenous antioxidant, and epidemiologic evidence suggests that it may protect against the development of gastric cancer. We therefore determined mucosal vitamin-C levels in the stomach and duodenum of subjects with and without Helicobacter pylori infection.. The patients were 30 subjects undergoing routine gastroscopy for investigation of dyspepsia. High-performance liquid chromatography with electrochemical detection was used to determine mucosal ascorbic acid and total vitamin-C levels.. In H. pylori-negative subjects with normal gastroduodenal histology the antrum contained significantly higher levels of ascorbic acid and total vitamin C than the corpus or duodenum (P < 0.05). No significant changes were seen in gastric mucosal ascorbic acid or total vitamin-C levels in the presence of H. pylori infection and related inflammation. The presence of gastric atrophy did not affect mucosal ascorbic acid or total vitamin C levels. Duodenal ascorbic acid and total vitamin-C levels did not change significantly in the presence of gastric H. pylori or duodenal inflammation.. Although high levels of vitamin C are present in the gastroduodenal mucosa, these are not altered in the presence of H. pylori infection and inflammation. These observations suggest that the mucosal antioxidant potential of vitamin C is not impaired by H. pylori infection.

Topics: Adult; Antioxidants; Ascorbic Acid; Biopsy; Case-Control Studies; Chromatography, High Pressure Liquid; Duodenitis; Duodenum; Female; Gastric Mucosa; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; Male; Middle Aged

Maori and Pacific Island ethnic groups in New Zealand have a high risk for gastric cancer. Low levels of gastric juice ascorbic acid (vitamin C) have been suggested to be a risk factor for gastric cancer. Previous studies have shown that gastric juice ascorbic acid may be independently associated with both ethnicity and Helicobacter pylori infection. This study aimed to examine the interrelationship between H. pylori and ethnicity in New Zealand.. Gastric juice was collected into 70% perchloric acid preservative and stored at -80 degrees C. Ascorbic acid was analysed by high-performance liquid chromatography using ion-pair chromatography and electrochemical detection. Inflammation and atrophy was graded from biopsies from multiple sites in the antrum and body. Gastric juice was collected from 89 patients during routine endoscopy.. There was a wide range of measured gastric juice ascorbic acid from 0.001 to 410 microg/mL. The median concentration of ascorbic acid for H. pylori-negative patients was 1.78 microg/mL (n = 57) and 0.12 microg/mL (n = 32) for H. pylori-positive patients (P = 0.001). Gastric juice ascorbic acid concentration was not associated with age, endoscopic diagnosis or intestinal metaplasia, but was significantly associated with the degree of acute inflammation (P = 0.01) and the presence of atrophy (P = 0.04). The median ascorbic acid concentration for European patients was 0.92 microg/mL (n = 44) and 0.09 microg/mL (n = 38) for Maori and Pacific Island ethnic groups combined (P = 0.1). Multiple step-wise regression analysis showed that only H. pylori infection was a significant factor for predicting ascorbic acid concentrations (r2 = 0.12).. This study has confirmed that gastric juice ascorbic acid concentration is lower in the presence of H. pylori infection.

Topics: Adult; Aged; Aged, 80 and over; Ascorbic Acid; Ascorbic Acid Deficiency; Biopsy; Cross-Cultural Comparison; Female; Gastric Juice; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Native Hawaiian or Other Pacific Islander; New Zealand; Risk Factors; Stomach Neoplasms

Gastric carcinogenesis is a multifactorial, multistep process, in which chronic inflammation plays a major role.. In order to ascertain whether free radical mediated oxidative DNA damage is involved in such a process, concentrations of 8-hydroxydeoxyguanosine (8OHdG), a mutagenic/carcinogenic adduct, and thiobarbituric acid reactive substances (TBARS), as an indirect measure of free radical mediated damage, were determined in biopsy specimens from patients undergoing endoscopy.. Eighty eight patients were divided into histological subgroups as follows: 27 with chronic non-atrophic gastritis, 41 with atrophic gastritis, six with gastric cancer, and 14 unaffected controls.. Intestinal metaplasia, Helicobacter pylori infection, and disease activity were semiquantitatively scored. 8OHdG concentrations were assessed by HPLC with electrochemical detection, and TBARS concentrations were fluorimetrically assayed.. 8OHdG concentrations (mean number of adducts/10(5) dG residues) were significantly higher in chronic atrophic gastritis (p = 0.0009). Significantly higher concentrations were also detected in the presence of severe disease activity (p = 0.02), intestinal metaplasia (p = 0.035), and H pylori infection (p = 0.001). TBARS concentrations were also higher in atrophic gastritis, though not significantly so. In a multiple logistic regression analysis, 8OHdG concentrations correlated best with the presence and severity of H pylori infection (r = 0.53, p = 0.002).. Chronic gastritis is characterised by the accumulation of oxidative DNA damage with mutagenic and carcinogenic potential. H pylori infection is the major determinant for DNA adduct formation.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Aged; Aged, 80 and over; Analysis of Variance; Ascorbic Acid; Chronic Disease; Deoxyguanosine; DNA Damage; Female; Gastric Juice; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Reactive Oxygen Species; Regression Analysis; Stomach Neoplasms; Thiobarbituric Acid Reactive Substances

Helicobacter pylori is an independent risk factor for gastric cancer, and this association may be due to the bacterium causing reactive oxygen species mediated damage to DNA in the gastric epithelium. High dietary ascorbic acid intake may protect against gastric cancer by scavenging reactive oxygen species.. To assess reactive oxygen species activity and damage in gastric mucosa in relation to gastric pathology and mucosal ascorbic acid level, and to determine the effect of H pylori eradication on these parameters.. Gastric biopsy specimens were obtained for analysis from 161 patients undergoing endoscopy for dyspepsia.. Reactive oxygen species activity and damage was assessed by luminol enhanced chemiluminescence and malondialdehyde equivalent estimation respectively. Ascorbic acid concentrations were measured using HPLC.. Chemiluminescence and malondialdehyde levels in gastric mucosa were higher in patients with H pylori gastritis than in those with normal histology. Successful eradication of the bacterium led to decreases in both parameters four weeks after treatment was completed. Gastric mucosal ascorbic acid and total vitamin C concentrations were not related to mucosal histology, but correlated weakly with reactive oxygen species activity (chemiluminescence and malodialdehyde levels).. Data suggest that reactive oxygen species play a pathological role in H pylori gastritis, but mucosal ascorbic acid is not depleted in this condition.

Topics: Adult; Aged; Ascorbic Acid; Chromatography, High Pressure Liquid; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Lipid Peroxidation; Luminescent Measurements; Male; Malondialdehyde; Middle Aged; Reactive Oxygen Species; Treatment Outcome

Colonization of the gastric mucosa with Helicobacter pylori H.p. reduces the vitamin C concentration of gastric juice. Eradication of H.p. within four weeks after completed treatment does not exert a significant effect on changes in the concentration of vitamins A, E and C in gastric juice or serum. Despite this after eradication a rising trend of vitamin E in gastric juice was recorded. Substitution of vitamin C and E in gastritis associated with colonization with H.p. has a favourable effect and may reduce the risk of malignization.

Topics: Ascorbic Acid; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Vitamin A; Vitamin E; Vitamins

The pathological processes by which Helicobacter pylori infection leads to the development of gastroduodenal disease are still incompletely understood. Oxygen-derived free radicals are important mediators of inflammation and potential carcinogens. Furthermore, dietary studies have suggested that antioxidant vitamins may protect against gastric cancer.. To determine plasma free radical activity and antioxidant vitamin levels in dyspeptic patients and to correlate the results with H. pylori infection and tobacco smoking.. Forty-three patients undergoing routine endoscopy for investigation of dyspepsia.. Plasma free radical activity was determined by measurement of thiobarbituric acid-reactive substances (TBARS). Plasma samples were also assayed for the antioxidant vitamins A, C and E. Gastroduodenal biopsies were obtained from all patients for histological examination.. Plasma TBARS levels were significantly higher in H. pylori positive versus negative subjects (P < 0.03), smokers versus non-smokers (P < 0.04) and males versus females (P < 0.01). Multiple regression analysis revealed that after correcting for male sex and smoking there was no significant association between plasma free radical activity and H. pylori infection. Smokers had significantly lower levels of plasma vitamin C than non-smokers (P< 0.05); no differences were seen in vitamin A and E levels. Gender and H. pylori infection did not significantly affect plasma antioxidant vitamin levels. Gastroduodenal disease was present in all of the smokers compared with 67% of the non-smokers (P < 0.05); 69% of the smokers were H. pylori positive versus 53% of the non-smokers.. Tobacco smoking and male sex, both recognized risk factors for gastroduodenal disease, appear to be the major determinants of increased plasma free radical activity in dyspeptic subjects, rather than H. pylori infection. The reason for the higher prevalence of H. pylori infection and gastroduodenal disease in dyspeptic smokers is unclear but may relate to weakened antioxidant defences.

Topics: Adult; Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; Dyspepsia; Female; Free Radicals; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Smoking; Thiobarbituric Acid Reactive Substances; Vitamin A; Vitamin E; Vitamins

Vitamin C may be protective against gastric cancer though infection with Helicobacter pylori is associated with a reduction in intragastric concentrations of vitamin C.. To examine the effects of H pylori infection, gastric juice pH, the severity and extent of gastric inflammation, and CagA antibody status of the individual on gastric juice and mucosal vitamin C concentrations.. One hundred and fifteen patients undergoing routine gastroscopy for investigation of dyspepsia.. High performance liquid chromatography was used to determine vitamin C concentrations. CagA antibody was detected by western blot analysis.. Gastric juice ascorbic acid concentration was significantly lower in patients infected with H pylori compared with those uninfected (19.3 mumol/l (interquartile range (IQR) 10.7-44.5) versus 66.9 mumol/l (IQR 24.4-94.2), p = 0.003). The reduction in gastric juice ascorbic acid concentration was inversely related to the severity of gastritis (p = 0.01). CagA positive patients had significantly lower gastric juice ascorbic acid concentrations than CagA negative ones (14.8 mumol/1 (IQR 7.9-52.2) versus 39 mumol/l (IQR 19.9-142.2), p = 0.05). Decreased gastric juice dehydroascorbic acid concentrations were observed in patients with gastric atrophy and intestinal metaplasia. Mucosal ascorbic acid concentrations were also significantly lower in infected patients than uninfected patients (p = 0.04).. The reduction in gastric vitamin C concentrations is related to gastric juice pH, the severity and extent of gastritis, the presence of H pylori, and the CagA antibody status of the individual. These findings may have implications in H pylori associated carcinogenesis.

Topics: Adult; Aged; Aged, 80 and over; Analysis of Variance; Antigens, Bacterial; Ascorbic Acid; Bacterial Proteins; Blotting, Western; Chromatography, High Pressure Liquid; Female; Gastric Juice; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Statistics, Nonparametric; Stomach Neoplasms

Helicobacter pylori infection occurs most frequently in impoverished populations; however, little is known about specific determinants of susceptibility. This report describes the relationship between H. pylori infection and nutritional indicators among children from a rural village in the Colombian Andes, where a prevalence of 69% was observed in children from 2 to 9 years old.. In a cross-sectional study of 684 children, comprising 92% of the 2- to 9-year-old population of Aldana, Colombia, information was obtained on dietary factors by questionnaire, height and weight by direct measurement, and H. pylori status using the carbon-13 urea breath test. Multivariate logistic regression was used to estimate relative risks for nutritional indicators.. The infection was least frequent among children who are several servings of fruits and vegetables daily, drank two or more cups of milk daily, and were in the upper quintile of height for their age. The odds of infection increased 19-fold (95% confidence interval, 4.0-91.9) among children who consumed less than two daily servings of fruits and vegetables compared with the modal intake of three to five daily servings. Children whose daily vitamin C intake from fruits and vegetables was less than 40 mg had greatly increased odds of infection (odds ratio, 7.2; 95% confidence interval, 1.5-34.1) compared to the modal intake of 80-119 mg; for beta-carotene, the odds ratio was 3.1 (95% confidence interval, 1.2-7.9) for intakes of less than 300 IU per day, compared with the modal daily intake of 900 IU or more.. The results of this population-based study suggest that nutritional factors may play a role in determining susceptibility to H. pylori infection.

Topics: Aging; Animals; Ascorbic Acid; Body Height; Child; Child, Preschool; Colombia; Cross-Sectional Studies; Diet; Fruit; Helicobacter Infections; Helicobacter pylori; Humans; Milk; Nutritional Status; Vegetables

Helicobacter pylori infection is a risk factor for gastric carcinogenesis. High dietary vitamin C intake appears to protect against gastric carcinoma. It has been suggested that vitamin C exerts the protective effect by scavenging free radicals that may be enhanced by H. pylori. However, vitamin C has not been investigated in relation to the direct action on H. pylori. In this study, the authors attempted to clarify this possibility both in vitro and in vivo.. Susceptibility testing of H. pylori (64 strains) was performed by the agar dilution method. Bactericidal actions were determined by a broth cultivation technique. The effect of vitamin C on in vivo H. pylori colonization was evaluated by using the Mongolian gerbil model.. At concentrations of 2048, 512, and 128 microg/mL (minimum inhibitory concentrations [MICs]), vitamin C could inhibit the growth of 90% of the bacterial stains incubated at pH values of 7.4, 6.0, and 5.5, respectively. The broth cultures exposed to the MICs of vitamin C displayed a 1.57 approximately 2.5-log decrease in the number of viable bacteria, and the loss of viability was observed in 24 hours at concentrations 8-fold higher than the MICs. In an in vivo experiment, H. pylori colonies decreased significantly in animals treated with vitamin C after oral administration of vitamin C (10 mg/head/day) for 7 days.. High doses of vitamin C inhibit the growth of H. pylori in vitro as well as in vivo.

Topics: Animals; Ascorbic Acid; Gastric Mucosa; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Microbial Sensitivity Tests; Risk Factors; Stomach Neoplasms

High dietary ascorbic acid intake appears to protect against gastric cancer. This may be due to its action as a scavenger of reactive radical species formed in the gastric mucosa, resulting in a reduced level of radical-mediated DNA damage. We have studied 82 patients, of whom 37 had Helicobacter pylori-associated gastritis, a condition which predisposes to gastric cancer. Using electron paramagnetic resonance (EPR) spectroscopy we have demonstrated, for the first time, that ascorbyl radicals are generated in human gastric mucosa, presumably as a result of scavenging of free radicals by ascorbic acid. Quantification of ascorbyl radicals demonstrates that there is a higher concentration in those patients with H.pylori gastritis compared with subjects with normal histology (P < 0.01). We also found gastric mucosal luminol-enhanced chemiluminescence and malondialdehyde concentrations (which are believed to be markers of radical generation and tissue damage) to be higher in patients with H.pylori gastritis compared with those with normal histology (P < 0.001 and P < 0.01 respectively). The observed concentrations of the ascorbyl radical correlate with the level of luminol-enhanced chemiluminescence (r = 0.41, P < 0.001), but not with malondialdehyde concentrations (r = 0.08, P = 0.47). Mucosal ascorbic acid and total vitamin C concentrations did not vary between histological groups, nor did they correlate with mucosal levels of the ascorbyl radical, chemiluminescence or malondialdehyde. These data suggest that ascorbic acid is acting as a scavenger of free radicals generated in human gastric mucosa. The experiments therefore provide direct supportive evidence for the hypothesis that ascorbic acid protects against gastric cancer by scavenging reactive radical species which would otherwise react with DNA, with resultant genetic damage.

Topics: Adult; Ascorbic Acid; Free Radical Scavengers; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Luminescent Measurements; Malondialdehyde; Middle Aged; Reactive Oxygen Species; Stomach Neoplasms

We have evaluated gastric juice pH, nitrites and vitamin C levels, mucosal glutathione, and malondialdehyde, a marker of lipid peroxidation, in patients with chronic gastritis undergoing endoscopy. Patients had chronic gastritis with (n = 28) or without (n = 60) atrophy and/or concomitant Helicobacter pylori infection. Nineteen healthy subjects, without major macroscopic or histologic changes, were included as controls. Ten subjects were studied before and after H. pylori eradication. Vitamin C levels were low in atrophic gastritis (p < 0.006) and H. pylori infection (p < 0.02). Nitrite concentrations and pH were significantly higher in atrophy (p < 0.005 and 0.0001). Glutathione turnover was higher than normal in gastritis, with higher levels of oxidized glutathione (p < 0.02). Gastric malondialdehyde levels were significantly increased by gastritis (p < 0.05) and H. pylori infection (p < 0.05). Overall, more active gastritis coincided with lower vitamin C levels and higher malondialdehyde levels. After H. pylori eradication a drop in mucosal MDA levels was observed (p = 0.04). In summary, chronic gastritis and H. pylori infection correlate with increased free-radical production, reduced gastric vitamin C levels, and increased glutathione turnover. The possible implications of these changes in the pathogenesis of gastric damage and in carcinogenesis are intriguing.

Topics: Adult; Aged; Aged, 80 and over; Ascorbic Acid; Female; Free Radicals; Gastric Juice; Gastric Mucosa; Gastritis; Gastritis, Atrophic; Glutathione; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Nitrites

Topics: Adult; Ascorbic Acid; Black People; Female; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Injections, Intravenous; Male; Middle Aged; Statistics, Nonparametric; White People

Topics: Adult; Ascorbic Acid; Cell Division; Child; Epithelium; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Male; Precancerous Conditions; Risk Factors; Stomach Neoplasms

H. pylori has recently been recognized as a novel risk factor of gastric cancer, but its precise role in gastric carcinogenesis is as yet unknown. The aim of the present study was to assess the relationship between H. pylori infection and vitamin C levels in gastric juice and also to examine whether eradication of H. pylori could have any impact on these levels. Gastric juice and plasma vitamin C levels were measured in 88 dyspeptic patients who had an upper gastrointestinal endoscopy. In the subgroup of H. pylori-positive patients, eradication was attempted with triple therapy. This subgroup was studied on two occasions, ie, before and after treatment. There were 58 H. pylori-positive and 30 -negative patients. Gastric juice vitamin C levels in H. pylori-positive patients were statistically lower (P < 0.001) than the levels in the H. pylori-negative patients. Triple therapy achieved eradication in 45 patients (77.6%) of the 58 H. pylori-positive patients. Before H. pylori was eradicated in these 45 patients gastric juice vitamin C levels were significantly (P < 0.001) lower than those after eradication, the latter being no different than the group of 30 H. pylori-negative patients. There was a significant (P < 0.001) improvement of gastritis after eradication, which paralleled the elevation of gastric juice vitamin C levels. No difference was noted in plasma vitamin C levels between H. pylori-negative and -positive patients or in the latter before and after H. pylori treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Amoxicillin; Anti-Bacterial Agents; Ascorbic Acid; Bismuth; Drug Therapy, Combination; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Organometallic Compounds; Stomach Neoplasms

Gastric juice ascorbic acid concentrations were examined in black and white patients. Significantly lower concentrations were found in blacks, in the absence of a significant difference in the plasma concentration of vitamin C between races. Blacks had higher prevalence of Helicobacter pylori infection, higher gastric pH, more severe acute and chronic inflammation of the gastric mucosa and higher frequency of Lewis (a-b-) phenotype. Although most of these factors have been related to low ascorbic acid levels in gastric juice, none of them could account entirely for the difference between races either individually or after joint consideration. These observations may help to explain the high incidence of gastric carcinoma among the black population in southern Louisiana.

Topics: Ascorbic Acid; Black People; Gastric Juice; Helicobacter Infections; Helicobacter pylori; Humans; Lewis Blood Group Antigens; Louisiana; Stomach Neoplasms; White People

To investigate the change of vitamin C concentration (ascorbic and dehydroascorbic acid) in gastric juice after anti-Helicobacter pylori treatment, and to relate any observed change to gastric pH, inflammatory compromise of the gastric mucosa, plasma vitamin C concentration, and smoking habits.. Plasma and gastric juice vitamin C, fasting gastric juice pH, gastric histology, and smoking status were studied in 70 patients with H. pylori-associated gastritis before and after therapy.. Gastric juice ascorbic acid increased significantly after H. pylori clearance. For the most part, this change was confined to patients who experienced reduction of gastric pH. It was also related to improvement of the compromise of the gastric epithelium, reduction of the proportion of vitamin C composed by dehydroascorbic acid, and increase of the gastric juice/plasma vitamin C concentration gradient. Smokers had lower vitamin C concentrations in plasma and gastric juice before and after H. pylori clearance than nonsmokers.. The findings are consistent with a causal association between H. pylori infection and low ascorbic acid levels in gastric juice, and support two mechanisms for this association: increased oxidation and a decreased secretion of ascorbic acid.

Topics: Amoxicillin; Ascorbic Acid; Bismuth; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Nitrofurantoin; Organometallic Compounds; Salicylates; Smoking

The presence of ascorbic acid in gastric juice may protect against gastric carcinoma and peptic ulceration. This study examined the effect of Helicobacter pylori (H pylori) on the secretion of ascorbic acid into gastric juice by measuring fasting plasma and gastric juice ascorbic acid concentrations in patients with and without the infection and also before and after its eradication. Gastric juice ascorbic acid concentrations in 19 H pylori positive patients were significantly lower (median 2.8, range 0-28.8 micrograms/ml) than those in 10 H pylori negative controls (median 17.8, range 5.6-155.4 micrograms/ml) (p < 0.0005) despite similar plasma ascorbic acid concentrations in both groups. The median gastric juice:plasma ascorbic acid ratio in the H pylori positive patients was only 1.16 (range 0.02-6.67), compared with a median ratio of 4.87 (range 0.76-21.33) in H pylori negative controls (p < 0.01). In the patients with H pylori infection there was a significant negative correlation between the severity of the antral polymorphonuclear infiltrate and gastric juice ascorbic acid concentrations (correlation coefficient -0.52, p = 0.02). After eradication of H pylori in 11 patients, gastric juice ascorbic acid concentrations rose from 2.4 (0-12.8 micrograms/ml) to 11.2 (0-50 micrograms/ml) (p = 0.01). The median gastric juice: plasma ascorbic acid ratio also increased from 1.33 (0.05-6.67) to 2.89 (0.01-166) (p = 0.01). In conclusion, the high gastric juice:plasma ascorbic acid ratio in H pylori negative subjects shows active secretion of ascorbic acid into gastric juice. Secondly, H pylori infection causes a reversible lowering of gastric juice ascorbic acid concentrations, which may predispose to gastric carcinoma and peptic ulceration.

Topics: Ascorbic Acid; Duodenitis; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Stomach; Time Factors

Patients infected with Helicobacter pylori have abnormally low ascorbic acid concentration in gastric juice. Low vitamin C intake and Helicobacter pylori infection have been related to an increased risk of gastric carcinoma. This report examines the association between ascorbic acid and Helicobacter pylori in patients referred for upper gastrointestinal endoscopy. Elevated gastric pH and the damage to the gastric surface epithelium were inversely associated with the ascorbic acid concentration in gastric juice. We postulate that these two factors mediate the ascorbic acid-decreasing effect of Helicobacter pylori. Patients with nonpremalignant conditions (normal gastric histology, diffuse antral gastritis, or duodenal ulcer) had lower gastric pH, less damage to the gastric epithelium, and higher levels of ascorbic acid in gastric juice than patients with atrophic gastritis, intestinal metaplasia, or dysplasia.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Ascorbic Acid; Endoscopy, Gastrointestinal; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Stomach

Gastric juice ascorbic acid, total vitamin C, nitrite and N-nitroso-compound concentrations were determined in fasting gastric juice from four second generation members of a gastric cancer family, all of whom had Helicobacter pylori-associated chronic gastritis and intestinal metaplasia. Juice pH, nitrite and N-nitroso-compound concentrations were low. Juice ascorbate levels were comparable to those found in subjects with normal histology. The findings are contrary to our previous experience with juice ascorbate in H. pylori gastritis.

Topics: Adult; Ascorbic Acid; Family Health; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Nitrites; Nitroso Compounds; Stomach Neoplasms

The symptomatology of a case of acute infection with Helicobacter pylori is described, together with the accompanying changes in gastric mucosal histology, local and systemic humoral immune response, and gastric ascorbic acid concentration. The patient was an endoscopist, previously negative for the carbon-14 urea breath test, who had a week of epigastric pain and then became asymptomatic. H pylori was detected by culture of antral biopsy specimens and was still present after 74 days. Five days after infection the histological findings showed acute neutrophilic gastritis; by day 74 changes of chronic gastritis were evident. The patient seroconverted by IgG enzyme linked immunosorbent assay by day 74, but a mucosal IgM and IgA response was evident as early as day 14. Infection was accompanied by a transient hypochlorhydria but a sustained fall in gastric juice ascorbic acid concentration.

Topics: Acute Disease; Adult; Antibodies, Bacterial; Ascorbic Acid; Gastric Juice; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male