ascorbic-acid and Gastritis

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

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

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

Topics: Ascorbic Acid; Gastric Juice; Gastritis; Humans; Tissue Distribution

This monograph on the clinical chemistry of vitamin B12 reviews the literature on daily requirements, methods for measurement, the effects of drugs on vitamin B12 metabolism absorption, pregnancy, clinical conditions associated with vitamin B12 deficiency, errors of metabolism, and reactions to vitamin therapy. Although only very small quantities of vitamin B12 are required to satisfy the daily requirement, a sufficient supply is stored in the liver to meet normal requirements for at least a 3-year period. A number of drugs are known to affect the absorption of vitamin B12, including neomycin, potassium chloride, p-aminosalicylic acid, and colchicine. Significantly reduced serum concentrations of vitamin B12 have been noted in users of oral contraceptives (OCs), although concentrations still remain within the limits of normal. It appears that the vitamin B12 level in OC users reestablishes itself at a different and somewhat lower level. Vitamin B12 binding protein appears to remain unchanged. A vitamin B12 deficiency is unusual in pregnant women who consume a normal, varied diet. On the other hand, lactating women whose diets are low in animal protein and dairy products may have problems providing enough vitamin B12 to meet their own and their infant's needs; supplementary oral vitamins should be considered.

Topics: Absorption; Adult; Alcoholism; Anemia, Pernicious; Ascorbic Acid; Autoantibodies; Biguanides; Biological Transport; Chemical Phenomena; Chemistry; Chlorpromazine; Contraceptives, Oral; Diet; Female; Gastrectomy; Gastritis; Humans; Intrinsic Factor; Malabsorption Syndromes; Male; Metabolism, Inborn Errors; Middle Aged; Neoplasms; Nervous System Diseases; Nitrous Oxide; Nutritional Requirements; Pancreatic Diseases; Parasitic Diseases; Pregnancy; Pregnancy Complications; Transcobalamins; Vitamin B 12; Vitamin B 12 Deficiency

Malabsorption of l-T4 is a major clinical problem. Changes in gastric pH caused by several medical illnesses are associated with difficulties in the control of patients with hypothyroidism receiving the hormone. Means to correct these alterations would be of clinical value.. Our objective was to study the effect of vitamin C on the absorption of l-T4 in patients with hypothyroidism and gastritis.. Thirty-one patients with hypothyroidism, 28 females age 47.5 ± 13.5 (mean ± SD) years and 3 males age 55.7 ± 11.2 years ingested the dose of l-T4 in 120 mL water containing or not containing 500 mg vitamin C in a solution of pH 2.9 ± 0.1 (mean ± SD). Serum concentrations of free T4 and TSH were measured at the end of 3 periods of 2 months each, 2 controls and 1 vitamin C. Serum total T3 was measured in 16 of the patients, before and at the end of the vitamin C period. Serum TSH and free T4 and T3 were measured by a solid-phase, enzyme-labeled chemiluminescent competitive immunoassay All patients had gastrointestinal pathology and were not in good control when taking l-T4 before the study, and 23 had autoimmune thyroiditis or idiopathic hypothyroidism. The median l-T4 dose was 100 μg with an interquartile range of 50 μg. The protocol was reviewed and approved by our institution's ethics committee. Patients were asked to sign a written consent to participate in the study.. Serum concentrations of TSH, free T4, and T3 improved while on vitamin C. Serum TSH decreased in all patients (control, 11.1 [10.5] μIU/mL, median [interquartile range]), vitamin C 4.2 (3.7) μIU/mL, P = .0001), and it was normalized in 17 patients (54.8%). The average decrease was 69.2%. Serum T4 was higher with vitamin C in 30 of the 31 patients (control, 1.1 [0.3] ng/dL; vitamin C, 1.3 [0.3] ng/dL; P < .0001), and serum T3 increased as well in all 16 patients in whom it was measured (control, 60.5 [16.5] ng/dL; vitamin C, 70 [21] ng/dL; P < .005).. In patients with hypothyroidism and gastrointestinal pathology, vitamin C improves the abnormalities in serum free T4, T3, and TSH concentrations. This approach is helpful in the management of these patients.

Topics: Adult; Aged; Ascorbic Acid; Female; Gastritis; Humans; Hypothyroidism; Intestinal Absorption; Male; Middle Aged; Thyroid Function Tests; Thyrotropin; Thyroxine; Triiodothyronine

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

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

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

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

Low intake of foods rich in vitamin C is associated with an increased risk of gastric cancer, and geographic variation in average vitamin C intake, therefore, could explain some of the wide international variation in gastric cancer rates. This multicentre study investigated the relationships between plasma levels of vitamin C, as an indicator of vitamin C intake, and gastric cancer rates, markers of gastritis and other socio-demographic variables. Fasting plasma samples from about 1,400 individuals from 9 centres in 7 countries worldwide were assayed for total vitamin C using a fluorometric assay. There was no association between average plasma vitamin C levels and either gastric cancer mortality or incidence rates in the populations studied. Therefore, variation in fasting plasma vitamin C levels, as an indicator of consumption of vitamin C, does not appear to explain any of the wide geographic variation in gastric cancer rates. Furthermore, there was no association between plasma vitamin C levels and Helicobacter pylori infection, low serum levels of pepsinogen A (as a marker of severe chronic atrophic gastritis) or the presence of DNA adducts in blood leukocyte DNA. Multivariate models showed that fasting plasma vitamin C levels were associated positively with female sex, higher levels of education, never having smoked and increasing height and negatively with number of cigarettes smoked per day and increasing weight. This suggests not only that gender and tobacco smoking, in particular, are important predictors of plasma vitamin C levels but also that their effects are consistent throughout the developed world.

Topics: Adult; Antigens, Bacterial; Ascorbic Acid; Cross-Sectional Studies; DNA Adducts; Educational Status; Female; Gastritis; Humans; International Cooperation; Male; Middle Aged; Multivariate Analysis; Pepsinogens; Sex Factors; Smoking; Socioeconomic Factors; Stomach Neoplasms

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

Epidemiological evidence suggests that high dietary ascorbic acid reduces gastric cancer risk. It may do this by either reducing N-nitroso compound formation in gastric juice, or by scavenging reactive oxygen species in gastric mucosa. The aim of this study was to discover if potential ascorbic acid protection might be increased by supplementation. Thirty two patients were supplemented with ascorbic acid, 500 mg twice daily for two weeks. Gastric juice, plasma, and upper gastrointestinal biopsy ascorbate concentrations were measured and compared with values in 48 unsupplemented patients. It was found that ascorbic acid and total vitamin C concentrations were considerably higher in biopsy specimens from oesophagus, body, antrum, duodenum, and rectum, compared with values in plasma or gastric juice. Plasma and mucosal concentrations were unaffected by the presence of chronic gastritis but gastric juice concentrations were substantially lower in patients with chronic gastritis than in patients with normal histological assessment (p < 0.01). Patients receiving ascorbic acid supplements had higher ascorbic acid concentrations in plasma (p < 0.001), gastric juice (p < 0.001), and at all biopsy sites in the upper gastrointestinal tract (p < 0.05). Gastric juice ascorbic acid and total vitamin C concentrations in gastritic patients, however, were still less after supplementation than in normal subjects (p < 0.01). These data suggest that high ascorbic acid intake could reduce gastric cancer risk, but its protective effect might be greater if gastritis is treated (for example, by Helicobacter pylori eradication).

Topics: Adult; Aged; Aged, 80 and over; Ascorbic Acid; Endoscopy, Gastrointestinal; Esophagus; Female; Gastric Juice; Gastric Mucosa; Gastritis; Humans; Hydrogen-Ion Concentration; Intestinal Mucosa; Male; Middle Aged; Pyloric Antrum; Rectum

Scurvy is a disease that is rarely encountered in modern medicine. A condition that was classically associated with sailors, its incidence has decreased dramatically since the discovery of its association with vitamin C deficiency. We present the case of a 2-year-old boy, whose treatment for neuroblastoma was complicated by gastrointestinal disease, which necessitated enteral feeding. While still undergoing treatment, he started to complain about increasing pain in his lower limbs, which appeared to be markedly tender on palpation. Radiographic findings suggested a diagnosis of scurvy, which was subsequently confirmed on serum biochemistry. This was an unexpected finding, as the child had been receiving adequate vitamin C in his enteral feeds. However, his absorption had become severely impaired due to pseudomembranous gastritis and enteritis, leading to his deficient state. He significantly improved after intravenous ascorbic acid replacement and demonstrated a full recovery, both clinically and radiologically. This case highlights the importance of considering scurvy in the differential diagnosis for at-risk patients. Early recognition can facilitate the simple treatment of this potentially serious condition.

Topics: Ascorbic Acid; Diagnosis, Differential; Enteral Nutrition; Enteritis; Gastritis; Humans; Infant; Leg; Male; Neuroblastoma; Scurvy

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

We examined the recurrence of gastric mucosal lesions in rats after a single treatment with compound 48/80 (C48/80), a mast cell degranulator. During the period of 0.5 h to 24 h after treatment with C 48/80 (0.75 mg/kg, i.p.), an apparent recurrence of gastric mucosal lesions was found 18 and 24 h after the lesion formation, progression, and recovery occurred during the period of 12 h. Gastric mucosal blood flow showed the maximum reduction at 0.5, 16, and 22 h after treatment followed by the maximum recovery of the decrease at 12, 20, and 24 h, respectively. Gastric mucosal myeloperoxide and xanthine oxidase activities and lipid peroxide content showed the maximum increase at 3, 18, and 24 h after treatment. Gastric mucosal superoxide dismutase activity unchanged after treatment and gastric mucosal catalase activity decreased only at 24 h. Gastric mucosal Se-glutathione peroxidase activity and vitamin E, ascorbic acid, and hexosamine contents showed their maximum decrease at 3, 18, and 24 h after treatment. Gastric mucosal non-protein SH content showed the maximum decrease at 0.5, 16, and 22 h after treatment. Serum histamine and serotonin concentrations increased rapidly after treatment but the increases in serum histamine and serotonin concentrations diminished completely until 12 and 14 h, respectively. These results indicate that lesions recur repeatedly accompanied with an ischemia-reperfusion-like change in blood flow, inflammation, and disruption of antioxidant defense systems in the gastric mucosa of rats in no relation to released histamine and serotonin after a single C48/80 treatment.

Topics: Animals; Ascorbic Acid; Autacoids; Catalase; Cell Degranulation; Gastric Mucosa; Gastritis; Glutathione Peroxidase; Hexosamines; Lipid Peroxides; Male; Mast Cells; p-Methoxy-N-methylphenethylamine; Peroxidase; Rats; Rats, Wistar; Recurrence; Regional Blood Flow; Severity of Illness Index; Sulfhydryl Compounds; Time Factors; Vitamin E; Xanthine Oxidase

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

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

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

To study the role of gastric mucosal ascorbic acid (AA) in the progression of acute gastric mucosal lesions induced by compound 48/80 (C48/80), a mast cell degranulator, in rats.. C48/80 (0.75 mg/kg) was intraperitoneally injected to fasted Wistar rats. Oral administration of AA (10, 50 or 100 mg/kg) was performed 0.5 h after C48/80 treatment. Determinations for gastric mucosal lesion severity and blood flow, and assays for gastric mucosal total AA, reduced AA, oxidized AA, vitamin E, thiobarbituric acid reactive substances (TBARS), adherent mucus, nitrite/nitrate (NOx), non-protein SH (NPSH), and myeloperoxidase (MPO), and serum total AA, reduced AA, oxidized AA, and NOx were conducted 0.5 and 3 h after C48/80 treatment.. Gastric mucosal lesions occurred 0.5 h after C48/80 treatment and progressed at 3 h. Gastric mucosal blood flow decreased 0.5 h after C48/80 treatment but the decrease was recovered at 3 h. Gastric mucosal total AA, reduced AA, vitamin E, and adherent mucus concentrations decreased 3 h after C48/80 treatment. Gastric mucosal oxidized AA concentration remained unchanged after C48/80 treatment. Gastric mucosal NPSH concentration decreased 0.5 h after C48/80 treatment, but the decrease was recovered at 3 h. Gastric mucosal TBARS concentration and MPO activity increased 0.5 h after C48/80 treatment and further increased at 3 h. Serum total AA and reduced AA concentrations increased 0.5 h after C48/80 treatment and further increased at 3 h, while serum oxidized AA concentration increased at 0.5 h. Serum and gastric mucosal NOx concentrations increased 3 h after C48/80 treatment. AA administration to C48/80-treated rats at 0.5 h after the treatment prevented the gastric mucosal lesion progression and the changes in gastric mucosal total AA, reduced AA, vitamin E, adherent mucus, NOx, and TBARS concentrations and MPO activity and serum NOx concentration found at 3 h after the treatment dose-dependently. The AA administration to C48/80-treated rats caused further increases in serum total AA and reduced AA concentrations at 3 h after the treatment dose-dependently.. Gastric mucosal AA plays a critical role in the progression of C48/80-induced acute gastric mucosal lesions in rats.

Topics: Animals; Antioxidants; Ascorbic Acid; Gastric Mucosa; Gastritis; Male; Microcirculation; Mucus; Nitrates; Nitrites; Oxidation-Reduction; p-Methoxy-N-methylphenethylamine; Rats; Rats, Wistar; Regional Blood Flow; Sulfhydryl Compounds; Thiobarbituric Acid Reactive Substances; 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

Topics: Antioxidants; Arthritis, Rheumatoid; Ascorbic Acid; Cardiovascular Diseases; Chronic Disease; Comorbidity; Diabetes Mellitus; Free Radicals; Gastritis; Inflammation; Oxidation-Reduction; Oxidative Stress; Pancreatitis

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

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

Topics: Adult; Ascorbic Acid; Ascorbic Acid Deficiency; Chronic Disease; Colitis, Ulcerative; Diagnosis, Differential; Dietary Proteins; Ecchymosis; Fruit; Gastritis; Humans; Male; Middle Aged; Purpura

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

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

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

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

Plasma concentrations of the antioxidant vitamin ascorbic acid were measured by high-performance liquid chromatography in critically ill patients in whom the excessive generation of reactive oxygen species could compromise antioxidant defense mechanisms. Median concentrations of both total vitamin C (ascorbic acid and dehydroascorbic acid) and ascorbic acid in these patients were < 25% (P < 0.001) of the values found in healthy control subjects and in subjects in two other disease groups (diabetes, gastritis) in which reactive oxygen species are reported to be increased. The low values could not be explained by age, sex, intake, or treatment differences, but were associated with the severity of the illness and were not prevented by the use of parenteral nutrition containing ascorbic acid. In addition, the vitamin was less stable in blood samples taken from critically ill patients than in similar samples from subjects in the other groups. The findings indicate that antioxidant defenses could be considerably compromised in these very sick patients. If this reduces the patient's capacity to scavenge reactive species, then the potential of these species to damage DNA and lipid membranes could be increased and compromise recovery.

Topics: Adult; Aged; Aging; Ascorbic Acid; Chromatography, High Pressure Liquid; Critical Illness; Dehydroascorbic Acid; Diabetes Mellitus; Female; Gastritis; Humans; Intensive Care Units; Male; Middle Aged; Reactive Oxygen Species

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

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

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

The effects of four fruit juices, processed vegetable juice, orange peel, green tea and low dose vitamin C on endogenous N-nitrosation in 86 subjects from a high-risk area for gastric cancer in Moping County, China were studied using urinary excretion of N-nitrosoproline (NPRO) as an indicator. After ingestion of 300 mg L-proline, urinary excretion of NPRO was significantly increased from a baseline of 2.5 +/- 1.6 micrograms/day to 8.7 +/- 6.2 micrograms/day. (P < 0.001). Vitamin C (75 mg) administration significantly reduced NPRO formation (62.3%, P < 0.002) although NPRO excretion remained higher than the baseline level (4.2 +/- 1.3 vs 2.2 +/- 1.2 micrograms/day, P < 0.001). Intake of fruit juices and green tea extracts (containing 75 mg vitamin C) or of orange peel powder (containing 3 mg vitamin C) together with 300 mg L-proline inhibited NPRO formation effectively to the baseline level or to levels significantly lower than the baseline level (P < 0.05-0.005). A processed juice of a number of vegetables (300 ml) significantly catalysed endogenous nitrosation (14.7 +/- 11.8 vs 9.4 +/- 4.7 micrograms/day, P < 0.05). Endogenous N-nitrosation was unaffected by the presence of intragastric lesions. The present study shows that endogenous nitrosation in this population is profoundly affected by environmental factors and that inhibitors, such as vitamin C, alpha-tocopherol and other non-nutritive compounds in the foods do inhibit endogenous nitrosation either synergistically or in an additive manner. The significance of fruits and vegetables in prevention of human cancers is discussed.

Topics: Ascorbic Acid; Beverages; China; Citrus; Female; Fruit; Gastric Mucosa; Gastritis; Humans; Male; Metaplasia; Middle Aged; Nitrosamines; Precancerous Conditions; Proline; Risk Factors; Stomach Neoplasms; Tea; Vegetables

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

Ascorbic acid, the reduced form of vitamin C, may protect against gastric cancer. Accordingly, this study assessed the variability of ascorbic acid and vitamin C in the gastric juice of 77 patients with dyspepsia. There was a vitamin C concentration gradient from gastric juice down to plasma in subjects with normal gastric mucosa, but not in those with chronic gastritis. Patients with chronic gastritis had significantly lower gastric concentrations of vitamin C and ascorbic acid, and ascorbic acid concentrations were especially low in subjects with hypochlorhydria. The presence of the concentration gradient suggests that a mechanism for the secretion of vitamin C into the stomach exists. This is compromised by chronic gastritis. The very low ascorbic acid concentrations in hypochlorhydria may be a consequence of oxidation by bacterial nitrite. Those patients who by the Correa model are at greatest risk for gastric cancer have the lowest gastric levels of ascorbic acid.

Topics: Adult; Alcohol Drinking; Ascorbic Acid; Biopsy; Dyspepsia; Female; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastritis; Humans; Male; Smoking

1. Concentrations of ascorbic acid (ascorbic and dehydro-ascorbic; A + D; measured by the 2,4-dinitrophenylhydrazine method) of nearly three times those of plasma are present in gastric juice samples from patients with normal gastric histology. 2. A significant reduction in gastric juice ascorbic acid (A + D) was observed in patients with chronic gastritis. This reduction in concentration was independent of the grade of gastritis. 3. Concentrations of ascorbic acid (A + D) in gastric biopsy specimens were consistently higher in the antrum than in the body of the stomach. 4. These data demonstrate that considerable quantities of ascorbic acid (A + D) are normally 'secreted' into the stomach. 5. Ascorbic acid (ascorbic only; A; measured by h.p.l.c.) was present predominantly in its biologically active form in the patients with normal gastric histology. However, in patients with gastritis, independent of grade, ascorbic acid was present predominantly in its oxidized, biologically inactive form.

Topics: Adult; Aged; Ascorbic Acid; Chromatography, High Pressure Liquid; Chronic Disease; Female; Gastric Juice; Gastritis; Humans; Hydrogen-Ion Concentration; Leukocytes; Male; Middle Aged; Phenylhydrazines

A survey was conducted of 513 men aged 65 74 years living in two British towns with high and low stomach cancer death-rates. The prevalence of severe atrophic gastritis (defined as a serum pepsinogen I less than 20 micrograms l-1) was significantly higher in the high-risk than in the low-risk town (14.5% and 7.7% respectively); it also tended to be higher in the manual workers, who are known to have a greater risk of stomach cancer than non-manual workers. The manual workers in the high-risk town were particularly likely to have had a partial gastrectomy. Plasma ascorbate concentration and fruit intake were lower in the high-risk area and lower social classes, suggesting a poorer vitamin C status. There was, however, no direct relationship between ascorbate concentration and the presence of severe atrophic gastritis. These findings are consistent with the hypothesis that risk of stomach cancer is determined in two stages--a long-term effect, producing atrophic gastritis; and a short-term effect in which vitamin C is protective.

Topics: Aged; Ascorbic Acid; Gastritis; Gastritis, Atrophic; Humans; Male; Risk; Stomach Neoplasms; United Kingdom

A hospital-based case-control study of gastric cancer precursor lesions was conducted in a high-risk black population in southern Louisiana. Ninety-three subjects with biopsy-proved advanced chronic atrophic gastritis were compared to two control series: a gastroscopy clinic series and a general hospital-admission series. Dietary case-control differences indicated a protective effect associated with fruit and vegetable intake and with dietary vitamin C and a risk elevation associated with milk consumption. The protective effect associated with consumption of fruits, vegetables, and vitamin C is consistent with findings for gastric cancer and with the etiologic hypothesis of intragastric nitrosation. A twofold increased risk was associated with cigarette smoking. Gastric juice pH, NO3-, and NO2- were determined for subjects undergoing gastroscopy, and comparisons were made between this high-risk U.S. group and a Colombian population with a much greater magnitude of risk; the latter had higher NO3- and NO2- levels. An increase in pH was associated with increasing severity of gastric lesions. Levels of pH and NO2- concentration were significantly correlated (P less than .0005); however, in Louisiana the large difference in NO2- concentration associated with pH elevation is not associated with histopathologic severity. Divergent trends with severity of lesions for NO3- concentration were seen in the two populations.

Topics: Adult; Age Factors; Aged; Animals; Ascorbic Acid; Black People; Chronic Disease; Diet; Female; Fruit; Gastric Acidity Determination; Gastric Juice; Gastritis; Gastritis, Atrophic; Humans; Male; Middle Aged; Milk; Nitrates; Nitrites; Sex Factors; Smoking; Sodium Chloride; Stomach Neoplasms; Vegetables

As part of an ongoing cohort study of gastric cancer precursors in Nariño, Colombia, blood levels of ascorbic acid, vitamin E, retinol, pre-albumin, retinol binding protein and carotenoids were measured and correlated with histopathologic findings of gastric biopsies. Carotene levels in both sexes and vitamin E levels in males were significantly lower in subjects with gastric dysplasia than in subjects with normal mucosa and subjects with less advanced gastric lesions (chronic atrophic gastritis and intestinal metaplasia). No other significant correlations were found.

Topics: Adolescent; Adult; Age Factors; Aged; Ascorbic Acid; Carotenoids; Female; Gastric Mucosa; Gastritis; Humans; Male; Metaplasia; Middle Aged; Prealbumin; Retinol-Binding Proteins; Sex Factors; Stomach Diseases; Stomach Neoplasms; Vitamin A; Vitamin E; Vitamins

Topics: Adolescent; Adult; Ascorbic Acid; Cholinesterases; Duodenal Diseases; Enteritis; Female; Gastritis; Humans; Male; Middle Aged

Topics: Adult; Ascorbic Acid; Chronic Disease; Female; Gastric Mucosa; Gastritis; Health Resorts; Humans; Male; Middle Aged; Stomach; Ukraine

Topics: Acute Disease; Ascorbic Acid; Blood Transfusion; Diet; Diet Therapy; Duodenal Ulcer; Endoscopy; Esophageal and Gastric Varices; Gastritis; Gastrointestinal Hemorrhage; Hematemesis; Hernia, Diaphragmatic; Humans; Melena; Myocardial Infarction; Peptic Ulcer Hemorrhage; Radiography; Stomach Neoplasms; Vagotomy; Vitamin K

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adrenal Glands; Ascorbic Acid; Child; Cholangitis; Cholecystitis; Gastritis; Humans

Topics: Adrenal Cortex Hormones; Adrenal Glands; Adult; Ascorbic Acid; Female; Gastric Mucosa; Gastritis; Humans; Male; Middle Aged; Sulfhydryl Compounds

Topics: Alcoholism; Ascorbic Acid; Beer; Beriberi; Electrocardiography; Gastritis; Heart Diseases; Humans; Male; Middle Aged; Radiography, Thoracic; Thiamine

Topics: Ascorbic Acid; Balanitis; Candidiasis, Oral; Carbonates; Female; Gastritis; Gingivitis; Herpes Simplex; Humans; Leukoplakia; Male; Mycoses; Osteomyelitis; Pressure Ulcer; Stomatitis; Tonsillitis; Vulvitis

Topics: Ascorbic Acid; Carbohydrate Metabolism; Gastritis; Guinea Pigs

Topics: Adrenal Cortex; Animals; Ascorbic Acid; Gastritis; Rats; Vitamins