Gastric Juice Ascorbic Acid Research Articles

Letter: effects of gastric microenvironment on the management of iron deficiency anaemia – authors' reply

We thank Kilincalp and colleagues for their interest in our investigation on patients with anaemia following acute upper gastrointestinal bleeding (AUGIB) and for highlighting the topic of oral iron absorption.1, 2 In our study, we measured the prevalence of Helicobacter pylori infection and found no difference between the treatment groups. Unfortunately, we do not have data on the response rate to H. pylori treatment. The primary aim of our study was to evaluate the effect of iron treatment in anaemic patients after AUGIB in a randomised controlled design, regardless of H. pylori infection and proton pump inhibitor (PPI) treatment. We are fully aware that several micro-environmental factors might influence the absorption of oral iron. A systematic review found a 2.8-fold increase in the relative risk of iron deficiency anaemia among H. pylori-infected patients.3 The infection itself consumes iron and decreases the concentration of gastric juice ascorbic acid.4, 5 As mentioned by Kilincalp et al., the presence of a gastric acidic environment is important for oral iron absorption.1 On the basis of our data, we cannot recommend a specific route of iron supplementation in anaemic patients after AUGIB with H. pylori infection. However, if intravenous iron is chosen, potential reduced iron absorption due to H. pylori infection will be avoided. Use of intravenous iron supplementation furthermore solves the risk of a changed intestinal iron absorption in patients treated with PPI.6 Intravenous iron is still much more expensive than oral iron. Therefore, it would be desirable if we were able to allocate the anaemic AUGIB patients to the most effective iron treatment. This calls for large well-designed studies with a focus on iron absorption in patients with AUGIB, stratifying for PPI treatment, H. pylori status and eradication of H. pylori infection. The authors' declarations of personal and financial interests are unchanged from those in the original article.2

Hostile Environment of the Gastroesophageal Junction

The gastroesophageal junction is remarkable for its high prevalence of mucosal pathology including inflammation, erosions, metaplasia, and adenocarcinoma. The incidence of disease focused at this site has increased in the West over recent decades and this has coincided with a decline in Helicobacter pylori infection and atrophic gastritis. This is consistent with most disease at the gastroesophageal junction being due to damage by refluxing acidic gastric juice. Several observations may explain the focusing of mucosa pathology at the gastroesophageal junction. Recent studies have demonstrated much greater acid exposure of the esophageal squamous mucosa near to the gastroesophageal junction than at 7-cm proximal to this where acid reflux has been traditionally measured. The mechanism of this short segment reflux is unclear but it is likely to be relevant to the high incidence of pathology affecting the most distal esophagus and in asymptomatic subjects. In addition, it has been recognized that the proximal cardia region of the stomach largely escapes the buffering effect of food and remains highly acidic after meals. This unbuffered acid pocket will be available for refluxing into the esophagus during the postprandial reflux when transient lower esophageal relaxations are most frequent. The gastroesophageal junction is also where saliva meets acidic gastric juice and this results in very active and potentially mutagenic luminal nitrosative chemistry. This arises from the reaction between the high concentrations of nitrite in saliva and the hydrochloric acid and ascorbic acid in gastric juice. The gastroesophageal junction is thus a site of very active chemical warfare, the primary function of which is to destroy potentially pathogenic ingested microorganisms. However, as with all legitimate targets, there is always a risk of collateral damage.

Basis of Decreased Risk of Gastric Cancer in Severe Atrophic Gastritis with Eradication of Helicobacter pylori

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.

Gastric histopathology, iron status and iron deficiency anemia in children with Helicobacter pylori infection.

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.

Gastric Histopathology, Iron Status and Iron Deficiency Anemia in Children with Helicobacter pylori Infection

ABSTRACTObjectivesHelicobacter 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 extragastrointestinal 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.MethodsFifty‐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.ResultsTwenty‐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.ConclusionsH. 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.

15-deoxy-Δ12,14-prostaglandin J2 stimulates cathepsin-L expression in human pancreatic cancer cells through multiple pathways

High concentrations of nitric oxide are generated at the gastroesophageal junction due to the reduction of salivary nitrite to nitric oxide by acidic gastric juice containing ascorbic acid. Salivary nitrite is derived from the enterosalivary recirculation of dietary nitrate and its reduction to nitrite by buccal bacteria. Aims: To determine whether nitric oxide generated in the above way will exert nitrosative stress on the adjacent epithelium. Methods: A benchtop model was constructed reproducing the chemistry occurring at the gastroesophageal junction including a lumen and an adjacent epithelial compartment. The latter was maintained at pH7.4 and separated from the acidic lumen by a thin hydrophobic barrier with the permeability properties of the epithelial cell membrane. The secondary amine morpholine was added to each compartment and N-nitrosomorpholine formation at 15 min measured. Results: Adding 100uM nitrite to the acidic (pill.5) luminal compartment in the absence of ascorbic acid generated 6.2 + 2.0uM (mean + SE) N-nitrosomorpholine in that compartment and 2.2 + O. luM in the adjacent epithelial compartment. When lOOuM nitrite was added to the acidic luminal compartment (pH 1.5) containing ascorbic acid, all the nitrite was immediately converted to nitric oxide and no N-iutrusomorpholine was formed within that compartment. However, the nitric oxide rapidly diffused into the adjacent epithelial compartment (pH 7.4) where it generated very high concentrations of N-nitrosomorpholine (137 + 5.6uM). The concentrations of N-nitrosomorpholine generated in the epithelial compartment decreased with increasing luminal pH being 9SuM at pH2.5, 65uM at pH3.5 and 12uM at pH4.5. The concentration of N-nitrosomorpholine generated in the epithelial compartment was directly related to the nitric oxide concentration in the lumen. The addition of ascorbic acid or ghitathione to the epithelial compartment could only reduce this nitric oxide induced nitrosation within the epithelial compartment by 40%. Conclusion: Ascorbic acid in gastric juice prevents acid-catalysed nitrosation within the gastric lumen. However, in doing so, it generates nitric oxide which exerts a far higher nitrosative stress on the adjacent epithelium. This mechanism is likely to be relevant to the aetiology of mutagenesis and neopfasia at the gastroesophageal junctio

Does vitamin C intake slow the progression of gastric cancer in Helicobacter pylori-infected populations?

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.

Increased intragastric pH and reduced gastric juice ascorbic acid may be related with iron deficiency anemia in patients with atrophic body gastritis (ABG) and pangastritis (PG)

Increased intragastric pH and reduced gastric juice ascorbic acid may be related with iron deficiency anemia in patients with atrophic body gastritis (ABG) and pangastritis (PG)

Patients with atrophic body gastritis (ABG) and pangastritis (PG) associated with iron deficiency anemia (IDA) Have similar reduction of gastric juice Ascorbic Acid due to inccreased pH

Patients with atrophic body gastritis (ABG) and pangastritis (PG) associated with iron deficiency anemia (IDA) Have similar reduction of gastric juice Ascorbic Acid due to inccreased pH

Patients with atrophic body gastritis (ABG) and pangastritis (PG) associated with iron deficiency anemia (IDA) Have similar reduction of gastric juice Ascorbic Acid due to inccreased pH

Patients with atrophic body gastritis (ABG) and pangastritis (PG) associated with iron deficiency anemia (IDA) Have similar reduction of gastric juice Ascorbic Acid due to inccreased pH

ASCORBIC ACID CONCENTRATION IN GASTRIC JUICE AND PLASMA BEFORE AND AFTER ERADICATION OF HELICOBACTER PYLORI

Ascorbic acid, the reduced form of vitamin - C, is secreted by the normal stomach and may protect against gastric carcinoma and peptic ulcera-tion . This study examined the effect of helicobacter Pylori (H.P) on the se­cretion of ascorbic acid into gastric juice and examined if H.P. eradication improves gastric juice ascorbate val­ues. Eighty six patients with dyspeptic symptoms were included into the study. Fasting plasma and gastric juice ascorbic acid measurement, anti H.P. IgG, rapid urease slide test and bacteriological examination for antral & corpus biopsy specimens during endoscopy were done for all patients at entery into the study. Gastric juice ascorbic acid concentrations in H.P. positive patients were significant­ly lower (374.9±66.6 micromol/dl) than those in 10 H.P. negative con­trols, (507.8±9.04 micromol/dl] (P<0.0001). Likewise, plasma ascor­bic acid concentrations in H.P. posi­tive patients were significantly lower (322.7 ± 92.2 micromol / dl) than those of H.P. negative control (513.1 ± 17.5 micromol /dl) (P<0.0001). Of the 76 H.P positive patients who re­ceived one - week triple therapy (Omeprazol, Amoxicillin & Metronida-zole), H.P. was successfully eradicat­ed in 66 (86.8%), and after one mo­nth, their mean gastric juice ascorbic acid concentrations rose to 453. + 76.01 micromol/dl (P< 0.0001) and their mean plasma ascorbic acid con­centration rose to (419.3± 104.4 mi)

The relation between gastric vitamin C concentrations, mucosal histology, and CagA seropositivity in the human stomach

Background—Vitamin C may be protective against gastric cancer though infection withHelicobacter pylori is associated with a reduction in intragastric concentrations of vitamin C.Aims—To examine the effects ofH pylori infection, gastric...

The effect of H. pylori eradication and antioxidant vitamin supplementation on gastric mucosal reactive oxygen species damage and gastric juice ascorbic acid

Introduction: H. pylori infection causes increased gastric mucosal reactive oxygen species (ROS) and reduced gastric juice ascorbic acid levels, processes that may underlie the increased risk of developing gastric cancer• We have studied the effect of supplementing dietary antioxidant vitamins in combination with H. pylori eradication on these mechanisms in a randomised, double blind, placebo controlled trial. Methods: Following gastroscopy, H. pylori positive patients (based on uease test, culture and histology) were randomised into four groups: Bismuth chelate 120mg qds, tetracycline 500mg qds, metronidazole 400rag tds (BTM) or placebo (plac) for 2 weeks, followed by vitamin C (200mg bd) and vitamin E (50mg bd) (vits) or placebo for four weeks. Gastroscopy was repeated at six weeks. Samples were taken for assay of plasma, gastric juice, and antral ascorbic acid (PAA ()amol/ml), JAA (~tmol/ml), AAA 0amol/g)) using HPLC, lipid peroxidation using thiobarbituric acid extraction of malondialdehyde (MDA) (pmol/g), and ROS estimation by chemiluminescence (cpm/mg). Results: 56 patients had normal gastric mucosa; 98 H. pylori positive patients returned for follow up. Mean ages 35 and 49 yrs, respectively. For patients receiving antibiotics, only data for those with successful eradication (36/49, 73.5%) is included. No significant changes were seen in the placebo group.

Dietary nitrate lowers gastric juice ascorbic acid concentrations

Dietary nitrate lowers gastric juice ascorbic acid concentrations

Omeprazole lowers gastric juice ascorbic acid & elevates gastric juice nitrite concentrations

Omeprazole lowers gastric juice ascorbic acid & elevates gastric juice nitrite concentrations

Gastric Juice Ascorbic Acid After Intravenous Injection: Effect of Ethnicity, pH, and Helicobacter PyloriInfection

Gastric Juice Ascorbic Acid After Intravenous Injection: Effect of Ethnicity, pH, and Helicobacter PyloriInfection

Ascorbic acid, Helicobacter pylori and Lewis phenotype among blacks and whites in New Orleans.

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.

Effect of Helicobacter pylori and its eradication on gastric juice ascorbic acid.

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.

Helicobacter pylori-associated gastritis and the ascorbic acid concentration in gastric juice.

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.

Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations.

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.