Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori is the main cause of chronic gastritis in humans. Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspective. Atrophic gastritis is a quite common late consequence of H. pylori gastritis and will develop on a multifactorial basis, but not in all infected persons. The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum and corpus are affected to dissimilar extent and degree. The distal part of the stomach is the site where the atrophic sequelae (atrophic gastritis and intestinal metaplasia) of H. pylori infection occur most often. A minority of cases develop corpus-limited, or corpus-predominant atrophic gastritis. Along with the worsening of atrophic gastritis, inflammation and density of colonization of the mucosa by H. pylori tend to decrease in grade. In general, the degree of gastric mucosal inflammation, acute and chronic, is positively related to the degree of colonization of the mucosa by H. pylori. Acid secretion and local acidity are factors which modulate the ecology and density of colonization of H. pylori in the stomach, and may thus also modulate the evolution of chronic gastritis into topographically dissimilar subtypes. Acid secretion varies among individuals, this variation being perhaps caused by hereditary differences in parietal cell mass, or by differences in the sensitivity of parietal cells to hormonal or neural stimuli. It is hypothesized that in genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then leads to further impairment of acid output. In these cases, H. pylori infection and gastritis may, finally, heal in the antrum, resulting in hypochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.
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PMID:The relationships between chronic gastritis and gastric acid secretion. 873 Feb 65

One hundred and two patients suffering from giardiasis and/or chronic gastritis were subjected for upper gastrointestinal endoscopy. Purified immune rabbit's serum against Giardia lamblia was used in ELISA and immunoperoxidase (IIP) techniques for detection of Giardia antigen in the stomach. Results showed that out of 70 cases with intestinal giardiasis, 8 (11.4%) by ELISA and 6 (8.6%) by IIP showed gastric giardiasis. Higher percentage of gastric giardiasis (14%) was encountered in cases with both giardiasis and chronic gastritis (50) than in cases with giardiasis alone (5%) but with statistically insignificant difference (P > 0.05). None of the cases with chronic gastritis alone (without giardiasis) was positive for gastric giardiasis. Dyspepsia was the main presenting symptom in cases with gastric giardiasis (P < 0.05) with significant (P < 0.05) association. Helicobacter pylori was encountered in 6 out of 8 cases (75%) with gastric giardiasis (P < 0.05) with significant (P < 0.05) association. Duodenogastric reflux was detected in 4 out of 8 cases (50%). Histopathological changes in antral mucosa were detected in all cases of gastric giardiasis. This study indicates that under abnormal circumstances most probably with decreased gastric acidity, gastric giardiasis can occur in concomitance with intestinal giardiasis. So, one has to search for Giardia in gastric biopsies, particularly those showing chronic atrophic gastritis and H. pylori. Also, one has to be aware of gastric giardiasis as a possible cause of upper gastrointestinal symptoms.
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PMID:Giardia lamblia and chronic gastritis. 875 56

H. pylori acquisition is the main cause of chronic gastritis in humans. After acquisition, non-atrophic gastritis appears which develops with time into atrophic gastritis in approximately one third of infected subjects. Gastritis may affect the gastric antrum, both antrum and corpus or, occasionally, corpus alone. Acid secretion and local acidity are factors which are considered to influence the ecology and flourishing of H. pylori infection in the stomach, and can, therefore, also modulate the evolution of gastritis into topographically dissimilar subtypes. In the present study, we analysed whether there occurs an association between the intensity of chronic gastritis (inflammation) of the corpus mucosa and the pentagastrin stimulated peak acid output (PAO) in 94 subjects who had an H. pylori positive, non-atrophic gastritis. It appeared that the mean PAO was significantly higher in subjects who had mild or no chronic corpus gastritis than in those who had severe corpus gastritis. The prevalence of subjects with mild or no gastritis was highest among those with a high PAO ( > or = 30 mmol/hr) and lowest among those with a low PAO ( < 30 mml/hr). Furthermore, the mean score of chronic corpus gastritis was significantly (P < 0.01) lower in those with PAO < or = 19 mmol/hr than among those with PAO > or = 40 mmol/hr. We conclude that the intensity of chronic inflammation (gastritis) in the corpus mucosa is inversely related to PAO. This supports the hypothesis that acid output may affect the course of H. pylori gastritis and can modulate the topographic distribution of gastritis in the stomach.
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PMID:H. pylori corpus gastritis--relation to acid output. 877 95

Helicobacter pylori (Hp) is considered as the major pathogen in Hp-associated gastritis but the mechanism of its action has not been fully explained. We investigated both the damaging and protective effects of intragastric (i.g.) application of ammonia (NH4OH) and ammonium ion (NH4Cl), the major products of Hp-derived urease, on the rat stomach with intact and capsaicin-deactivated sensory nerves or suppressed prostaglandin (PG) and nitric oxide (NO) synthesis. NH4OH given i.g. resulted in a concentration-dependent mucosal damage starting at 30 mM and reaching maximum at 250 mM (pH 11), the extent of damage being similar to that obtained with 100% ethanol. NaOH solution (1 mM) at pH 11 given i.g. did not affect mucosal integrity. The damage caused by NH4OH was accompanied by the fall in gastric blood flow (GBF) reaching at 250 mM NH4OH about 30% of the vehicle control value. The NH4OH-induced gastric damage was augmented by capsaicin-induced deactivation of sensory nerves, the suppression of nitric oxide (NO) synthase with L-NAME or the decrease of i.g. acidity by ranitidine. The pretreatment with scavengers of reactive oxidants significantly reduced the area of NH4OH-induced gastric lesions. When the mucosa was first exposed to a low 15-mM concentration of NH4OH and then insulted with large 250 mM NH4OH or with 100% ethanol, the lesion area was markedly reduced as compared to that obtained with 250 mM NH4OH or 100% ethanol alone. This adaptive protection by 'mild' concentration of NH4OH against strong irritants (250 mM NH4OH or 100% ethanol) was reversed, in part, by pretreatment with L-NAME and indomethacin. NH4Cl (60-500 mM) given i.g. alone failed to affect the mucosal integrity but when applied before 100% ethanol it produced a concentration-dependent fall in the mucosal damage by these irritants. We conclude that; (1) ammonia at higher concentrations damages the gastric mucosa, while ammonium ion exerts the protective activity; (2) the ammonia-induced gastric damage may involve the formation of reactive oxidants; (3) ammonia at lower concentration acts like a mild irritant via the activation of sensory nerves, NO-arginine pathway and PG.
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PMID:Gastric mucosal damage and adaptive protection by ammonia and ammonium ion in rats. 891 6

We measured gastric juice fluid output, acidity, tonic strength (osmolality), and pepsin concentrations basally and after the injection of pentagastrin in 120 healthy African Americans and 60 Caucasian Americans of similar age and gender. Sera for basal gastrin concentration and IgG for antibody to Helicobacter pylori (Hp) organisms also were obtained, as were gastric body mucosal biopsies to ascertain the presence or absence of Hp or gastritis. Gastric juice hydrogen ion concentrations and osmolality were significantly lower in African Americans than in Caucasians. At the same time, African Americans had significantly higher gastric juice fluid outputs than did Caucasians. From measurements of gastric juice fluid output, acidity, and osmolality, we used a previously validated method for calculating gastric HCO3- and H+ secretion, as well as nonparietal and parietal fluid secretion. Gastric HCO3 secretion and nonparietal fluid were significantly higher in African Americans, while H+, parietal fluid, and pepsin secretion rates were nearly identical in the two racial groups. Basal serum gastrin concentrations and antibody titers to Hp also were significantly higher in African Americans (p < .001). Mucosal biopsies demonstrated a much higher prevalence of Hp infection and chronic active superficial gastritis in African Americans than Caucasians (p < .001). When only Hp-negative subjects were considered, racial differences in gastric secretion and basal serum gastrin concentration were still present. The mechanism or mechanisms causing higher gastric bicarbonate and nonparietal fluid secretion and for higher serum gastrin concentrations in African Americans remains to be elucidated.
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PMID:Racial differences in gastric function among African Americans and Caucasian Americans: secretion, serum gastrin, and histology. 895 72

Helicobacter pylori has been established as the major causative agent of human active gastritis and is an essential factor in peptic ulcer disease and gastric cancer. The mechanism that has been proposed for H. pylori to control its inhospitable microenvironment happens to coincide with the pH control technique developed by us. This technique was developed to separate an acidic environment from a basic environment for a sequential enzymatic reaction by the hydrolysis of urea within a thin layer of immobilized urease. In this paper, a mathematical model is presented to consider how H. pylori survives the gastric acidity. The computed results explain well the experimental data available involving H. pylori.
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PMID:Helicobacter pylori survival in gastric mucosa by generation of a pH gradient. 925 24

Symptomatic gastro-oesophageal reflux disease is a common disorder characterized by pathological exposure of the distal oesophagus to acid. The management requires the control of symptoms, prevention of relapse and complications. Proton pump inhibitors are without doubt the most effective agents in the management of gastro-oesophageal reflux disease. In Helicobacter pylori-negative individuals the efficacy of ranitidine, but more pronounced of omeprazole, on the nocturnal intragastric acidity, is less than in Helicobacter pylori-positive patients. Curing the Helicobacter pylori infection in gastro-oesophageal reflux disease patients might, therefore, have the disadvantage of losing efficacy of antisecretory therapy. Conversely, several studies have shown that long-term use of proton pump inhibitors is associated with progression and worsening of body gastritis exclusively in Helicobacter pylori-positives. This observation makes Helicobacter pylori eradication indicated before starting long-term treatment with proton pump inhibitors for gastro-oesophageal reflux disease and other acid-related diseases. The data reported, so far, however, are not conclusive. The Federal Drugs Administration Advisory Committee concluded on available data, that there is no evidence that longterm proton pump inhibitors treatment leads to gastric atrophy, intestinal metaplasia or gastric cancer. Eradication of Helicobacter pylori infection might lead to reduction in the efficacy of antisecretory agents, but might prevent worsening of the gastric corpus gastritis. More data are needed to really answer these clinically relevant questions.
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PMID:Should Helicobacter pylori be eradicated before starting long-term proton pump inhibitors? 951 35

The reverse transcription polymerase chain reaction (RT-PCR) was performed to detect genes of RNA viruses in the freshly biopsied gastric mucosa of seven patients with low gastric acidity. Although nucleoprotein genes of Sendai virus and hemmaglutinin genes of influenza virus A were not detected, nucleoprotein genes of influenza virus B were detected in samples from three of the seven patients. The first patient had had antrectomy and vagotomy for gastric ulcer, the second patient was receiving a histamine type 2 receptor blocker for gastritis, and the third patient was receiving a proton pump inhibitor for gastric ulcer. Virus isolation from gastric mucosa and from gargles was negative for all seven patients. These findings suggest that genes of influenza viruses may exist in the gastric mucosa of patients with low gastric acidity.
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PMID:Detection of genes of RNA viruses from freshly biopsied gastric mucosa by reverse transcription polymerase chain reaction. 960 41

Helicobacter pylori gastritis is common, but effects on gastric secretion are not well understood. We measured basal and pentagastrin-stimulated gastric acidity, pepsin activity, and fluid output, as well as serum gastrin concentrations and H. pylori antibody levels, before and after treatment of H. pylori gastritis in 28 men and women. Subjects were studied before and 1 and 3 mo after a course of bismuth, metronidazole, and tetracycline. Elimination of H. pylori gastritis, accomplished in 14 subjects, increased basal and pentagastrin-stimulated gastric acidity (by 15 meq/l) and basal acid output significantly (by 2.1 meq/h 1 mo after therapy). Elimination of H. pylori had an opposite effect on pepsin secretion, significantly decreasing pepsin output by 30%. Elimination of H. pylori significantly reduced nonparietal fluid output by 35%, without affecting fluid output from parietal cells. Serum gastrin and H. pylori antibody levels declined significantly after elimination of H. pylori. None of these changes was observed in 14 subjects whose H. pylori gastritis was resistant to antimicrobial therapy. In summary, eradication of H. pylori infection increases gastric acidity by reducing nonparietal gastric secretion from peptic and other cells.
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PMID:Effects of Helicobacter pylori gastritis on gastric secretion in healthy human beings. 969 99

Helicobacter pylori acquisition is the main cause of chronic gastritis in humans. In up to half of the infected subjects, chronic gastritis progresses to atrophic gastritis and intestinal metaplasia. During this course, various mechanisms are triggered that may contribute to the pathogenesis of gastric cancer. Such mechanisms include the inflammation-related cascades of cytokine and free radical reactions, up- and downregulation of growth factors and their receptors, and the atrophy-related impairment of acid output and intraluminal acidity. An array of other factors may also have become significant including overgrowth of bacteria other than H. pylori in the hypochlorhydric or achlorhydric stomach, a high dietary consumption of salt, nitrate, or nitrite, smoking, deficiency of vitamins or micronutrients, influence of sex hormones, or an inherited liability of the dividing epithelial cells to gene errors. These factors may vary in effect between populations and individuals but, if active, may affect the cell genome which may further influence the course and progression of chronic gastritis, and can finally result in overt gastric neoplasia. The molecular biology of gastric cancer has revealed a spectrum of gene errors which vary in type and extent between different histological types of cancer, and between individual cases. There now is evidence that the intestinal metaplasia or the gastric epithelium in atrophic gastritis reveal signs of abnormal expression of various regulatory genes well before the appearance of gastric neoplasia. It is possible that the mechanisms leading to mutation of the genes in epithelial cells are triggered very early in the H. pylori gastritis cascade, and that atrophic gastritis and intestinal metaplasia result from these processes.
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PMID:Review article: Pathogenesis of the transformation from gastritis to malignancy. 970 Oct 4


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