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)

In order to obtain an additional information concerning a possible functional role of the main types of the endocrine cells (EC and ECL) on investigation of aspiration biopsy specimens taken from the middle third of the stomach in patients with ulcerative disease of the duodenum and chronic gastritis was carried out. Changes in morphology, distribution and number of the endocrine cells in pathology of the mucosa and in various acidity of the gastric juice were followed up. On the basis of the data obtained the conclusion is made that serotonin-producing (EC) cells seem to have nothing to do with the regulation of the activity of the fundal glands, whereas the enterochromaffin-like cells (ECL) influence the production of hydrochloric acid by pavement cells.
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PMID:[Endocrine cells of the gastric mucous membrane]. 0 52

Bleeding from hemorrhagic erosions in the stomach or duodenum of seriously ill patients is associated with a high mortality. While the pathogenesis of such lesions is by no means certain, it is known that they are universal after shock, sepsis or severe burns. Fiberoptic endoscopy has become the most valuable means of diagnosis. This should be preceded by gastric irrigaiton, which usually sufficies to control bleeding caused by acetylsalicylic acid or alcohol, or both. Neutralization of gastric acidity is essential. The histamine HI-receptor antagonist, cimetidine, was used in 27 patients with erosive gastritis, and bleeding ceased in 24. There is a prospect that sugh agents will obviate the necessity of total gastrectomy in the occasional resistant cases in favour of conservative surgery.
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PMID:Symposium on intensive care: 3. Upper gastrointestinal bleeding in the intensive care unit. 2 13

Sclerosing of the gastric mucosa with a 60% fresh sterile solution of glucose was applied in 60 selected patients with chronic conflictual duodenal ulcers, hyperacidic gastritis by vagal neurogenic hyper-reactivity, associated with ischaemic gastropathy developed on an sympathico-adrenergic background. The immediate operatory results were good. The late results (between 1 and 5 years) were as follows: the clinical, radiological and metabolic results were good in 57 patients. Gastric chemical analysis, the values of the hourly basal output remained high in 16,6% of the patients, and those of acidity stimulated by histamine administration remained high in 13,3% of the patients. No peptic recidive was recorded. Unsatisfactory late results were noted in 3 patients (of which forced indication of the method in one patient and non-association of drainage in two patients).
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PMID:[Treatment of duodenal stress ulcer by means of chemical sclerosis of the gastric mucosa induced with a 60 percent glucose solution (results after 1--5 years)]. 49 72

Alterations in gastric physiology caused by selective embolization and vasopressin infusion of the left gastric artery were evaluated in 29 dogs. Gastric acidity was not significantly altered following Gelfoam embolization but decreased sharply with vasopressin infusion. These results suggest that the segmental occlusion caused by Gelfoam embolization permits significant collateral blood flow to the gastric mucosa, while the arteriolar and capillary constriction caused by vasopressin effectively decreases mucosal blood flow. These findings are consistent with the clincal observation that embolization is more effective in controlling bleeding ulcers, while vasopressin infusion is more effective for controlling hemorrhagic gastritis.
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PMID:Alterations in gastric physiology caused by selective embolization and vasopressin infusion of the left gastric artery. 108 10

In pigs treated with various doses of prednisone, pathologic changes appeared in the glandular region of the stomach, mainly in the fundic area and rarely and less severely in the cardiac and pyloric mucosae. The characteristic lesion was hemorrhagic gastritis; this was associated with massive gastric hemorrhages in pigs given the larger doses of prednisone. Epithelial changes were found in the esophageal area, but there were no ulcers. In pigs with gastric fistulas, prednisone administered at dose levels of 10 mg/kg of body weight for 8 days produced a significant increase in the volume and the acidity of gastric secretion. Hexosamine output, but not concentration, increased significantly during the treatment period. Change in pepsin secretion was sit significant. Prednisone did not produce an immediate change in gastric secretion--there being a latent period lasting 1 to 2 days before marked changes were observed. After peak changes occurred (3rd or 4th day of treatment), acidity gradually decreased to pretreatment level toward the end of the treatment period. This indicates that although increased acidity may be involved in the development of lesions in the glandular region, other factors probably have a role also in the pathogenesis of steroid-induced stomach lesions in swine.
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PMID:Effects of prednisone on gastric secretion and development of stomach lesions in swine. 109 Feb 20

In most cases of alkali ingestion, the stomach is protected from injury by its contents and gastric acidity, so that the esophagus is usually the main site of injury. The authors describe a case of severe corrosive gastritis following ingestion of a large amount of alkali. Huge gastric bullae, an unusual manifestation, were an early roentgen finding. As healing occurred, the stomach was reduced to a shrunken, aperistaltic pouch.
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PMID:Gastric bullae. An early roentgen finding in corrosive gastritis following alkali ingestion. 112 69

The incidence of parietal cell antibodies (P.C.A.) in patients with various diseases was investigated by complement fixation test (C.F.T.). The relationship between the incidence of P.C.A. and clinical and pathological findings was also investigated. The incidence of P.C.A. with simple atrophic gastritis was 34.8% in total cases, 29.0% in male and 48.1% in female, respectively. The difference between the sexes was statistically significant (p less than 0.05). The incidence of P.C.A. in superficial gastritis was 37.5%, showing the same incidence as atrophic gastritis. The difference between the two groups was not statistically significant (p less than 0.05). The incidence in patients with hypo- and hyperactivity was 43.0% and 11.8%, respectively. The difference was statistically significant, but that between hypo- and normoacidity was not significant (p less than 0.05). The author postulated the conclusion that the superficial gastritis could be included in the category of atrophic gastritis. The dissociation of correlation of titer of C.F.T. with acidity and histological findings was found. The correlation was more significantly observed with acidity than with histological findings. The relatively high incidences of P.C.A. were noted in patients with peptic ulcer, gastric carcinoma and chronic thyroiditis. The incidence of P.C.A. in other diseases showed the nearly equal incidence to that of other investigators. Three cases of postgastrectomy patients were noted, in which the P.C.A. disappeared four to six months after total or subtotal gastrectomy.
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PMID:Parietal cell antibodies. Part I. Clinical and pathological studies of parietal cell antibodies. 123 86

Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. H pylori was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower in H pylori negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p < 0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmol/l, 19 (7.1-33.1) mmol/l, 44 (25.1-63.1) mmol/l, and 36 (31.6-39.8) mmol/l respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During all predefined time periods, intragastric acidity was significantly higher in patients with H pylori positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between the H pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylori infection have normal gastric acidity.
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PMID:Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer. 139 25

Helicobacter pylori is a recognized cause of chronic active gastritis and is frequently associated with peptic ulcer disease, but its effect on acid secretion is unclear. Transient hypochlorhydria occurs with acute infections. Despite the theoretical possibility of an increase in parietal cell mass or a response to stimulation occurring secondary to the associated hypergastrinaemia observed with H. pylori, no consistent increase in basal, pentagastrin-stimulated acid secretion or 24-h intragastric acidity has been reported. Although H. pylori is accepted as one of the many factors involved in peptic ulcer disease, and eradication results in decreased ulcer recurrence, its pathogenic role is still poorly understood. The progression of chronic active gastritis to atrophic gastritis and hypochlorhydria may in part explain the natural tendency for duodenal ulcer disease to resolve.
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PMID:Helicobacter pylori and gastric acid secretion: the ulcer link? 177 27

Nine patients with Helicobacter pylori-related antral gastritis and history of duodenal ulceration were studied before and at 1 and 7 months after eradication of the infection by a 4-week course of tripotassium dicitrato bismuthate, metronidazole, and amoxycillin. The median basal gastrin concentration before eradication was 30 ng/l (range, 20-60) and fell to 20 ng/l (5-20) at 1 month (p less than 0.02) and 15 ng/l (5-20) at 7 months (p less than 0.01) after eradication. The integrated gastrin response to a peptide meal was 3650 ng/l.min (range, 1875-6025) before treatment compared with 1800 ng/l.min (range, 1200-3075) at 1 month (p less than 0.01) and 1312 ng/l.min (875-2625) at 7 months (p less than 0.03). Daytime intragastric pH (0900-2100 h) was similar before treatment (median, 1.4; range, 1.1-2.1) and at 1 month (1.4; 1.1-2.3) and 7 months (1.4; 1-2.2) after eradication. In five of the patients nighttime acid output (2300-0900 h) was also studied and was similar before (median, 86 mmol/10 h; range, 52-114) and at 1 month (76 mmol/10 h; 50-143) and 7 months (94 mmol/10 h; 63-106) after eradication. In conclusion, eradication of H. pylori is accompanied by a sustained fall in serum gastrin concentrations but is not accompanied by an early or late reduction of daytime intragastric acidity or nighttime acid output.
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PMID:Plasma gastrin, daytime intragastric pH, and nocturnal acid output before and at 1 and 7 months after eradication of Helicobacter pylori in duodenal ulcer subjects. 185 58


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