Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Electrophoretic separation of proteases from human gastric mucosal extracts of five patients with gastric ulcer, one with duodenal ulcer and three with gastric cancer were investigated by agar-gel electrophoresis at pH 8.3 and pH 5.0. 2. In the fundic mucosal study, there were seven faster moving proteases in all nine cases, but the slowest moving protease showed a slightly different picture in each case. In the antral mucosal study, two of eight cases showed mainly group II pepsinogens, seven of nine cases, however, showed the same results as in the fundic mucosal study. 3. In the cases of the nine mucosal extracts activated at pH 1.5 or pH 4.0, they all showed the same electrophoretic separation at each pH level. At these two pH levels, however, quite different electrophoretic patterns were observed. The presence of pepsin 3 appeared to diminish at the higher levels of pH, although that of pepsin 5 and pepsin 7 appeared to increase at pH 4.0 and above. Pepsin 6 appeared for the first time at pH 4.0 and existed at higher pH levels. 4. We thus conclude that electrophoretic patterns of pepsins in the gastric mucosal extracts are changeable depending on the pH level of the incubating medium, and further that diversity of pepsins in gastric juices may also depend on the pH level of gastric juices.
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PMID:Studies on the pepsinogens of human gastric mucosal extracts. 74 87

This case-control study of Hawaiian Japanese indicated that gastric ulcer in the proximal portion of the pyloric antrum has features similar to those of gastric cancer. Such ulcers occurred at sites most frequently and most severely affected by intestinal metaplasia, although metaplasia tended to be more extensive with cancer than with ulcer. Metaplastic mucosa was more vulnerable to the action of pepsin and acid than was normal mucosa. The risk of ulceration would rise when a sufficiently lagrge area of the antrum was intestinalized and when the corpus continued to produce significant quantities of these substances. This study showed a strong association between salt intake, ulcer, and metaplasia. Significant but less dramatic associations were demonstrated between metaplasia and the use of traditional Japanese foods and smoking. The question was raised as to whether salt promotes ulceration or whether it potentiates the action of a mutagen that causes intestinal metaplasia.
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PMID:Epidemiologic pathology of gastric ulcer and gastric carcinoma among Japanese in Hawaii. 83 57

A significant association has previously been found between a betazole-induced decrease in serum group I pepsinogen (PG I) levels and a low peak acid output (PAO) in symptomatic patients with vagotomy and gastric resection or a drainage procedure. This study compares the effect of betazole on serum PG I levels and gastric acid output in 245 unoperated patients (115 duodenal ulcer, 25 prepyloric ulcer, 32 gastric ulcer, 73 nonulcer) and in 73 symptomatic postoperative patients (15 subtotal gastric resection, 28 vagotomy and gastric resection, 30 vagotomy and drainage). A negative serum PGI response (2-hr serum PG I level less than 92% of basal) occurred in 10 (4.1% of the unoperated patients and in 31 (42.5%) of the postoperative patients. Seven (70%) of the former and 29 (93.5%) of the latter patients had a PAO of less than 10 mEq per hr, indicating that a negative serum PG I response is associated with a low PAO in both unoperated and postoperative patients. The PAO was greater than 10 mEq per hr in 93.1% of the 277 patients with a 2-hr serum PG I level of more than 92% of basal. Additional studies revealed that neither aspiration of gastric juice nor perfusion of the stomach with acid altered the serum PG I response. This suggests that topical acid does not modulate the effect of betazole on serum PG I levels. Finally, a negative serum PG I response has been shown to be paradoxical, in that gastric pepsin levels have been found to increase over basal concurrently with the decrease in serum PG I levels.
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PMID:Effect of betazole on serum group I pepsinogen levels: relationship to gastric acid output in unoperated and postoperative patients. 84 14

1) In chronic gastric ulcer bed rest, leaving out smoking and carbenoxolone have increased the rate of healing. 2) In chronic duodenal ulcer it has yet to be shown that any medical measure so far significantly altered the course of the disease. 3) The surgical approach to the treatment of chronic duodenal ulcer is based upon three principles, all of them aiming at reducing the acid-pepsin secretion: a) Removal of the acid secreting mucosa decreases the acid secretory capacity of the stomach; b) Removal of the pyloric antrum eliminates the main source of gastrin, the major known humoral excitant of acid secretion; c) Section of the vagi probably renders the acid secreting cells less responsive to humoral stimulation (Brooks). The major problem, however, which is the prevention of recurrent duodenal ulcer is yet unsolved. There is some hope that the new receptor blocking agent metiamid is the first step, and there is even more hope in that the proceedings of this symposium will show us further steps forward.
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PMID:The rationale in the treatment of peptic ulcer disease. 97 73

Pepsin secretion is stimulated by the back-diffusion of acid across the mucosa of the vagally denervated canine pouch. If back-diffusion is enhanced by damage, pepsin secretion increases. The current study investigates whether this mechanism exists in man. The stomach of normal human volunteers were irrigated for 1 hour with either buffer of 0.01 N HCl, 1 hour with 0.2 N HCl, and a final hour with buffer or 0.01 N HCl. During the middle hour both the concentration and output of pepsin increased three- or fourfold. From these studies it appears that the human gastric mucosa contains a mechanism similar to the dog's which results in the stimulation of pepsin secretion when exposed to acid. This mechanism could be of etiologic significance in gastric ulcer disease, which has been shown to be associated with increased gastric-mucosal permeability.
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PMID:Stimulation of human pepsin output by tropical hydrochloric acid. 109 97

This study has examined the inhibition produced by metiamide on the gastric secretion of acid and pepsin in 13 patients with duodenal and three with gastric ulcer. The effect of metiamide on the response to a range of doses of pentagastrin in three normal individuals was determined, as was the interaction of metiamide and atropine on prolonged basal secretion. Metiamide inhibited the secretion of acid more than pepsin and the gastric secretion of patients with gastric ulcer more than duodenal ulcer. Metiamide inhibited both the maximal secretory response attainable with pentagastrin and decreased the sensitivity to pentagastrin. Atropine augmented and prolonged the action of metiamide.
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PMID:Aspects of the effect of metiamide on pentagastrin-stimulated and basal gastric secretion of acid and pepsin in man. 109 68

Stepwise increasing doses of pentagastrin (0.166, 1, and 6 mug/kg-hr) were given to 21 healthy volunteers (HV), 22 patients without peptic ulcer disease (MI), and 22, 18, and 19 patients with duodenal (DU), pyloric (PU), and gastric ulcer (GU) respectively. Maximal response (Vmax) and half maximal dose of pentagastrin (Km) were calculated for both acid and pepsin. The ability to secrete acid and pepsin was in PU and GU slightly higher and lower, respectively, than in the non-ulcer groups. Markedly elevated values were found in DU, and the pepsin secretion was relatively more increased than that of acid. The values for Km suggested a different behavior of the chief cells and the parietal cells in DU. Whereas the sensitivity of the parietal cells appeared to be abnormally high, that of the chief cells tended to be lower than normal. The discrimination between DU and the non-ulcer groups was better by estimation of pepsin than of acid secretion and tended to improve with increasing stimulation. Superiority was however, found for a submaximal dose of pentagastrin for acid secretion. No superiority in discrimination between groups was found for Vmax. Km was poorly reproducible for acid and pepsin and showed little diagnostic significance. The study suggests that pentagastrin dose-response does not provide more diagnostic information than a single dose (1 mug/kg-hr), which is maximal for pepsin and submaximal for acid.
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PMID:Pentagastrin dose-response in peptic ulcer disease. 110 72

The course reviews the present status in the field of Vagotomy with reference to pathophysiology, gastrin release, anatomy, neural changes in the antrum, acid secretion, GI hormones, gastric motility, pepsin concentration, mucus production, O2 tension in the gastric mucosa, changes in the numbers of parietal cells, glucose tolerance, indications, diagnosis, necessity for drainage, acute complications, exclusion of malignancy in gastric ulcer; technique, intraoperative tests, results with TV, SV with antrectomy, recurrences, SPV and pyroplasty (controlled study), training. Nonresecting surgery of GDU is possible if vagotomy (SPV) and drainage (pyloroplasty) are correctly combined.
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PMID:[Vagotomy (author's transl)]. 120 35

It would seem that a gastric ulcer is the product of an interaction between chronic gastritis, the acid (and pepsin) of the gastric juice, and one or more precipitating factors. In a group of 194 consecutive patients with gastric ulceration particular note was made of whether they smoked, drank alcohol, used salicylates, were depressed or had experienced recent stress. There was an extraordinarily high incidence of depression among White women.
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PMID:Alcohol, aspirin, depression, smoking, stress and the patient with a gastric ulcer. 126 62

A slow-release zinc complex, zinc monoglycerolate (ZMG) was examined for its potential gastroprotective activity in various gastric ulcer models. These models comprised (a) oral or parenteral non-steroidal anti-inflammatory drugs (NSAIDs) given to rats whose gastrointestinal mucosa was pre-sensitized by prior development of arthritis, oleyl alcohol-induced inflammation and cold exposure, (b) oral ethanol (12.5-100%) with and without added 4% HCl, (c) intraperitoneal reserpine (5 mg kg-1) in arthritic and normal rats and in normal mice, (d) oral NSAIDs given to mice in which acid and pepsin production was stimulated by co-administration of intraperitoneal bethanechol chloride (5 mg kg-1) to enhance ulcer development, and (e) NSAIDs given to carrageenan-inflamed rats to determine effects of ZMG on paw inflammation. In these models, ZMG given orally was effective in preventing development of gastric lesions, except with propionic acid NSAIDs; the effective doses being apparently dependent on the severity of the mucosal injury. In many of the models ZMG was superior to zinc sulphate and other zinc salts or metal ion complexes investigated but was slightly more effective or equipotent compared with zinc acexamate. ZMG did not impair the anti-oedemic effects of NSAIDs. ZMG is thus an effective agent in preventing ulcer development in a wide range of model systems and may be more effective than zinc salts because of the controlled slow-release of zinc from the complex.
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PMID:Anti-ulcer activity of a slow-release zinc complex, zinc monoglycerolate (Glyzinc). 135 71


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