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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have established an experimental model of chronic gastric ulcer, in rats which transection of the lower horizontal portion of the duodenum and anastomosis of the forestomach to the upper part of the jejunum caused regurgitation of all duodenal juice into the stomach. After 3, 6, 12, and 30 wk, all treated rats developed an ulcer in the prepyloric region on the lesser curvature of the stomach. More than half of the antrum was finally involved in the ulcer. Histologic studies revealed chronic ulcers quite similar to human ones. As a control series, transection at the pylorus failed to produce an ulcer. Although many papers have appeared regarding the experimental production of chronic gastric ulcer, most of the studies reported have applied chemicals, drugs, or mechanical injury to the gastric mucosa. Our model produced chronic regurgitation of duodenal juice as a natural phenomenon, and uniformly resulted in ulcer formation. Intragastric total bile acid concentrations were significantly elevated in the reflux group. Serum gastrin levels, the thickness of the fundic mucosa, and the height of fundic gland were also significantly increased. Thus, the detergent action of bile acids and the increased acid secretion were assumed to play an important role in ulcer formation. Further studies using this model are warranted on the pathogenesis of chronic peptic ulceration.
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PMID:A new model for production of chronic gastric ulcer by duodenogastric reflux in rats. 356 68

The present study explored the 24-hr variations in serum gastrin and pepsinogen in clinically healthy subjects and in patients with gastric ulcer, duodenal ulcer, and erosive gastroduodenopathy. Time-qualified data were analyzed by means of cosinor procedures. Significant changes in rhythmometric properties were documented in patients with peptic disease when compared to clinically healthy subjects. In essence, it was discovered that gastric ulcer patients exhibit a higher mesor and amplitude for both gastrin and pepsinogen, whereas duodenal ulcer patients and those with erosive gastroduodenopathy show only a significant increase in the pepsinogen mesor. These characteristics are so specific in the groups investigated that one can hypothesize that the disorders in the circadian rhythmicity of gastrin and pepsinogen have a role in determining the clinical manifestations of peptic disease.
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PMID:Peptic disease and 24-hr patterns of serum gastrin and pepsinogen. 360 74

In gastric ulcer disease the operative procedure of choice is still partial gastrectomy, mostly carried out as Billroth I reconstruction with preservation of the duodenal passage. Indications for gastric resection are as follows: suspicion of malignancy, non-healing ulcers under conservative therapy, recurrent ulcer following conservative treatment, multiple and giant ulcers and ulcer complications like penetration, perforation, or bleeding. In duodenal ulcer gastric resection represents the exception. The routine operation is selective proximal vagotomy. The indication for partial gastrectomy in duodenal ulcer disease is: Recurrent ulcer after selective vagotomy (refractory to drugs), gastrin cell hyperplasia (hyper-function) and in rare cases of technical problems during surgery.
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PMID:[Peptic ulcer: status of resecting stomach surgery]. 366 Aug 97

Fasting hypergastrinemia was noted in 13-41% of 82 of outpatients with definite or classical rheumatoid arthritis. No differences were noted between the normogastrinemic and the hypergastrinemic subjects in their age, sex, duration of rheumatoid disease, serological status, or medications. The food-stimulated gastrin response was 117 mg/L, or 216% above the basal levels, and the integrated gastrin response was increased to the level previously reported in patients with duodenal or gastric ulcer disease. These results suggest that hypergastrinemia is a feature of patients with rheumatoid arthritis, the gastrin response to food may be abnormal in some rheumatoid patients.
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PMID:Hypergastrinemia in rheumatoid arthritis. 369 60

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxta-pyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9 +/- 1.2 ng/mg (mean +/- 1 SEM) in control patients. Duodenal gastrin concentration was similar to control values in patients with duodenal ulcer, pyloric channel ulcer, vagotomy and pyloroplasty, and gastric atrophy and hypergastrinemia. In gastric ulcer patients, duodenal gastrin concentration, 2.8 +/- 0.6 ng/mg, was significantly less than the control value (P less than 0.05). Duodenal gastrin concentration was approximately one third of antral gastrin concentration in control, duodenal ulcer, and gastric ulcer patients and was approximately one fifth of antral gastrin concentration in vagotomy and pyloroplasty patients and gastric atrophy patients. Duodenal and antral gastrin concentrations were significantly correlated in normal controls and in gastric ulcer patients. The finding of normal duodenal gastrin concentration in patients with vagotomy and pyloroplasty and patients with gastric atrophy suggests that, unlike antral gastrin concentration, duodenal gastrin concentration is unaffected by a decrease in acid secretion rate. The low duodenal gastrin concentration in gastric ulcer patients indicates that the duodenum may be involved in the pathophysiology of gastric ulcer disease.
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PMID:Duodenal gastrin concentration in upper gastrointestinal disorders. 376 3

A hybridoma monoclonal antibody against human pepsinogen I was used to develop an enzyme-linked immunosorbent assay for pepsinogen I in serum. In the two-step competitive procedure using antimouse immunoglobulin F(ab')2 fragment coupled to alkaline phosphatase, the measurable assay range was 8-256 micrograms/l. No cross-reactivity with rat pepsinogen 1, human pepsinogen II, gastrin I, bombesin, somatostatin and peptide YY was shown. However, there was slight cross-reactivity (0.09%) with porcine pepsinogen. The coefficients of variation within and between series were 7.6% and 13.0%. This enzyme-linked immunosorbent assay for serum pepsinogen I correlated positively with radioimmunoassay (r = 0.87, n = 92). The concentration range of serum pepsinogen I in 354 healthy controls was 15-100 micrograms/l with a lognormal distribution. Serum pepsinogen I levels were significantly higher in the subjects who developed active duodenal ulcer or active gastric ulcer, but significantly lower in those who had gastric cancer, than in control subjects.
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PMID:Enzyme-linked immunosorbent assay of serum pepsinogen I. 380 50

The aim of this survey was to examine the incidence of duodenogastric reflux in patients with abdominal complaints and the relations between the nature and extent of reflux abdominal complaints, the use of drugs, smoking, the drinking of coffee and alcohol and histological changes in the gastric mucosa. A comparison was also made between gastric ulcer patients and patients with upper abdominal complaints with respect to the nature and extent of reflux. The patients examined included 107 with abdominal complaints and 33 with a gastric ulcer. Gastroscopy was performed, followed by determination of intragastric bile acids and lysolecithin and a duodenogastric isotope reflux examination using technetium-99m-diethyliminodiacetic acid (Tc-99m HIDA). Intragastric bile acid concentrations in the patients with upper abdominal complaints were in the range 7-21,458 mumol/l (mean 964 +/- 2342 mumol/l) and lysolecithin concentrations in the range 0-1992 mumol/l (mean 70 +/- 273 mumol/l). Isotope reflux was observed in 48% of the patients, the reflux index varying in the range 0-70% (mean 4 +/- 9%). The patients suffered more frequently from nausea, epigastric fullness and flatulence with increasing reflux, as assessed by the various methods used here, but only the increase in epigastric fullness symptoms with rising intragastric bile acid concentrations was statistically significant (p less than 0.05). Similarly the various measures of reflux were higher in those patients taking anticholinergic, psychotherapeutic or cardiovascular drugs, antacids or metoclopramide than in the patients not taking the respective drugs, although the only statistically significant increases were in intragastric bile acids among the users of antacids and metoclopramide (p less than 0.01 and p less than 0.05, respectively) and the increase in lysolecithin concentrations among those taking metoclopramide (p less than 0.05). Those abstaining from alcohol had an intragastric bile acid concentration over 1000 mumol/l significantly more often than those who drank alcohol (p less than 0.05), but smoking and the drinking of coffee showed no significant correlation with duodenogastric reflux. The body gastritis score increased significantly with the extent of isotope reflux and the concentrations of intragastric bile acids (p less than 0.05 and p less than 0.01, respectively), and the latter also showed a significant correlation with serum gastrin (p less than 0.05). No significant relationship could be detected between intragastric lysolecithin concentrations and the gastritis score.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Duodenogastric reflux in patients with upper abdominal complaints or gastric ulcer with particular reference to reflux-associated gastritis. 386 29

The effects of the addition of carprofen (Roche), a new nonsteroidal antiinflammatory agent, to regular 4-5 week ranitidine (300 mg/day) therapy on gastric secretion, serum gastrin level and ulcer healing, have been examined in 15 gastric ulcer (GU) and 60 duodenal ulcer (DU) patients. Carprofen at a therapeutic dose (300 mg/day) was well tolerated by both GU and DU patients and did not give rise to any major adverse effects. In an open trial on 15 GU (all receiving carprofen), complete endoscopic ulcer healing was found in 9 patients after 3 weeks and in 6 others after 5 weeks of treatment. In a double blind, placebo controlled trial on 60 DU (30 receiving carprofen and 30 receiving placebo), complete ulcer healing was seen after 2 weeks in 23 on carprofen and 22 on placebo, and after 4 weeks in all tested patients. Pentagastrin-induced maximal acid secretion examined 24 h after the last dose of treatment was significantly reduced in DU, but not in GU, patients, and was accompanied by a significant rise in plasma gastrin levels. No change in gastric histology was observed in any patient tested. This study provides evidence that carprofen added to antiulcer ranitidine therapy shows excellent gastrointestinal tolerance, and does not interfere with ulcer healing; it is, therefore, recommended in the treatment of arthritic patients with peptic ulcer disease.
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PMID:Carprofen and the therapy of gastroduodenal ulcerations by ranitidine. 387 36

Gastric acid secretion, incidence of gastric mucosal lesion, and gut hormone responses were studied in 24 patients with liver cirrhosis. Gastric acid output in these subjects showed normal acidity and was nearly similar to that in patients with gastric ulcer. The incidence of gastric mucosal lesion was high, especially in patients whose plasma disappearance rate of indocyanine green was low. Plasma levels of both gastrin and gastric inhibitory polypeptide were higher in cirrhotic patients than in control subjects both in the fasting state and after the ingestion of a test meal. Gel chromatography of the postprandial plasma of cirrhotics showed a higher immunoreactivity at the second peak than in controls. This is because cirrhotics have a higher percentage of authentic gastric inhibitory polypeptide, although the elution patterns were similar in both groups. It is suggested that impairment of extraction of some molecular components of both gastrin and gastric inhibitory polypeptide may occur in the cirrhotic liver.
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PMID:Gastric acid secretion and gastrin and gastric inhibitory polypeptide release in cirrhotic patients. 388 51

A case of a bombesin-producing carcinoid tumor of the lung is reported. Morphologically, the tumor was a typical argentaffinic carcinoid which contained bombesin as demonstrated by diffuse granular cytoplasmic staining using the immunoperoxidase method. Electron microscopy revealed dense-core granules measuring 100-150 nm, consistent with bombesin-containing endocrine cells. In man, bombesin-producing endocrine cells are found predominantly in the bronchopulmonary tree and scattered throughout the intestinal tract. The majority of previously reported bombesin-producing tumors have arisen, as in this case, in the lung; thus the demonstration of bombesin-like immunoreactivity in a widely metastatic tumor should direct the search for a primary lesion to the lung. Bombesin is known to have gastrin-releasing hormone activity. The presence of a gastric ulcer in the present patient raised the possibility of a bombesin-mediated Zollinger-Ellison-like syndrome, an association not previously described.
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PMID:Disseminated bombesin-producing carcinoid tumor of pulmonary origin. 388 21


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