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

A 76 year-old man with a benign gastric ulcer and pernicious anemia is reported. The etiology of the ulcer is unexplained.
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PMID:Achlorhydria and benign gastric ulcer. 52 20

Idiopathic chronic gastritis is an autoimmune disease and the cause of this gastritis probably act through a final common immunologic pathway. Specific gastric antibodies are diagnostic of this gastritis and the tissue of the gastric mucosa is characterized by infiltrations of mononuclear cells damaging the glandular parenchyma with concomitant loss of gastric secretory function. With suitable predisposing factors operating, the patient with simple chronic gastritis can have pernicious anemia develop. Chronic gastritis is frequently associated with chronic gastric ulcer and carcinoma of the stomach but not with duodenal ulcer. Chronic gastritis clinically presents with vague dyspeptic symptoms. Females are more commonly affected than males and the incidence rises with advancing age. Treatment of chronic gastritis is supportive in nature and also similar to the treatment of other autoimmune diseases. The author has suggested a new treatment of duodenal ulcer whereby the patients are immunized against mucosal antigen with a view to induction of chronic gastritis. The resulting biochemical damage of the parietal cells will produce hypochlorhydria.
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PMID:Idiopathic chronic gastritis. 79 68

In spite of reduction in mortality, gastric carcinoma is still one of the most frequent types of carcinoma. For this reason precanceroses - pernicious anemia and diffuse adenomatous polyposis of the stomach - must be particularly watched. Whether gastric ulcer and chronic gastritis are precanceroses is discussed. Clinical aspects, therapy and prognosis are described in detail.
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PMID:[Gastric carcinoma (author's transl)]. 81 83

Although many facts on epidemiology of gastric cancer and on the preceding atrophic gastritis are known, sufficient scientific foundations for planning primary prevention are lacking. It is suggested that with rising standards of living and hygiene and with dissemination of optimal nutrition according to physiologic aspects, incidence of gastric cancer will further decrease. 2. It is possible to identify some high risk groups: elderly persons with familial aggregation of stomach cancer, blood group A, pernicious anemia, atrophic gastritis and intestinal metaplasia, anacidity, and patients operated upon for benign epithelial neoplasms or gastric ulcer. Prophylactic supervision of this segment of the population seems mandatory but by this means, only a small percentage of all gastric cancer can be detected early. 3. Our knowledge is sufficient for the planning of intervention studies, e.g. long tome prophylactic application of ascorbic acid or vitamin A or intensive drug treatment of atrophic gastritis. Therefore we have started such a trial using carbenoxolon. 4. Screening methods for detection of early gastric cancer in asymptomatic persons have been evaluated in Japan. Their application in Europe cannot be generally recommended. The cost-benefit ratio is prohibiting. 5. Today, the main route to detect stomach cancer when curable is the thorough examination of persons with dyspeptic complaints. Radiological examination holds the first place and is supplemented by fibergastroscopy which enables aimed biopsy and cytologic examination of gastric juice. All other methods have only limited value in selected situations. 6. Without resignation we must realize that a solution of the problem cannot be expected in the near future. Further efforts are necessary in order to gain solid scientific foundations and to introduce research results into medical practice.
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PMID:[Scientific foundation of gastric cancer control (author's transl)]. 86 74

This is the report of the presence of a benign gastric ulcer in a patient with achlorhydria and documented pernicious anemia. The pernicious anemia was established by a Histalog-fast achlorhydria, a Schilling test of 2.1% excretion of tagges vitamin B12 in a 24-hr urine, and reticulocytosis after administration of cyanocobalamine. Following Histalog (1.5 mg per kg of body weight), the gastric volume was 40 ml, there was no acid, and the pH was 8.1. The ulcer demonstrated by gastroscopy was confirmed at gastrectomy. Histological examination of the ulcer and the remainder of the stomach showed no malignancy. The principal conclusion of this paper is that the patient did not have an acid-produced ulcer, but that bile regurgitation coupled with alcohol ingestion produced the lesion. Surgical investigation of the ulcer seemed mandatory because of the known increased incidence of gastric carcinoma in patients with pernicious anemia.
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PMID:Benign gastric ulcer in a patient with pernicious anemia. 115 91

The development of gastric enterochromaffin-like (ECL)-cell hyperplasia in humans may be associated with extreme hypergastrinaemia, as occurs in Zollinger-Ellison syndrome (ZES) and pernicious anaemia (type A gastritis). More recently, endocrine cell hyperplasia has been found in all forms of chronic atrophic gastritis and even in cases of focal atrophy. Serum gastrin levels, non-antral gastric endocrine (argyrophil) cell growth, and the severity and type of concomitant gastritis were monitored in 66 unoperated and 8 antrectomized patients with poorly responsive peptic ulcer or reflux oesophagitis during up to 5 years' treatment with high-dose omeprazole, 40 mg daily. A small subgroup of patients (23%) had serum gastrin concentrations of more than four times the normal upper limit. These patients also had hyperplasia of the gastric argyrophil cells. More importantly, the same subgroup of patients had high-grade (atrophic) gastritis. Micronodular hyperplasia of argyrophil cells was significantly more frequent in biopsies showing atrophic gastritis (48%) than in biopsies showing only superficial gastritis (3.6%). It is concluded that, as previously demonstrated in untreated patients with gastric ulcer, the argyrophil cell hyperplasia observed during high-dose omeprazole therapy is related to the progression of chronic atrophic gastritis rather than to serum gastrin levels.
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PMID:Inter-relationship between serum gastrin levels, gastric mucosal histology and gastric endocrine cell growth. 139 48

We have developed enzyme-linked immunosorbent assay (ELISA) for pepsinogen group I and II (PG I.II) in human serum, and clinical significance of serum pepsinogen measurement was evaluated. Serum PG I.II levels in patients with gastric and duodenal ulcer were higher than those in normal healthy subjects. On the other hand, serum PG I levels in patients with pernicious anemia were significantly low levels. In both gastric ulcer and duodenal ulcer, serum PG I.II levels at active stage were higher than healing stage. These results suggested that the measurement of PG I.II levels was useful for screening or monitoring test for the injury of gastric and duodenal mucosa.
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PMID:[Clinical significance of the measurement of serum pepsinogen group I and II by enzyme-linked immunosorbent assay]. 143 35

The formation of a benign gastric ulcer in an achlorhydric milieu is a rare phenomenon. Since 1971, only 12 cases have been reported. Early cases were treated surgically for fear of gastric cancer, but since that time such ulcers have been successfully treated medically. The authors describe the case of a patient who had no concomitant ulcerogenic factors and whose ulcer occurred in the gastric cardia at the esophagogastric junction. We believe this is the first case report of a patient with pernicious anemia meeting these conditions.
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PMID:Benign gastric ulcers and pernicious anemia. 235 81

There are reasons to believe that chronic antral gastritis and chronic body gastritis are different clinical conditions. While both are associated with aging, chronic antral gastritis is much more commonly associated with gastric or duodenal ulcer. The natural history of chronic antral gastritis in asymptomatic normals and patients with peptic ulcer appears the same. Chronic body gastritis deteriorates rapidly with age in patients with gastric ulcer, but does not progress in patients with duodenal ulcer. With spontaneous healing of duodenal ulcer, chronic antral gastritis improves but persists. All these observations suggest that gastric ulcer, duodenal ulcer, and chronic antral gastritis are involved in a common mucosal inflammatory process. C. pylori occurs commonly on the antral mucosa affected by chronic gastritis, but is found to a much less extent at the site of peptic ulceration, and spontaneous ulcer healing is not affected by the presence of the organisms. It remains to be established whether C. pylori is the cause of chronic antral gastritis, is an aggravating factor of the gastritis, or is simply an inhabitant of the inflamed antral mucosa. Other known associations of chronic gastritis include pernicious anemia, bile reflux, and gastric cancer. Whether chronic antral or body gastritis is associated with clinical symptoms remains controversial. Histological improvement can be obtained with the use of prostaglandins, sucralfate, or bismuth compounds, which have one common property--they all possess mucosal-protective mechanisms.
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PMID:Etiology and management of chronic gastritis. 264 23

Fasting gastric juice pH and concentrations of vitamin C in gastric aspirate and plasma were measured in 73 patients undergoing endoscopy. Vitamin C concentrations were significantly lower in those with hypochlorhydria (pH greater than 4; n = 23) compared with those with pH less than or equal to 4 (p less than 0.005) and there was a significant correlation between gastric juice and plasma concentrations (p = 0.002). Patients with normal endoscopic findings had significantly higher intragastric concentrations of vitamin C than those with gastric cancer (p less than 0.001), pernicious anaemia (p less than 0.005), gastric ulcer (p less than 0.01), duodenal ulcer (p less than 0.05), or after gastric surgery (p less than 0.01). There was a strong trend (0.05 less than p less than 0.1) towards lower intragastric concentrations of vitamin C in patients with chronic atrophic gastritis. In vitro, vitamin C concentrations remained stable in acidic but fell significantly over 24 hours in alkaline gastric aspirate. Gastric secretory studies in five volunteers showed that vitamin C concentrations increased significantly after intramuscular pentagastrin. These findings suggest that the low fasting levels of vitamin C in hypochlorhydric gastric juice may be caused by chemical instability and that vitamin C may be secreted by the human stomach.
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PMID:Vitamin C in the human stomach: relation to gastric pH, gastroduodenal disease, and possible sources. 271 77


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