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

A total of 36 patients with advanced non-small-cell lung cancer (NSCLC) were treated with a combination of 5-day continuous i.v. infusion of cisplatin (25 mg/m2 daily), bolus infusion of vindesine (3 mg/m2) on days 1 and 8, and s.c. injection of recombinant human granulocyte-colony-stimulating factor (2 micrograms/kg daily) on days 6-21. Treatment was repeated every 3-4 weeks. Responding patients with stage IIIA or IIIB disease received chest radiation therapy (50-60 Gy) after this treatment. One complete response and 23 partial responses were observed, for an overall response rate of 66.7% (24/36; 95% confidence limits, 51.3%-82.1%). The median duration of response was 5.7 months and the median overall survival was 10.1 months. WHO grade 3 or 4 leukopenia and neutropenia occurred in 22 (61%) and 27 (75%) patients, respectively, but the mean duration of leukopenia (< 2,000/mm3) and neutropenia (< 1,000/mm3) was 3.4 and 3.5 days, respectively, and there was no instance of life-threatening infection. Thrombocytopenia and anemia of grade 3 or 4 occurred in 28% and 36% of our subjects, respectively. Grade 2 nausea and vomiting occurred in 47% of the patients. Elevated serum creatinine levels (> 1.5 mg/dl) were observed in 3 (8%) of the 36 patients. One patient died of acute renal failure induced by hemorrhage of a gastric ulcer. This regimen is effective in the treatment of NSCLC and further studies of this combination are warranted.
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PMID:Phase II study of cisplatin as a 5-day continuous infusion with vindesine plus recombinant human granulocyte-colony-stimulating factor in the treatment of advanced non-small-cell lung cancer. 128 May 37

Results of semiquantitative culture of the gastric mucosa for Campylobacter pylori (C. pylori) are reported. The samples were obtained by biopsy at the pyloric antrum along the lesser curvature from 197 patients with various gastric or duodenal disorders. 1) C. pylori was found in most cases with duodenal ulcer (100%), gastric ulcer (87.7%) and acute gastric mucosal lesion (AGML) (87.5%). Relatively heavy infestation was usual in these diseases, while relatively small amounts of the organism were found in various frequencies in other gastroduodenal disorders. 2) Samples from gastric ulcer cases under H2-blocker treatment had reduced amount of C. pylori as compared with those from untreated cases (p less than 0.01). C. pylori decreased in quantity in each case of AGML after successful treatment with a H2-blocker but not in a case without favorable response. 3) C. pylori distributed evenly among the gastric mucosa sampled at the margin of the ulcer and that at a relatively healthy portion in the pyloric antrum of the same stomach. 4) There was a modest, positive correlation between the amount of C. pylori and that of inflammatory cells, especially of neutrophilic granulocyte, in the gastric mucosa (r = 0.679), while there was a weak, negative correlation between the former and the extent of intestinal metaplasia of the epithelial cells (r = -0.479). 5) Quantitative rather than qualitative observation of C. pylori seems mandatory for considering the relevance of the bacterium to gastric and duodenal disorders. Although C. pylori can be found in the mucosa of the stomach with any type of disorder, its quantity tends to parallel with the activity of duodenal as well as gastric ulcer.
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PMID:[Semiquantitative culture of Campylobacter pylori in gastroduodenal disorder]. 233 3

Nonsteroidal anti-inflammatory drugs elevate gastric acid secretion, possibly contributing to their ability to interfere with gastric ulcer healing. Inhibitors of cyclooxygenase-2 have been shown to delay experimental gastric ulcer healing. In the present study, we tested the hypothesis that cyclooxygenase-2-derived prostaglandins modulate gastric acid secretion. Studies were performed in normal rats and in rats with iodoacetamide-induced gastritis. Inflammation in the latter group was confirmed histologically and by a threefold increase in tissue levels of the granulocyte marker myeloperoxidase and was also associated with overexpression of cyclooxygenase-2 in the stomach. Basal acid secretion in both groups of rats was not affected by pretreatment with DuP-697, a selective inhibitor of cyclooxygenase-2. A nonselective cyclooxygenase inhibitor, indomethacin, had no effect on acid secretion in normal rats but caused a doubling of acid secretion in the rats with gastritis. DuP-697 had no effect on pentagastrin-induced secretion in either group of rats. Gastritis itself was associated with significantly increased pentagastrin-induced acid secretion, and this was further increased in rats pretreated with indomethacin. These results suggest that in a setting of gastric inflammation, prostaglandins derived from cyclooxygenase-1, not cyclooxygenase-2, exert inhibitory effects on acid secretion.
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PMID:Role of cyclooxygenase-2 in modulating gastric acid secretion in the normal and inflamed rat stomach. 1109 53

The changes caused by Helicobacter pylori are a slow, progressing inflammatory process developing from several to dozen years. H. pylori infection leads to an inflammatory response in the gastric mucosa with granulocyte infiltrates in an acute form of the inflammation, and lymphocytes, plasmatic, macrophages and eosinophils in a chronic form inducing the development of gastric and duodenal ulcers and gastric cancer in some patients. The frequency and the type of morphological changes in the gastric mucosa were analyzed in children with positive IgG against H. pylori and the incidence of gastric and duodenal ulcers in family members of children examined was evaluated in our study. Gastritis was reported in 68.8% of children with positive IgG against H. pylori. Gastric ulcer was confirmed in 37.1% of families of children included in the study. Duodenal ulcers were found in 22.9% of families. The results obtained, indicate the usefulness of long-term observation and clinical follow-up of children with chronic gastritis of H. pylori ethiology taking into consideration bacterium eradication as prophylaxis of peptic ulceration.
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PMID:Helicobacter pylori eradication as prevention against chronic peptic ulcer disease in children. 1611 48