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)

We examined the pathophysiological roles of the urea-urease-ammonia system in gastric ulcer disease using rats. Exposure of the stomach to ammonia (0.01-1.0%) decreased the transmucosal potential difference (PD) and histological injury in a concentration-dependent manner. Exposure of the stomach for 20 min to urea (0.025-0.2%) together with urease (100 IU) produced a decrease in PD and microscopic injury similarly, and the lesion was closely associated with the amount of ammonia produced. Urea and urease alone had no effect on the gastric mucosa. These results suggested the pathophysiological importance of urea, urease and ammonia in gastric ulcer disease.
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PMID:Effect of ammonia on the gastric mucosa in rats: pathophysiological importance of urease in gastric ulcer disease. 322 33

Campylobacter pyloridis infection of the stomach has been associated with gastric ulcer, duodenal ulcer, nonulcer dyspepsia, and gastritis. The etiological role of C. pyloridis in most of those conditions remains unclear. We reviewed what is known about C. pyloridis infections in man. Considerable clinical data on C. pyloridis infections was available in older literature concerning gastritis and gastric urease. C. pyloridis causes a form of type B gastritis. In some individuals the acute infection is associated with abdominal pain and transient hypochlorhydria. C. pyloridis infection is difficult to eradicate with current therapies. The mechanisms by which C. pyloridis infection may lead to development of peptic ulcers, nonulcer dyspepsia, or atrophic gastritis are discussed. Recent technological advances, such as the 13C-urea breath test, provide rapid noninvasive methods of identifying active C. pyloridis infection. These methods will permit the rapid execution of definitive investigations of the epidemiology, transmission patterns, and possible reservoirs of C. pyloridis infection and will delineate the spectrum of C. pyloridis-associated disorders.
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PMID:Campylobacter pyloridis gastritis: the past, the present, and speculations about the future. 355 84

From Oct. 1986 to Jan. 1987, a total of 74 patients presenting for endoscopy were studied. These included 30 cases of active chronic gastritis and 44 cases of peptic ulcer. Biopsy specimens were taken during the endoscopy and sent to the laboratory for Campylobacter pyloridis culture within 2 hours. The culture was done by inoculated with chocolate agar, Brucella agar and 0.2% urea broth for urease activity. Results showed that, 53% (16/32) of active chronic gastritis, 77% (10/13) of gastric ulcer and 84% (26/31) of duodenal ulcer were positive for Campylobacter pyloridis. The specificity and sensitivity of urease positive rate are 64% and 90% respectively. It is higher as compared with bacteria culture. In addition, we found that 10 days would be needed for the routine culture and identification of this organism. But it took only 30 minutes to 6 hours for urease activity test. Therefore, we suggested that urease activity test could be a rapid diagnostic method for detecting Campylobacter pyloridis.
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PMID:[Campylobacter pyloridis in active chronic gastritis and peptic ulcer]. 365 84

1. The gastrin concentrations in serum were elevated after nephrectomy in rats and mice indicating the importance of the kidney for elimination of gastrin in these species. In guinea-pigs and rabbits nephrectomy did not cause increased serum gastrin concentrations. In rats there was a gradual rise in the serum gastrin level up to 48 hr after bilateral nephrectomy and also after ureteral ligation. After the latter operation the concentrations of gastrin in serum were lower than after nephrectomy. Significant elevation of the gastrin level 48 hr after ureteral ligation indicates that gastrin is eliminated at least partly through glomerular filtration. The gastric histidine decarboxylase activity after nephrectomy or ureteral ligation generally reflected the concentration of circulating gastrin.2. After bilateral ureteral ligation gastric acid secretion in conscious fistula rats was uniformly inhibited with no response to pentagastrin or histamine 24 or 48 hr after the operation. After nephrectomy basal acid secretion was reduced and there was no response to pentagastrin. The response to histamine was still present, although reduced at all dose levels. Linear transformation of the dose-response curve indicated mixed inhibition. The incidence of gastric ulcer was 75% 48 hr after nephrectomy and 30% after ureteral ligation. Since basal and pentagastrin-stimulated acid secretion were unaffected by nephrectomy in rats with the upper two-thirds of the intestine removed, the intestine appears to produce factors which are responsible for the inhibition of gastric secretion.2. On the whole, the gastrin concentration in serum and gastric histidine decarboxylase activity were not increased after five-sixths nephrectomy. Gastric ulcers were seen in the rats with the highest serum urea levels; one in addition had high serum gastrin concentration and gastric histidine decarboxylase activity. Basal, pentagastrin- and histamine-stimulated acid secretion were not affected by subtotal nephrectomy. It appears that in the rat about one sixth of the renal mass is the minimum required for handling gastrin degradation and excretion.
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PMID:Importance of the kidneys for gastrin elimination and gastric function. 738 64

This study attempted to determine the efficacy of lansoprazole plus clarithromycin therapy in the eradication of Helicobacter pylori in gastric ulcer patients. The influence of H. pylori eradication on healing and relapse of ulcers was also studied. Thirty-nine patients received either lansoprazole 30 mg daily for 8 weeks (group 1) or clarithromycin 200 mg twice daily for 2 weeks and lansoprazole 30 mg daily for 8 weeks (group 2). Before treatment, H. pylori status was evaluated by a rapid urease test and histologic examination. H. pylori clearance and eradication were evaluated by a rapid urease test, polymerase chain reaction, and a [13C]urea breath test. Clearance of H. pylori was 0% in group 1 and was 33% in group 2. Eradication of H. pylori was 0% in group 1 and 21% in group 2. Although all five ulcers were healed in patients with H. pylori eradication, ulcers were not healed in the five patients without eradication. Relapse of ulcer was observed in three patients in whom eradication had failed. In this study, for H. pylori-positive gastric ulcer patients, better results were obtained when lansoprazole plus clarithromycin therapy was used, and H. pylori eradication was achieved.
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PMID:Eradication of Helicobacter pylori with lansoprazole and clarithromycin in gastric ulcer patients. 759 28

We investigated the eradication and recurrence rate of Helicobacter pylori-infected gastric ulcer patients by combination therapies. Eighty-six H. pylori-positive gastric ulcer patients were assigned randomly to one of seven groups: I, omeprazole 20 mg (n = 9); II, lansoprazole (LPZ) 30 mg (n = 16); III, LPZ 30 mg plus plaunotol 480 mg (n = 13); IV, LPZ 30 mg plus ecabet sodium 2 g (n = 11); V, LPZ 30 mg plus clarithromycin 600 mg (the first 2 weeks; n = 11); VI, LPZ 30 mg plus plaunotol 480 mg plus clarithromycin 600 mg (the first 2 weeks; n = 13); and VII, LPZ 30 mg plus ecabet sodium 2 g plus amoxicillin 1,500 mg (the first 2 weeks; n = 13). All therapy was for 8 weeks except where otherwise noted. H. pylori eradication rates as diagnosed by culture, histology, urease test, and [13C]urea breath test 4 weeks after stopping therapy were 0, 0, 8, 45, 6, 46, and 62%, respectively, in groups I-VII. No patient achieving H. pylori eradication suffered recurrence. The combination therapies with proton pump inhibitors in addition to antibiotics and antiulcer agents are safe and effective in H. pylori eradication.
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PMID:Combination therapies with a proton pump inhibitor for Helicobacter pylori-infected gastric ulcer patients. 759 30

The [13C]urea breath test was adapted for use in squirrel monkeys (Saimiri spp.) for identification of experimentally induced infection with Helicobacter pylori, the bacterium causing gastric ulcer in humans. A canine anesthesia inhalation mask was modified with a volume-reducing insert allowing sufficient breath collection from these small primates within 30 sec. Fourteen milligrams of [13C urea per kilogram of body weight was adequate for clear distinction between experimentally infected and noninfected animals. Initial infection of five squirrel monkeys resulted in increased 13CO2 in breath within 3 days after inoculation with H. pylori. Additional inoculation with H. pylori superimposed on an existing gastric population caused a transient increase in breath 13CO2 values, which gradually declined over the following 15 days. Breath test results indicating H. pylori infection were confirmed by high [13C] concentration in blood, by urease-positive culture, modified Steiner stain reaction, and Western blot analysis. This modified [13C]urea breath test provides a rapid, reproducible, noninvasive method for screening small primates used as nonhuman models for the study of gastric infection with H. pylori.
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PMID:Adaptation of the [13C]urea breath test as a noninvasive method for detection of Helicobacter pylori infection in squirrel monkeys (Saimiri spp.). 765 Aug 91

About 90% of patients with duodenal ulcer and 65% of those with gastric ulcer are infected with Helicobacter pylori. H. pylori infection can be diagnosed by examination of biopsy material obtained at endoscopy; by 14C or 13C-urea breath tests, or by serological means. The relapse rate of duodenal and gastric ulcers can be considerably reduced if the bacteria are eradicated. Some of the current treatment regimens are discussed.
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PMID:Clinical aspects of infection with Helicobacter pylori. 769 51

In a prospective study 27 patients (13 women, 14 men; mean age 62 [45-83] years) with Helicobacter (H.) pylori associated disease received over 7 days pantoprazole (40 mg twice daily), clarithromycin (500 mg twice daily) and metronidazole (500 mg twice daily). Six patients had gastric ulcer, 4 duodenal ulcer, 4 erosive gastritis, 6 erosive duodenitis and 7 had H. pylori-positive functional dyspepsia. Pre-treatment oesophago-gastro-duodenoscopy was combined in 4 patients with antral and in 4 others with body-of-stomach biopsies to demonstrate H, pylori (urease test, specific culture and histology). The H. pylori status was checked with the 13C-urea breath test 4 weeks after the end of treatment. In addition, 9 patients with peptic ulcer were examined endoscopically at least 2 weeks after onset of the treatment to check for any healing of the ulcers, 25 of the patients completed the study according to the protocol. The H. pylori eradication rate was 100% (25 of 25 patients), while the "intention to treat" analysis gave a rate of 92.6% (25 of the 27 patients). The peptic ulcers were found to be healed in all 9 patients who had been endoscoped. One woman developed a reversible stomatitis, but the drug treatment did not have to be stopped. -These findings indicate that short-term triple treatment in the described manner is efficacious in curing H. pylori infection and any peptic ulcer. It is thus a highly promising treatment of H. pylori-associated diseases.
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PMID:[Short-term triple therapy with pantoprazole, clarithromycin and metronidazole for the healing of Helicobacter pylori infection]. 788 16

We treated 143 Helicobacter pylori positive ulcer patients (duodenal ulcer 81, gastric ulcer 24, pyloric ulcer nine, previous duodenal ulcer 27, others two) with a ten days regimen of bismuth subnitrate, oxytetracycline and metronidazole. Four weeks after cessation of treatment the 14C-urea breath test showed that the infection was eradicated in 133 out of 140 patients (95%). The ulcer had healed in 129 (97%) of the H. pylori negative patients. Status at one year after treatment showed that 121 (98.4%) of 123 patients who had become H. pylori negative had remained negative. None of the H. pylori negative patients experienced ulcer relapse. The results show that the treatment is effective and that the rate of recurrence of H. pylori during the first year is very low.
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PMID:[10 days of triple treatment of Helicobacter pylori infection and peptic ulcer. Status after treatment of 4 weeks and of one year]. 794 Apr 47


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