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)

Prostanoids decrease gastric acid secretion and exert cytoprotective properties. The effect of several synthetic prostanoids on gastric ulcer healing was evaluated. The first trials were performed on a small number of patients with PGE2 analogs and their results were inconclusive. Two huge multicenter trials tested the efficacy of misoprostol, a synthetic PGE1 analog, in comparison to placebo and cimetidine. In the placebo-controlled trial, following 8 weeks of therapy, misoprostol 100 micrograms q.i.d was significantly better than placebo. In the cimetidine controlled trial, 2 doses of misoprostol were tested, 50 micrograms and 200 micrograms q.i.d. Ulcer healing rates following 4 weeks were 39%, 51%, and 58% in the misoprostol 50 micrograms, 200 micrograms, and cimetidine treatment groups, respectively. There was no statistically significant difference in the healing rates at 4 weeks between the misoprostol 200 micrograms and cimetidine 300 mg q.i.d groups (P = 0.16). The healing rate with the misoprostol 200 micrograms dose was significantly better than with the 50 micrograms dose (P = 0.008). Cimetidine 300 mg relieved global pain significantly better than misoprostol 200 micrograms at 2 weeks (P = 0.047) but not at 4 weeks. The 200 micrograms dose of misoprostol relieved pain significantly better than the 50 micrograms dose at 4 weeks (P = 0.019), but not at 2 weeks. All 3 treatments were well tolerated. Severe adverse events were rare. The efficacy of enprostil, another PGE2 analog, on gastric ulcer healing was also found to be better than placebo and not significantly different from ranitidine. The synthetic prostanoids, misoprostol and enprostil, appear to be safe and effective in the treatment of gastric ulcer.
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PMID:Efficacy of prostanoids in the treatment of gastric ulcer. 311

In order to investigate whether truncal vagotomy effects on the wound-healing of highly located gastric ulcer or not, the ratio of epithelialization of ulcer, gastric acidity, mucosal blood flow, mucosal PGE2 and labelling index of mucosa after vagotomy were studied by using the mongrel dogs which were prepared highly located penetrated gastric ulcer. Following results were obtained. 1. The ratio of epithelialization of vagotomized dogs at the third week after preparing ulcer showed significant high ratio compared with non-vagotomized dogs. Comparing thoracic truncal vagotomy with abdominal truncal vagotomy, the former was more effective than the latter. 2. Mucosal blood flow and gastric acidity were reduced after vagotomy. 3. Mucosal PGE2 decreased at the first week after vagotomy, however, reduced PGE2 recovered up-to the level with non-vagotomized dogs at the second week after thoracic truncal vagotomy and at the third week after abdominal truncal vagotomy, respectively. 4. Labelling indexes showed significant high counts after vagotomy compared with non-vagotomy. In conclusion, it was suggested that truncal vagotomy would be effective on the wound-healing of ulcer due to the reduction of acid out-put and only a transient decrease of PGE2, however, mucosal blood flow decreased after vagotomy.
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PMID:[Experimental study of truncal vagotomy for healing of highly located gastric ulcer]. 316 29

The ability of mucosal specimens from the stomach and duodenum to synthesize and degrade prostaglandin E2 has been determined in normal subjects and peptic ulcer patients. Significant reduction in fundic PGE2 synthesis capacity was observed in gastric ulcer patients. There was also significant reduction in the PGE2 degradation capacity of antral, fundic, and duodenal mucosal specimens in gastric ulcer patients. Patients with gastritis showed significant elevation of both antral and fundic PGE2 synthesis capacity compared with normal but no alteration in PGE2 degradation. No differences were observed in PGE2 synthesis and degradation rates in patients with duodenal ulcer. The results argue in favour of an association between impairment of PGE2 metabolism in the mucosa of patients with gastric but not duodenal ulceration.
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PMID:Simultaneous measurement of in vitro gastroduodenal prostaglandin E2 synthesis and degradation in peptic ulcer disease. 347 73

Biopsies were taken endoscopically from the fundic, antral, and upper duodenal region of healthy volunteers and gastric ulcer patients and were incubated in carbogen-saturated and buffered Medium 199 at 37 degrees C. The rate of DNA synthesis, estimated as incorporation of tritiated thymidine into tissue DNA, was determined as an index of cellular integrity. During the 30-min incubation, ethanol (25% v/v) significantly (p less than 0.01) depressed DNA synthesis by about 50% in the gastroduodenal mucosa of normal subjects and even by two thirds in the gastric mucosa of gastric ulcer patients. Prostaglandin E2 (PGE2) by itself (1 mg/50 ml) had no stimulatory effect on DNA synthesis; it did, however, reduce the drastic fall in DNA synthesis due to ethanol (p less than 0.005) when administered concomitantly. The basic process underlying cytoprotection by PGE2 in vitro remains to be elucidated. Some indirect mechanisms, such as stimulation of gastric mucosal blood flow, are ruled out by these experiments.
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PMID:Partial prevention of ethanol damage of human gastroduodenal mucosa by prostaglandin E2 in vitro. 620 94

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.
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PMID:Pathogenesis of gastric ulceration produced by acetazolamide in rats. 632 41

The present study demonstrated that acetazolamide (100 and 200 mg/kg, s.c.) induced severe gastric hemorrhagic ulceration in rats. The ulceration was aggravated by oral administration of HCl, but was inhibited by NaHCO3. Furthermore, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were accompanied by an increase in serotonin and histamine released from the stomach. Acetazolamide injection also increased the protein level but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increase in serotonin and histamine release also may have been the contributing factors for gastric ulcer formation.
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PMID:Study of the damaging effects of acetazolamide on gastric mucosa in rats. 644 31

This study shows that human fundic mucosa generates various PGs, particularly PGE2, and thromboxanes and this generation appears to be significantly lower in gastric ulcer than in duodenal ulcer patients or normal subjects. Non-steroidal antiinflammatory compounds (NOSAC), such as aspirin and indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage including mucosal erosions and haemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, carprofen, a novel NOSAC with good antiinflammatory properties and gastric tolerance, failed to affect mucosal generation of PGs and did not influence gastric mucosal integrity. This study indicates that the deficiency of endogenous PGs may play a role in the pathogenesis ulcer and that the degree of gastric mucosal damage by NOSAC is closely related to the alteration in the capability of the mucosa to generate PGs.
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PMID:Prostaglandins in peptic ulcer disease: effect of nonsteroidal anti-inflammatory compounds (NOSAC). 658 26

The effect of different antacids has been investigated on ulcer development, parameters of mucus barrier disruption and gastric PGE2 content in rats. Al(OH)3-containing antacids inhibit gastric ulcer formation induced by alcohol or acetylsalicylic acid (ASA). Changes in parameters of mucus barrier disruption evoked by sodium taurocholate can be significantly diminished by treatment with antacids. This protective effect of antacids is abolished in animals pretreated with indomethacin. PGE2 contents both in gastric mucosa and instillate are increased by pretreatment with antacids. PGE2 content in gastric mucosa or instillate diminished by sodium taurocholate can be normalized by antacid treatment. Although acidic isotonic or acidic hypertonic solutions increase gastric PGE2 content, they are not ulceroprotective. In these solutions, detectable amounts of released PGE2 are minimal. Under in vitro circumstances, the lifetime of PGE2 in gastric juice is shortened by decreasing pH. It has been concluded that Al(OH)3-containing antacids increase PGE2 content in the gastric mucosa. Furthermore, they are capable of lengthening the lifetime of PGE2 in the gastric content. Thus, the clinical use of Al(OH)3-containing antacids in low doses is to be emphasized in the management of gastric ulcer disease.
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PMID:Functional cytoprotection by certain antacids. 659 1

Human fundic mucosa generates various prostaglandins (PGs), particularly PGE2, and tromboxanes. This generation appears to be significantly lower in gastric ulcer patients than in duodenal ulcer patients or normal subjects. Nonsteroidal antiinflammatory compounds (NOSAC), such as aspirin or indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage, including mucosal erosions and hemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, paracetamol or carprofen, a novel NOSAC, fails to affect mucosal generation of PGs and does not influence gastric mucosal integrity. This study indicates that endogenous PGs may be involved in the pathogenesis of gastric ulcer and that normal generation of mucosal PGs is essential for the mucosal integrity.
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PMID:Generation of prostaglandins in gastric mucosa of patients with peptic ulcer disease: effect of nonsteroidal antiinflammatory compounds. 659 41

Prostaglandin E was measured by radioimmunoassay in endoscopic biopsy specimens obtained from 7 normal healthy volunteers, 28 patients with a benign gastric ulcer, and 10 with a malignant gastric ulcer. Biopsy specimens were taken from the antral and body mucosa and from the ulcer edge in patients. The median value in normal antrum specimens was 5.15 (4.44-8.40) ng PGE/mg protein which was more than the body with 3.50 (1.86-9.28), p less than 0.05. In the 28 patients with benign gastric ulcer the ulcer edge contained 2.33 (0.48-7.67) ng PGE/mg protein which was more than the antrum with 1.06 (0.30-4.17) or the body with 0.97 (0.20-7.67), p less than 0.01 respectively. The antral and body levels in patients with gastric ulcers were lower than those found in the normal volunteers, p less than 0.01. There was no difference between the levels found in patients with malignant as opposed to benign gastric ulcer. In patients with gastric ulcer lower levels of PGE were found in body mucosa with atrophic gastritis 0.83 (0.53-2.66) ng PGE/mg protein as compared with histologically normal body mucosa 2.55 (0.63-7.67), p less than 0.05. These results suggest that mucosal PGE levels are reduced in patients with gastric ulcer disease and that this may be due to the presence of atrophic gastritis.
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PMID:Gastric mucosal prostaglandin E levels in patients with gastric ulcer disease and carcinoma. 705 27


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