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)

Following a multicenter, double-blind trial comparing cimetidine, antacid, and placebo for the treatment of gastric ulcer, patients whose ulcers had healed were followed prospectively to assess the frequency of ulcer relapse. Fifty-eight patients entered the follow-up study. Patients were encouraged to discontinue smoking and excessive ethanol intake, but were not maintained on antiulcer medications. Clinical evaluation was performed at monthly intervals; repeat endoscopy was performed at the time of symptom recurrence or at 6 to 9 months after ulcer healing. Gastric ulcer recurred in 20 of 58 patients (35%). While 15 (75%) with ulcer recurrence had symptoms, 5 (25%) had asymptomatic recurrences. There were no differences in the incidence of ulcer relapse or symptom recurrences between groups. We conclude that gastric ulcers recur in approximately one-third of patients within 9 months of ulcer healing.
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PMID:Gastric ulcer recurrence: follow-up of a double-blind, placebo-controlled trial. 264 57

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis. Most of the available data regarding the prevalence of upper and lower gastrointestinal sites of bleeding in cirrhotic patients have been obtained in individuals with alcoholic cirrhosis evaluated in the course of an acute gastrointestinal bleeding episode. Few data exist, however, as to the prevalence of either potential bleeding sites or of normal endoscopic findings in hemodynamically stable individuals with cirrhosis of any etiology. Five hundred ten cirrhotic subjects, who were evaluated for possible liver transplantation (OLTx) between January 1985 and June 1987, were included in this study. Seventy-five had alcoholic cirrhosis and 435 had nonalcoholic cirrhosis of various etiologies. Of these 510 patients, 412 underwent combined upper and lower gastrointestinal endoscopy and 98 underwent upper gastrointestinal endoscopy alone. Gastritis, gastric and duodenal ulcer disease were found significantly (each at least p less than 0.025) more often in patients with alcoholic liver disease than in those with nonalcoholic liver disease. The prevalence of the various lower gastrointestinal lesions in both groups was similar. Of particular interest is the fact that in alcoholic cirrhotics, the prevalence of gastritis, gastric ulcer and duodenal ulcer disease was unrelated to the degree of portal hypertension, whereas in the nonalcoholic cirrhotics the prevalence of gastritis and duodenal ulcer disease but not gastric ulcer disease was associated significantly with the degree of portal hypertension as assessed by the presence or absence of large esophageal varices, ascites, and hepatic encephalopathy.
Alcohol Clin Exp Res 1989 Dec
PMID:Combined upper and lower gastrointestinal endoscopy: a prospective study in alcoholic and nonalcoholic cirrhosis. 269 Jun 64

1. The effects of sulphasalazine (SZP) and PhCL28A on macroscopic lesion formation and ex vivo prostaglandin inactivation were studied in the ethanol (ETOH) and phenylbutazone (PBT) models of gastric ulcers in the rat. Prostaglandin 'synthesis' during homogenisation of the stomachs was also studied in the latter model. 2. Both PhCL28A and SZP when injected i.p. prevented the formation of ETOH- and PBT-induced gastric ulcers with ED50 values of 13 and 41 mgkg-1 (vs ETOH) and 3 and 32 mgkg-1 (vs PBT) for PhCL28A and SZP respectively. However, neither compound was active orally in the dose ranges used (up to 30 mg kg-1 for PhCL28A and 100 mg kg-1 for SZP). 3. Irrespective of the route of administration, SZP (100 mg kg-1) and PhCL28A (30 mg kg-1) produced slight but statistically significant decreases in ex vivo prostaglandin inactivation by 100,000 g cytosolic supernatants prepared from stomachs not receiving ulcerogen. When tested in vitro, PhCL28A (IC50 = 230 nM) was approximatively 480 times mor potent than SZP (IC50 = 110 microM) against rat stomach cytosolic prostaglandin inactivation. 4. Both ETOH (50%, 5 ml kg-1, orally) and PBT (200 mg kg-1, orally) significantly decreased ex vivo gastric cytosolic prostaglandin inactivation. PhCL28A (30 mg kg-1, orally or i.p.) decreased prostaglandin inactivation still further after ulcerogen treatment except when given i.p. before ETOH treatment. SZP (100 mg kg-1) had a similar effect when given orally before PBT treatment. 5. When the prostaglandin content of the stomach homogenates was used as a measure of ex vivo prostaglandin synthesis in the PBT experiments, PhCL28A 30 mg kg-' orally (but not i.p.) produced an 88% increase in prostaglandin E2 (PGE2) levels, but had no effect on 6-keto-PGF,, or thromboxane B2 formation during homogenization. SZP (100mg kg' i.p. or orally) was without effect. 6. We conclude from these results that the anti gastric ulcer activity of SZP and PhCL28A is independent of prostaglandin inactivation and endogenous prostaglandin formation is probably not involved.
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PMID:Sulphasalazine and PhCL28A inhibit the formation of ethanol- and phenylbutazone-induced rat gastric ulcers: lack of involvement of endogenous prostaglandins? 289 15

The calcium channel antagonists verapamil and nifedipine were examined for their effects on conscious basal gastric acid output, stress ulcer formation and on ethanol-induced ulcers. Both compounds significantly reduced gastric acid secretion, however verapamil did so in a dose-related manner. Both verapamil and nifedipine significantly attenuated stress gastric ulcer formation. Nifedipine, at a dose of 32.0 mg kg-1, virtually abolished stress ulcers. Verapamil exacerbated, while nifedipine, at 32.0 mg kg-1, attenuated ethanol-induced gastric ulcers. The differential gastrointestinal effects of these calcium channel antagonists support the existence of multiple classes of calcium channels in the gut and suggest an important role for intracellular calcium and hence, its blockade, in gastric pathophysiology.
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PMID:Verapamil and nifedipine effects on gastric acid secretion and ulcer formation in rats. 290 96

N,N-Diethyl-2-[4-(phenylmethyl)-phenoxy]-ethanamine hydrochloride (DPPE) is a para-diphenylmethane derivative that binds selectively and with high affinity to the microsomal antiestrogen binding site (AEBS). Recent studies with DPPE indicate that AEBS is closely related to a lower affinity non-H1, non-H2 histamine site that may be associated with calcium channels; the DPPE-AEBS site is different from that which verapamil binds, however, DPPE, but not verapamil, demonstrates antiproliferative effects in vitro and is antiestrogenic in vivo. We now show that DPPE profoundly inhibits restraint and cold stress and ethanol-induced gastric ulcer formation, accelerates ulcer healing, attenuates the stress-induced rise in plasma corticosterone level, and significantly reduces basal and H2 agonist (dimaprit)-stimulated and, to a lesser extent, bethanechol-stimulated gastric acid output in conscious rats. A nonulcerogenic but prostaglandin-depleting dose of indomethacin completely blocks the inhibitory effects of DPPE on stress ulcer formation. Conversely, verapamil only slightly attenuates dimaprit-stimulated gastric acid secretion and exacerbates ethanol-induced gastric ulcers; its anti-stress ulcer effects are only partially attenuated by indomethacin. These findings support the likelihood that the site of action of DPPE is different from that of verapamil, and that an effect on prostaglandins may, at least in part, contribute to its antiulcer and apparent cytoprotective effects.
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PMID:Antiulcerogenic and antisecretory effects of a novel diphenylmethane derivative and antiestrogen binding site ligand. 290 33

The aetiology of ethanol-induced gastric ulceration, and its interaction with zinc, were studied in rats. Oral administration of ethanol (40, 50 or 80%) to conscious rats reduced the stomach mucus content and increased gastric ulcer formation in a concentration-dependent manner. Histological examination indicated that mucus, both on the surface and within the epithelium, was depleted because of epithelium being shed from the gastric mucosa. Zinc sulphate abolished mucus loss and ulcer formation in the ethanol-treated animals. Using an ex-vivo gastric chamber preparation in anaesthetised animals, it was found that an ethanol (50%)-HCl (100 mmol/l) solution produced severe glandular haemorrhagic ulceration, elevated Na+, K+ and protein levels in the luminal solution, and reduced the H+ content in this fluid. Zinc sulphate pretreatment dose-dependently prevented all these changes. On the other hand, prostaglandin E2 (PGE2) administration only antagonised ethanol ulceration and H+ loss from the chamber; it did not significantly influence the Na+ and K+ fluxes and protein leakage into the luminal solution. It is concluded that the antiulcer mechanisms of zinc sulphate and PGE2 may be different. Protection by the former drug could be due partly to preservation of mucus adhering to the gastric mucosa. The possibility of the membrane-stabilising action of zinc contributing to the observed effects is also discussed.
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PMID:Protection by zinc sulphate against ethanol-induced ulceration: preservation of the gastric mucosal barrier. 294 51

There is both morphological and functional evidence that capsaicin-sensitive sensory neurons innervate the digestive tract. The possible function of these neurons in gastric ulceration and gastrointestinal motility was investigated in rats which had been systemically pretreated with capsaicin (50-125 mg/kg). It was found that capsaicin-sensitive afferent neurons do not participate in the physiologic control of gastrointestinal propulsion. However, the inhibition of gastrointestinal transit due to surgical trauma or peritoneal irritation with iodine was reduced in capsaicin-treated rats. It was concluded that capsaicin-sensitive sensory neurons may be involved in sympathetic reflex inhibition of gastrointestinal propulsion. Gastric ulceration induced by the intraperitoneal injection of indomethacin or intragastric administration of ethanol was greatly aggravated in capsaicin-treated rats. Since an involvement of the autonomic nervous system as well as of histamine and prostaglandins in this effect of capsaicin treatment could be ruled out, further support was lent to the previously proposed hypothesis that sensory nerve endings can protect the gastric mucosa against ulceration by the local release of vasodilator substances.
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PMID:Involvement of capsaicin-sensitive sensory neurons in gastrointestinal function. 331 May 22

A metallothionein isoform metallothionein-II was isolated from the livers of zinc acetate-treated rats. Metallothionein-II, which showed a single band on polyacrylamide gel electrophoresis, was subjected to two kinds of anti-ulcer screening systems. It was shown that intravenously administered metallothionein-II suppressed the formation of rat water-immersion stress- and HCl-ethanol-induced gastric ulcer significantly. The effect may partly be derived from the zinc contained in the metallothionein-II. However, the effect of metallothionein-II was much stronger than that of an equivalent mole of zinc. Apparently, metallothionein-II had an anti-ulcerogenic activity not based on the effect of intrinsic zinc.
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PMID:Suppression of gastric ulcer induced by stress and HCL-ethanol by intravenously administered metallothionein-II. 334 6

Endoscopic dehydrated ethanol injection was attempted in 48 patients with substantial bleeding of the upper gastrointestinal tract; most of the patients had associated serious medical conditions. The causes of bleeding were: gastric ulcer in 17; duodenal ulcer in 11; gastric or duodenal vascular ectasias, or both, in five; Mallory-Weiss tear in three; acute gastric mucosal lesion in six; esophageal ulcer in two; marginal ulcer in two; gastric leiomyoma in one, and carcinoma of the stomach in one. The mean age was 57 years old (a range of 18 to 91 years old). The mean amount of blood loss prior to time of injection was 4.5 units (a range of 3 to 10 units). Ethanol injection was initially successful in 45 of 48 patients but rebleeding occurred within 72 hours in three of these patients. All instances of treated vascular ectasia disappeared by the time of follow-up endoscopy. No complications were attributable to the injections. Endoscopic local ethanol injection may be the treatment of choice in selected patients with bleeding of the upper gastrointestinal tract.
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PMID:Endoscopic hemostasis of bleeding of the upper gastrointestinal tract by local injection of ninety-eight per cent dehydrated ethanol. 351 55

An uncontrolled study for the assessment of the hemostatic effects of endoscopically injected hypertonic saline-epinephrine (HS-E) solution and pure ethanol (PE) was carried out in 67 patients with nonvariceal gastrointestinal bleeding. The HS-E group included duodenal ulcer (18), gastric ulcer (9), gastric cancer (2), polyp (2), marginal ulcer (1), and esophageal cancer (1). Bleeding was active in 15 (pulsating, 3; oozing, 12). The hemostatic effect was permanent in 29 cases (87.9%) but failed in four cases (12.1%). The PE group consisted of 34 patients with duodenal ulcer (25), gastric ulcer (4), polyp (2), marginal ulcer (2), and gastric cancer (1). There was active bleeding in 14 (pulsating, 3; oozing, 11). The hemostatic effect was permanent in 31 cases (91.2%), temporary in 1 case (2.9%), and failed in 2 cases (5.9%). We conclude that endoscopic local injection with HS-E or PE is a simple maneuver with reasonable cost, high safety, and satisfactory hemostatic efficacy in the treatment of nonvariceal gastrointestinal bleeding.
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PMID:Hemostatic effect of endoscopic local injection with hypertonic saline-epinephrine solution and pure ethanol for digestive tract bleeding. 353 2


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