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)

Peptic ulcer disease mortality patterns of California Japanese are compared with those of their home and host countries for even years from 1960 to 1988, as well as 1989. Data presented are consistent with the hypothesis that Helicobacter pylori is a necessary but not sufficient causal factor in peptide ulcer disease, and that other co-factors including cigarette smoking and salt intake may be important. Deaths due to peptic ulcer numbered 106 among California Japanese, 12,793 for California Caucasians, 107,461 in Japan, and 117,737 for United States Caucasians during the study period. Data for California Japanese were analyzed separately for California Japanese migrants (i.e., those born in Japan) and U.S.-born California Japanese. California Japanese exhibit site-specific peptic ulcer mortality patterns more similar to those of Japan than of the United States. California Japanese migrants (gastric ulcer:duodenal ulcer = 3.2:1), like Japanese in Japan (gastric ulcer:duodenal ulcer = 6.8:1), die more often from gastric than duodenal ulcer, while California and U.S. Caucasians die as often from duodenal ulcer as gastric ulcer (gastric ulcer:duodenal ulcer = 1:1). California Japanese born in the United States exhibit a ratio between those of California Japanese migrants and California Caucasians (gastric ulcer:duodenal ulcer = 2.3:1). U.S.-born California Japanese have the lowest age-adjusted mortality rates for duodenal ulcer and the second-lowest gastric ulcer rates of all populations examined, even though their gastric to duodenal ratio is similar to that for Japan (which has the highest overall ulcer mortality rate).
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PMID:Peptic ulcer disease mortality. Comparison of native Japanese, Japanese Americans, and Caucasian Americans. 818 11

CI-986 (5-[3,5-bis(1,1-dimethylethyl)-4-hydroxyphenyl]-1,3,4-thiadiazole-2(3H)- thione-2-hydroxy-N,N,N-trimethylethanaminium salt) is a novel anti-inflammatory compound classified as a dual inhibitor of cyclooxygenase and 5-lipoxygenase. Studies were undertaken to characterize the preclinical toxicology of the compound. CI-986 was administered to rats for 2 weeks (0, 50, 250, 750, and 1500 mg/kg) or 13 weeks (0, 20, 250, 500, and 1000 mg/kg), dogs for 2 weeks (0, 50, 150, and 500 mg/kg) or 13 weeks (0, 20, 100, and 200 mg/kg), and to monkeys for 2 weeks (0, 50, 250, and 1000 mg/kg). No drug-related deaths resulted. Mild clinical signs of toxicity were noted in rats given doses of 250 mg/kg and above. Drug-related emesis and diarrhea were absent at the low dose in the dog and monkey but increased in incidence and severity at higher doses. Severe clinical signs in monkeys (emesis and diarrhea) necessitated the lowering of the top dose to 500 mg/kg/day (administered b.i.d.) during the second week of the monkey study. Slight decreases (< 23%) in serum protein and/or albumin were noted in all studies at the higher doses. A dose-related increase in alkaline phosphatase was noted in both dog studies, with no other drug-related effect on clinical pathology parameters. A gastric ulcer occurred in one rat administered 500 mg/kg CI-986 for 13 weeks. Gastrointestinal ulcers were not noted at any other dose in rats or at any dose in dogs or monkeys. A dose-related eosinophilia of glandular stomach submucosa was noted in rats after 2 and 13 weeks of drug administration but not in dogs or monkeys. In the 2-week rat study, mean combined sex plasma drug concentrations monitored 2 hr after dose on Day 14 were 0.59, 1.10, 2.64, and 3.43 micrograms/ml for the 50, 250, 750, and 1,500 mg/kg dose groups, respectively. In the 2-week dog studies, maximum plasma drug concentrations on Day 10 or Day 11 were achieved within 2 hr of dose with mean combined sex Cmax values of 0.73, 2.05, and 2.62 micrograms/ml for the 50, 250, and 750 mg/kg groups, respectively. Hepatic microsomal induction characterized by increased microsomal protein, increased microsomal cytochrome P450 content, and increased p-nitroanisole O-demethylation activity was noted in dogs and monkeys but not rats. CI-986 was well tolerated in rats and dogs at the doses employed and in monkeys at doses up to 500 mg/kg (b.i.d.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subacute and subchronic toxicology studies of CI-986, a novel anti-inflammatory compound. 831 60

An international comparison of the ratio of mortality rates from gastric and duodenal ulcers (GU/DU) reveals a positive correlation with gastric carcinoma death rates. This correlation is driven by the rates of gastric ulcer and has decreased in recent decades. Genetic susceptibility factors appear to be involved in the pathogenesis of peptic ulcers: non-secretor phenotypes of blood groups predispose to both types of peptic ulcers, while blood group A predominates in gastric ulcer and group O in duodenal ulcers. Environmental factors such as smoking increase the risk for both types of ulcers while excessive salt intake increases the risk of gastric ulcer only. Such aetiological factors may modulate the outcome of Helicobacter pylori infection. Factors associated with duodenal ulcer lead to a non-atrophic diffuse antral gastritis while those associated with gastric ulcer lead to multifocal atrophic gastritis. The latter, but not the former, type of gastritis provides a micro-environmental favouring neoplastic transformation of the gastric epithelium.
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PMID:The relationship between gastric cancer frequency and the ratio of gastric to duodenal ulcer. 854 23

Maintenance treatment with antisecretory agents, and above all with H2-RA, is a therapeutic option still largely favoured by physicians. However, in the last decades the pathogenetic role of Helicobacter pylori (Hp) in duodenal and gastric ulcer has met with increasingly convincing confirmation. Actually, Hp eradication brings about a dramatic and persistent decrease in ulcer relapse rate. At present, there is a general agreement that Hp-positive patients, with ulcer whether ab initio or recurrent, need to be treated with anti-Hp regimens. The first choice therapy, according to some clinicians, should be the classic triple therapy (colloidal bismuth, metronidazole and tetracicline or amoxicillin) associated or not with a proton pomp inhibitors (PPI) or H2-RA. Though supported by other gastroenterologists, dual therapy with a PPI plus amoxicillin raises some perplexity due to the unpredictable variability of the results. Non-bismuth triple therapy, consisting in 2 antimicrobial and 1 antisecretory agent, for which a duration of only 1 week would seem sufficient even at low dosage, is currently meeting with greater favour. The FDA approval is probably imminent for 2 anti-Hp regimens consisting in clarithromycin plus a PPI or the complex salt ranitidine-bismuth citrate.
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PMID:[The eradication of Helicobacter pylori and the prevention of ulcer recurrence. The certainties and the open problems]. 876 57

Ranitidine bismuth citrate (Pylorid, Glaxo-Wellcome) is a novel salt of ranitidine which provides a unique combination of properties: inhibition of secretion of gastric acid by competitive antagonism of the action of histamine at the histamine H2-receptor on the gastric parietal cell, mucosal protective effects and anti-Helicobacter pylori action. Ranitidine bismuth citrate provides effective healing and symptom relief, both in duodenal ulcer disease and in gastric ulcer disease. When coprescribed with certain antibiotics (clarithromycin alone or combined with amoxicillin or nitro-imidazole), it heals ulcers, eradicates Helicobacter pylori and prevents recurrence of the disease. Several clinical studies demonstrated that ranitidine bismuth citrate is well-tolerated and has quite similar efficacy as proton pump inhibitors.
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PMID:[Drug clinics. The drug of the month. Ranitidine bismuth citrate (Pylorid)]. 955 83

c-Kit is a receptor tyrosine kinase, and it is encoded by the mouse W locus. Mutant W/Wv mice develop spontaneous gastric antral ulcers. The aim of the present study was to investigate the pathogenesis of these gastric ulcers and to examine the effects of two antiulcer drugs; a proton pump inhibitor (2{[4-(3-methoxypropoxy)-3-methylpyridine-2-yl]methyl-sulfinyl}-1H -benzimidazole sodium salt, rabeprazole) and a mucosal protective drug (geranylgeranylacetone, GGA), on the gastric ulcers. The inhibition of the gastric acid secretion by rabeprazole (30 mg/kg body weight, subcutaneous injection once a day for six weeks) significantly increased the gastric ulcer formation compared to the controls. In contrast, the GGA treatment (100 mg/kg body weight, oral administration for six weeks) significantly inhibited the ulcer formation. Bile reflux was seen in these mutant mice, and they showed no cyclic intense contractions in the gastric antrum. These results suggest that bile reflux due to the disturbance of gastric antral movement is a cause of the spontaneous gastric ulcers in W/Wv mice.
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PMID:Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/Wv mice. 1038 93

Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1

The Republic of Kalmykia possesses a great deal of therapeutical peloids awaiting biomedical investigations. Mud formation in Kalmykia is characterized by an intensive accumulation of sulfide salt. Therapeutical peloids form in the Manych Lake region. An experimental murine model of acetate-induced gastric ulcer was used to evaluate the therapeutical efficacy of Manych mud. There was a statistically significant difference in the rate of ulcer healing between the study and control groups.
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PMID:[Effect of mud applications on acetate-induced ulcer in albino rats]. 1155 Mar 76

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
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PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84

This article describes changes in the basic digestive functions (motility, secretion, intraluminal digestion, absorption) that occur during aging. Elderly individuals frequently have oropharyngeal muscle dysmotility and altered swallowing of food. Reductions in esophageal peristalsis and lower esophageal sphincter (LES) pressures are also more common in the aged and may cause gastroesophageal reflux. Gastric motility and emptying and small bowel motility are generally normal in elderly subjects, although delayed motility and gastric emptying have been reported in some cases. The propulsive motility of the colon is also decreased, and this alteration is associated with neurological and endocrine-paracrine changes in the colonic wall. Decreased gastric secretions (acid, pepsin) and impairment of the mucous-bicarbonate barrier are frequently described in the elderly and may lead to gastric ulcer. Exocrine pancreatic secretion is often decreased, as is the bile salt content of bile. These changes represent the underlying mechanisms of symptomatic gastrointestinal dysfunctions in the elderly, such as dysphagia, gastroesophageal reflux disease, primary dyspepsia, irritable bowel syndrome, primary constipation, maldigestion, and reduced absorption of nutrients. Therapeutic management of these conditions is also described. The authors also review the gastrointestinal diseases that are more common in the elderly, such as atrophic gastritis, gastric ulcer, colon diverticulosis, malignant tumors, gallstones, chronic hepatitis, liver cirrhosis, Hepato Cellular Carcinoma (HCC), and chronic pancreatitis.
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PMID:Changes, functional disorders, and diseases in the gastrointestinal tract of elderly. 2247 8


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