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[Influence of an acute hypercalcemia on the gastric secretion in duodenal ulcer, peptic ulcer of the jejunum and Zollinger-Ellison syndrome].

In 36 patients with ulcer without Zollinger-Ellison-syndrome (25 patients with recurrent duodenal ulcer, 11 with an ulcus pepticum jejuni after B II-resection of the stomach) and 2 patients suffering from ulcus pepticum jejuni with an ascertained gastrinoma the secretion of acid was compared after stimulation of pentagstrin (6 mug/kg) and calcium (4 mg Ca++/kg/h). The secretion of hydrochloric acid was statistically significantly stimulated in all patients suffering from ulcer by the hypercalcaemia (increase of the serum calcium concentration from 5.0 +/- 0.3 mval/1 to 6.2 +/- 0.8 mval/1). But in patients suffering from ulcer with gastrinoma the stimulatory effect was larger than in such patients without autonomous source of gastrin: the calcium-stimulated secretion of hydrochloric acid was on the average in cases of duodenal ulcer 40% (2 to 68%), in the ulcera peptica jejuni 47% (17 to 75%), in the 4 comparative examinations of the two patients with Zollinger-Ellison-syndrome, however, always more than 100% (106 to 177%) of the pentagastrin-stimulated peak secretion. The comparative test of the pentagastrin and calcium-stimulated secretion of hydrochloric acid could be a help for the proof of autonomous places of the formation of gastrin.

Acute Disease↗

Is there any difference in Helicobacter pylori eradication rates in patients with active peptic ulcer, inactive peptic ulcer and functional dyspepsia?

Omeprazole triple therapy has been shown to produce Helicobacter pylori eradication rates of up to 96% in patients with current or recent peptic ulceration. Such therapy is also now being used without endoscopy in H. pylori-positive patients who may have an inactive ulcer or dyspepsia, and in whom their effectiveness has been less well documented. Compliance is an important variable affecting H. pylori eradication; with 1-week omeprazole triple therapy, however, compliance is uniformly high, and this allows more detailed analysis of other causes of treatment failure. The strains of H. pylori in patients with functional dyspepsia may be associated with a lower degree of inflammation. Two new, large studies (DU-MACH and GU-MACH) have therefore looked at the impact of inflammation on H. pylori eradication. Polymorph infiltration in the antrum of patients with inflammation of grades 2/3 was associated with a significantly higher eradication rate when compared with inflammation of grades 0/1. Inflammation may be important for a number of reasons, including degradation of the mucus and epithelial layers (which may allow better penetration of charged antibiotics from the gastric lumen) and altered vascular and epithelial permeability (which may allow better systemic delivery of drugs). Alternatively, inflammation may be a marker for more aggressive H. pylori subtypes, which are also more vulnerable to antibiotic therapy.

Amoxicillin↗

[Physiopathological basis for the treatment of peptic ulcer].

Peptic ulcer pathophysiology has advanced in several ways during the last years; the following facts has been put forward: a) There has been recognized specific receptors controlling oxyntic cell secretion for histamine, acetylcholine, gastrin and prostaglandins. Agonists and antagonists for the above mentioned receptors has been synthesized. The physiology of the proton-pump located at the luminal side of the mucous membrane has been clarified. This pump is responsible for HCl secretion and can be blocked with omeprazole and trimeprazole. b) There is a comprehensive view of the gastric mucosal barrier, which is important for gastric self-protection, against inner or outer noxious stimuli. The mucosal barrier rupture can be the initial step of some gastroduodenal diseases, so the understanding of its functioning is very important to explain the pathophysiology of peptic ulcer. Finally, some etiopathogenic factors has been proved in the development of peptic ulcer, as Helicobacter pylori, which adheres to gastric cells mucus, damaging the cells after colonization, and producing the rupture of the mucosal barrier; which in turn favours peptic ulcer disease. The use of non-steroidal antiinflammatory drugs (NSAID) can act at several levels; the most important one seems to be the alteration of prostaglandins synthesis and consequent decrease of mucus and bicarbonate secretion. At the same time NSAID can cause antro-pyloric motor disturbances which contributes to peptic ulcer development. The understanding of all those pathophysiological factors has promoted the designs of new pharmacological approaches to the medical treatment of peptic ulcer, so new antiulcer drugs can act at different stages of peptic-acid secretion, like H2-antagonists, proton-pump blockers, cytoprotector drugs and antimicrobial agents for Helicobacter pylori eradication.

Gastric Acid↗

Diagnosis method of Helicobacter pylori infection in bleeding peptic ulcer.

Peptic ulcer lesions are the most frequent cause of upper gastrointestinal bleeding and are responsible for more than 50 per cent of cases. Several etiologic factors of peptic ulcer are known, the principle one being Helicobacter pylori (H. pylori). Recent studies indicate that H. pylori eradication is associated with the marked reduction in rebleeding rate. In peptic ulcer bleeding which requires surgical intervention, knowledge H. pylori status may help to determine the choice of procedure (simple sewing in H. pylori positive patients vs full-blown ulcer surgery in H. pylori negative patients). We suggest to use the invasive combination of histology and biopsy-rapid urease test in stable bleeding peptic ulcer patients without coagulopathy for H. pylori diagnosis. Cases with positive result do not need further investigation for H. pylori diagnosis. If negative, the serology test was suggested to confirm the absence of H. pylori. However, in unstable patients, the serology test seem to effectively detect H. pylori infection.

Biopsy, Needle↗

Continuous intravenous famotidine for haemorrhage from peptic ulcer.

Peptic ulcer bleeding often stops spontaneously but rebleeding may be catastrophic. Emergency surgery carries risks so safe medical therapies are needed. Since platelet function and plasma coagulation are both pH sensitive and since pepsin lyses clot at low pH the maintenance of gastric pH close to neutrality might influence rebleeding rates. Previous trials with H2 antagonists have been inadequate although a 1985 meta-analysis did support an important clinical effect. We report here a large multicentre trial of famotidine in ulcer bleeding. 1005 patients admitted to one of sixty-seven hospitals in the UK or Eire with haemorrhage from peptic ulcer with endoscopic signs of oozing, black slough, fresh clot or visible vessel were randomly allocated to famotidine (10 mg bolus followed by 3.2 mg/h intravenously) or matching placebo for 72 h. This famotidine regimen had previously been shown to maintain pH near 7 in such patients. 497 patients received famotidine and 508 placebo. The treatment groups were similar in respect of age, sex, ulcer site, and signs and severity of bleeding. Case fatality (6.2% famotidine vs 5.0% placebo), rebleeding (23.9% vs 25.5% placebo), and surgery (15.5% vs 17.1% placebo) rates were not significantly different between the two groups. This trial suggests that potent inhibition of gastric secretion does not influence the natural history of peptic ulcer haemorrhage.

Aged↗

Plasma and gastric mucosal endothelin-1 concentrations in patients with peptic ulcer.

Peptic ulcer in the human stomach causes localized destruction of the gastric wall, which may be associated with focal vascular insufficiency. Endothelin-1, an extremely potent vasoconstrictor peptide, modulates regional blood flow in the vasculature of stomach, suggesting a role for endothelin-1 in peptic ulcer. We examined the relationship among endogenous plasma and mucosal endothelin-1 concentrations and the severity and area of ulcer in 19 patients with gastric ulcers and eight healthy adults. Endothelin-1 concentrations were measured by enzyme immunoassay in plasma and gastric mucosal specimens from ulcer margins, corpus, and antrum. The severity and area of ulcer were assessed endoscopically. Plasma endothelin-1 concentrations in active (P < 0.01 compared with normal) and healing (P < 0.05) stages of ulcer were significantly greater than those in normal subjects. Plasma endothelin-1 concentrations, but not mucosal endothelin-1 concentrations in the ulcer margin, were significantly associated with the severity of the ulcer. There was a significant positive correlation between plasma endothelin-1 concentrations and area of ulcer (r = 0.70, P < 0.01). In conclusion, locally increased endothelin-1 may be an important mediator contributing to the pathogenesis of peptic ulcer.

Adult↗

[TREATMENT OF PEPTIC ULCER]

Peptic ulcer disease has been the reason for extensive studies throughout the 20th Century. During the first 75 years, investigation and study of the production of acid and in which cases it leads to the formation of ulcers were carried out. The last 25 years have been of major importance due to the finding of powerful suppressants of acid formation. At first, the Histamine H2-antagonist, then the blockers of the proton bomb; and also the Helicobacter pylori finding, as an important factor in peptic ulcer disease. During these last years, studies report about how the Helicobacter pylori works in the stomach of patients who are liable to produce ulcers. Now, we also know more about the action of the antiulcerative drugs, and how to use them in the best way. Lately, the recurrence of peptic ulcer and bacterial resistance of the Helicobacter pylori are concepts that are being studied most profoundly.

Journal Article↗

Perforated peptic ulcer.

Peptic ulcer disease has declined significantly since 1950 in industrialized nations. However, the number of patients with perforated and bleeding ulcers has been constant or has declined only slightly, except for older patients, in whom the frequency has increased. In patients with perforated ulcers, operative management is preferable to non-operative treatment. The operative choices are simple closure of the perforation or definitive surgery. Patients who have significant risk factors should undergo simple closure. Closure of the ulcer with parietal cell vagotomy is the author's first choice for definitive operative treatment when this procedure can be performed.

Abdomen, Acute↗

Maintenance therapy for prevention of recurrent peptic ulcers.

Peptic ulcer disease is a chronic, relapsing disease. Successful healing of duodenal and gastric ulcers with antacids, cimetidine, ranitidine, famotidine, or sucralfate is frequently followed by ulcer recurrence. The need for long-term, low-dose maintenance therapy is based on disease severity, ulcer history, complications, therapeutic intervention, response to treatment, and potential risk factors. Comparison of ulcer maintenance trials requires consideration of important factors such as frequency of endoscopy, duration of follow-up period, and the method used to calculate ulcer recurrence rates. Clinical trials indicate that chronic treatment with low-dose cimetidine, ranitidine, famotidine, and probably sucralfate decreases the frequency of duodenal ulcer recurrence and that ranitidine may be superior to cimetidine. Preliminary studies indicate that higher doses of these same medications may be required to prevent gastric ulcer recurrence. Long-term maintenance therapy with these agents must be continuous in order to prevent relapses, but treatment should be limited to one year because of unknown consequences beyond this period.

Anti-Ulcer Agents↗

The pathogenesis of peptic ulcer.

Peptic ulcers of the stomach and duodenum look much alike and the reaction around them is nonspecific, yet other evidence indicates that ulcers in the two locations do not represent the same disease. It is suggested that a common causal factor is the digestive effect of gastric juice, and that hypersecretion may produce duodenal ulcer without any predisposing change in the relatively susceptible duodenum. The development of a gastric ulcer, which may occur without hypersecretion, presumably requires some previous alteration of the normally resistant gastric mucosa. Focal metaplasia of the gastric mucosa to tissue resembling the lining of the small intestine, which is observed frequently in association with gastric ulcer, may be a factor in providing decreased resistance to peptic injury.

Digestion↗

Drug therapy and peptic ulceration.

Peptic ulceration can be treated by various types of drugs including antacids, protectors, antimicrobials and acid-secretion reducers. Nurses have a role to play in administering medicines, educating patients and, in future, prescribing drugs.

Anti-Ulcer Agents↗

Aetiology of peptic ulcer.

Peptic ulcer should no longer be regarded as a single disease entity but as a group of heterogeneous conditions, as evident epidemiologically, genetically, clinically and pathophysiologically. In duodenal ulceration, "hyperacidity" must be the major culprit since specific therapeutic reduction of gastric acidity results in ulcer healing in about 70% of patients. However when the physiologic abnormalities leading to hyperacidity are analysed, it is obvious that each abnormality occurs usually in about a third of the patients only. Each of these abnormalities, however, can theoretically lead to an abnormal postprandial acid output or abnormal nocturnal acid output, and may explain why the majority of patients appear to have "hyperacidity". Indeed, controlling the meal-stimulated acid secretion alone and controlling the nocturnal acid secretion alone have been shown to heal duodenal ulcer. Corpus gastric ulcers, prepyloric ulcers, and gastric ulcers associated with duodenal ulcers appear physiologically distinct, and often behave differently on clinical grounds. This may explain why therapeutic reduction of acid secretion is less successful in healing gastric ulcer than duodenal ulcer.

Adult↗

Endoscopic and radiological assessment of recurrent ulceration after peptic ulcer surgery.

One hundred and eighteen patients with dyspepsia after peptic ulcer surgery were assessed by a double contrast barium meal and fibre-optic endoscopy, for the possibility of recurrent ulceration. There was overall endoscopic-radiological agreement in 89%. It is concluded that the two techniques are complementary and that a double contrast barium meal performed and interpreted by an experienced radiologist can demonstrate the presence or absence of a recurrent peptic ulcer with an acceptable degree of accuracy.

Gastroscopy↗

Three treatment schemes with colloidal bismuth subcitrate (Q-ULCER) in peptic ulcer with Helicobacter pylori.

BACKGROUND: Since the discovery, several decades ago, of the infection of the gastric mucosa with Helicobacter pylori and its association with chronic antral gastritis and peptic ulcer, the treatment of ulcer illness has recently been revolutionized. METHODS: In this study, the clinical effectiveness of three schemes of treatment with colloidal bismuth subcitrate (CBS) were compared. Fifty-three patients suffering from gastroduodenal peptic ulcer with Helicobacter pylori were distributed randomly into three groups. Group I (n = 17) received 240 mg CBS every 12 h for 6 weeks. Group II (n = 17) received 240 mg CBS every 12 h for 6 weeks, pus metronidazole 500 mg every 8 h plus tetracycline 500 mg every 8 h for 10 days. Group III (n = 19) received 240 mg CBS every 12 h for 6 weeks, plus metronidazole 500 mg every 8 h plus amoxicillin 750 mg every 12 h for 10 days. A duodenoscopy investigation with antrum biopsy for a morphologic study and detection of the germ was carried out by means of urease test and histological study (Warthin-Sarry and hematoxylin-eosin). RESULTS: The three schemes of treatment were effective for ulcerous healing with 70.5%, 82.3%, and 78.2%, respectively, without significant differences. The highest clearing index (52.6%) was obtained in group III. CONCLUSIONS: With these treatments, the Helicobacter pylori eradication was only observed in 47.3% of the patients studied.

Amoxicillin↗