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)

Gastric acid secretion under basal conditions and in response to graded balloon distension (50 ml, 100 ml, 150 ml) of the antrum was determined in healthy subjects and in peptic ulcer patients. In patients with a quiescent duodenal ulcer or a gastric ulcer antrum distension produced slight acid responses. The acid response to antrum distension was of quantitative importance only in patients with an active duodenal ulcer, amounting to 35 percent of the maximal acid response to pentagastrin. The healthy subjects did not respond with acid secretion to antrum distension. The pH of the gastric contents in the present series was 1.8-3.0, being lowest in patients with an active duodenal ulcer. Thus, the acid secretory effect of mechanical stimulation of the antrum seems qualitatively different in healthy subjects and ulcer patients, with a marked acid response in patients with an active duodenal ulcer.
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PMID:Gastric acid response to antrum distension in man. 23 87

Bile salts have been implicated in the pathogenesis of gastritis and gastric ulcer. Because the bile salt binding agent cholestyramine has been suggested as a possible therapy for gastric ulcer, we studied the effects of cholestyramine, in the form of Questran, on bile salt-induced injury to mouse gastric mucosa. Solutions of taurocholate or of glycochenodeoxycholate, with or without added Questran, were instilled into the stomachs of fasted mice at pH 1, 3, 5, and 7. Taurocholate damaged the mucosa only at pH 1, whereas glycochenodeoxycholate caused injury at pH 1 and 3. Questran failed to prevent mucosal damage by either bile salt. The ineffectiveness of cholestyramine to prevent injury may be due to the nonionized fraction of bile salts at pH's below their pKa's which will not be sequestered by the anion exchange resin. This phenomenon may help explain the insignificant effect of Qestran treatment in promoting healing of gastric ulcers in a previous clinical trial.
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PMID:Failure of cholestyramine to prevent bile salt injury to mouse gastric mucosa. 23 72

A study was made of the treatment received by 135 gastric ulcer patients within one month and within six months of diagnosis. The treatment was divided into three types. Effective measures included surgery and those measures that have been shown favourably to influence the initial healing rate of chronic gastric ulcer (i.e. hospital admission and carbenoxolone sodium). Ineffective measures included those that have been shown convincingly not to accelerate ulcer healing--diet, antacids, sedatives and no treatmen at all. Anticholinergic drugs were included in the third group where the evidence is conflicting. The patient's therapeutic status was assessed one month and six months after diagnosis. Within six months of diagnosis only 32% of patients received treatment that clinical trials have shown favourably to influence the course of gastric ulcer and approximately half received treatment that has never been shown favourably to influence the course of gastric ulcer. The social class of the patients and whether they were seen by a consultant physicians or family doctor made no difference to the form of therapy received.
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PMID:Treatment of chronic gastric ulcer a study of the treatment recived by 135 gastric ulcer patients in a western community. 26 84

The effect of Mucaine and Aludrox on basal and food stimulated immunoreactive gastrin has been assessed in normal control subjects and patients with duodenal or gastric ulcer. No differences in gastrin responses were observed either in the basal period or after the protein meal with the two antacids. As previously described, release of gastrin was greatest in gastric ulcer patients but in contrast to previous results,normal subjects seemed to show a greater response than duodenal ulcer patients but this was not statistically significant. Thus the combination of a local anaesthetic oxethazaine with aluminium hydroxide gel does not lead to diminished gastrin release and is not the prime mechanism of action of this agent.
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PMID:The effect of mucaine on gastrin release in man. 28 54

Eighty patients with chronic gastric ulcer, shown to have complete healing by gastric photography, were followed for 18 months to nine years. Ulceration recurred in 24, always at the site of the original ulcer, the majority (14) of relapses occurring within 12 months. Those with recurrent ulcers were more likely to show delayed healing of their initial ulcer, than the ulcers not shown to recur. At two months, this was statistically significant (P = 0.004) and even more so at three months (P = 0.004). Recurrences were more frequent in males (P = 0.09). There were no differences in ulcer site or size compared with those ulcers not known to have occurred. The appearance of complications such as perforation, haemorrhage, or malignancy was rare after complete healing.
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PMID:Prognosis of completely healed gastric ulcer. 28 49

Two cases of gastro-colic fistula occurring in analgesic abusers are described. In both patients, the fistulous communication was diagnosed at endoscopy and subsequently verified by upper gastrointestinal tract barium studies. Gastro-colic fistula is a rare complication of benign peptic ulcer disease. Whilst salcylates and cortico-steroids have been implicated as aetiological agents, abuse of compound analgesics has not previously been reported. Since the first description of gastro-colic fistula in 1755, thirty documented cases associated with benign gastric ulcer have been reported. Most often, gastro-colic fistula occurs secondary to gastric or colonic malignancy. Barium enema examination is the most accurate diagnostic study. Endoscopy has been confined to the visual inspection of the ulcer and establishing the benign nature of these lesions.
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PMID:Gastro-colic fistula complicating benign gastric ulcer in analgesic abusers. 28 2

The effect of a single dose of 400 mg of the H2-receptor antagonist cimetidine on protein meal stimulated immunoreactive gastrin was assessed in ten patients with gastric ulcer and ten patients with duodenal ulcer. In gastric ulcer patients, serum gastrin (mean +/- SE) rose from 34 +/- 2.2 pmol.l-1 to a peak of 80 +/- 5.0 pmol.l-1 at 45 minutes without and from 36 +/- 2.2 to 107 +/- 8.0 pmol.l-1 at 60 minutes with cimetidine; in duodenal ulcer it rose from 26 +/- 3.0 to 47 +/- 5.1 pmol.l-1 at 45 minutes without and 26 +/- 3.2 to 52 +/- 5.1 pmol.l-1 at 60 minutes with cimetidine. Integrated gastrin responses in gastric ulcer were 4900 +/- 800 pmol.l-1 120 minutes without and 7000 +/- 900 pmol.l-1 120 minutes with cimetidine and 1560 +/- 300 pmol.l-1 120 minutes without and 2620 +/- 400 pmol.l-1 120 minutes with cimetidine in duodenal ulcer patients. These gastrin increases after cimetidine are comparable to those achieved with continuous intragastric neutralisation with alkali.
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PMID:The effect of cimetidine on gastrin release in ulcer disease. 29 75

A retrospective study examined the clinical course of 32 patients with hiatal hernia in whom hemorrhage of the upper gastrointestinal tract was a prominent symptom. Hemorrhagic esophagitis was the most common source of bleeding. Duodenal ulcer, gastritis, and gastric ulcer of the herniated stomach were other less frequent causes of hemorrhage in these patients. Hemorrhage from esophagitis is usually mild and chronically recurrent. Surgical correction of the hiatal hernia and reflux is adequate treatment for the patient with hemorrhage from esophagitis or gastritis of the herniated stomach. Hemorrhage from duodenal ulcer as well as gastric ulcer requires a procedure directed at these lesions. Because of the association of upper gastrointestinal bleeding in hiatal hernia with lesions other than esophagitis, a vigorous diagnostic approach with endoscopy is essential.
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PMID:Diagnosis and treatment of hemorrhage in patients with hiatal hernia. 30 Jan 32

Seven elderly cases with reversible electrocardiographic changes simulating acute myocardial infarction in the absence of gross myocardial infarction on postmortem examination were observed following the blood transfusion. The underlying diseases were cancer of gastrointestinal tract or gall bladder in 4, gastric ulcer in 2, and 1 of pseudomembranous enterocolitis. The electrocardiogram revealed the abnormal Q waves with monophasic ST elevation and following coronary T inversion. These findings lasted only for 2 to 7 days and returned to the previous normal tracings. The hematocrit was elevated from 28.9 to 47.7 after the blood transfusion of 800 to 1,800 ml. The disseminated intravascular coagulation was shown in 5 cases. GOT levels were within normal ranges except 1 case. Pathological findings in cases with recent electrocardiographic changes were characterized by the mural thromboses, extending into the myocardium through the Thebesian vein. The focal small necroses of the adjacent myocardium or around the thrombosis of small vessels were also observed. In the later phase the fine interstitial fibrosis took place after the resorption of the thrombi and necrotic foci. From these clinical and pathological findings we proposed a new concept of reversible myocardial infarction induced from the hypercoagulability, disseminated intravascular coagulation, and elevated hematocrit.
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PMID:Acute reversible myocardial infarction after blood transfusion in the aged. 30 Aug 14

This report is of the results of management in a haematemesis and melaena unit at Prince Henry's Hospital, Melbourne. The unit was established in October, 1972, in response to unpublished data for the decades 1950 to 1959 and 1960 to 1969, which showed a mortality of about 15%. In the 39 months to December, 1975, 513 patients were received into a semi-intensive care setting. The unit staff consisted of a group of four surgeons and four physicians working a weekly roster. Primary care and liaison were the responsibility of the gastroenterology registrar. The basic diagnostic measure taken was the routine early use of fibreoptic duodenoscopy. The unit was set up with an agreed policy of management of the common causes of haematemesis and melaena, and data were prospectively recorded in a form suitable for computer analysis in every case. Of the 513 admissions, 378 were of males and 135 were of females. Forty-five patients died, giving an overall admission mortality of 8-8. There were 143 admissions for bleeding duodenal ulceration, 102 for acute peptic ulceration, 47 for chronic gastriculceration, 43 for oesophageal varices, 33 for Mallory-Weiss syndrome and 45 for less common causes of upper gastrintestinal bleeding. In 100 cases the source of bleeding was not discovered. Of the 143 patients admitted for chronic duodenal ulcer, either patients died, giving a mortality of 5-6%; 72 patients underwent operation, with an operative mortality of 9-7%. Of the 47 admitted with bleeding gastric ulcer, nine died (19-1%), while 26 came to operation; the operative mortality was 26-9%. There were 102 admissions for acute peptic ulceration, with an overall mortality of 11-7% (12 patients); 16 patients came to operation, with an operative mortality of 43-7%. Eleven deaths occurred in the 43 patients admitted for bleeding oesophageal varices (25-6%), with 10 patients coming to operation; the operative mortality was 30-0%. An age of greater than 50 years and shock on admission were the most significant factors for poor prognosis in this group of patients.
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PMID:The experience of a haematemesis and melaena unit: a review of the first 513 consecutive admissions. 30 Aug 34


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