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PubMed1982

Gastric carcinoma in patients with unoperated duodenal ulcer disease.

Gastric cancer may develop in the presence of active or chronic duodenal ulcer disease in the unoperated stomach. This association is considered rare, especially since the presence of a duodenal ulcer is believed to protect against the development of a gastric malignancy. In this review, we describe two patients in whom gastric cancer was diagnosed after a long history of duodenal ulcer disease. Also presented is a review of 236 additional cases from the literature Patients with gastric cancer associated with duodenal ulcer disease tended to be younger than patients who develop gastric cancer not associated with duodenal ulcer. When compared to patients with gastric remnant (stump) cancer, the latency from onset of ulcer symptoms to the diagnosis of gastric cancer was shorter than the latency for stump cancer development, but the risk of developing stump cancer appears to be greater. The natural history and prognosis of this entity is otherwise similar to gastric cancer unassociated with duodenal ulcer and to stump cancer. A change in ulcer symptoms is an insensitive clue to the presence of gastric cancer in this group. The diagnosis may be delayed in some individuals whose gastric cancers respond to cimetidine or other agents.

Adenocarcinoma↗
PubMed1989

Proximal gastric vagotomy for duodenal ulcer disease.

Proximal gastric vagotomy is a useful operation for duodenal ulcer disease that is intractable to medical management. It is also useful in selected patients with acute duodenal ulcer perforation. We present an overview of the indications for proximal gastric vagotomy, along with its results. The major benefits of proximal gastric vagotomy are low operative mortality and a low incidence of late complications.

Acute Disease↗
PubMed1985

Altered solid and liquid gastric emptying in patients with duodenal ulcer disease.

Alteration in gastric emptying has been implicated in duodenal ulcer disease. The precise abnormalities remain controversial. We have used a radionuclide technique to assess solid and liquid gastric emptying in 14 patients with endoscopically proven duodenal ulcer and 22 healthy controls. Solid gastric emptying values for the patient group fell within the normal range. The median time taken for 50% (T50) of the liquid marker to empty from the stomach was 12 minutes (range 6-23 minutes) which was significantly faster (p less than .005) than controls (median 18 minutes, range 11-35). In 10 of the 14 patients, however, the rate of liquid emptying was within the normal range. There was no significant difference in the T50 for gastric emptying of solids between the groups, but in duodenal ulcer patients food left the stomach significantly earlier than in controls (p less than .05). After this, however, the linear rate at which duodenal ulcer patients emptied solid food from the stomach was a median 0.75%/minutes (range 0.5-1.4 minutes), which was slower (p less than .0005) than controls, median 1.25/minutes (range 0.7-2.3). These results show that the pattern of gastric emptying of digestible solids and liquids in patients with duodenal ulcer disease, as a group, is significantly altered.

Adult↗
PubMed1996

Gastric emptying and Helicobacter pylori infection in duodenal ulcer disease.

The pathogenetic link between Helicobacter pylori gastritis and duodenal ulcer is still unknown. Fast gastric emptying of liquids might be important in the pathogenesis of gastric metaplasia of the duodenum and duodenal ulcer through an increased exposure of the duodenum to gastric acid. In H. pylori-infected subjects, an abnormal gastric emptying could affect urea breath test results and correlate with histological gastritis. This study was performed to evaluate the gastric emptying of liquids in duodenal ulcer patients with H. pylori infection and the possible relation between the bacterial load, gastric emptying, and urea breath test results. Seventeen duodenal ulcer patients with H. pylori gastritis and 15 healthy volunteers were studied by a [14C]octanoic acid and [13C]urea breath test to evaluate gastric emptying rate and H. pylori status simultaneously. Endoscopy with antral biopsies were performed in all duodenal ulcer patients. Duodenal ulcer patients with H. pylori infection have a normal liquid gastric emptying that is unrelated with histological severity of gastritis. The urea breath test results and the gastric emptying parameters do not correlate with histology. A significant correlation between the gastric emptying and the urea hydrolysis rate is found. It is concluded that H. pylori infection and duodenal ulcer disease is not associated with abnormally fast liquid gastric emptying, and this finding should be taken into account when a casual link between H. pylori infection and duodenal ulcer disease is searched for. The correlation between gastric emptying and urea hydrolysis rate explains why no conclusions on intragastric bacterial load can be drawn from the urea breath test results.

Adult↗
PubMed1990

[Incompetence of the sphincter of Oddi in duodenal ulcer disease].

The association of post-bulbar duodenal scarring and incompetence of the sphincter of Oddi is rare. Radiographic and endoscopic procedures should exclude concomitant neoplastic disease invading the duodenum, and duodenal Crohn's disease. The pancreatico-biliary system should be visualized before attributing ampullar reflux to duodenal ulcer disease. The treatment is that of the primary disease.

Duodenal Ulcer↗
PubMed1983

Role of luminal acidity in the pathogenesis of stress-induced gastroduodenal disease.

Infusion of progressively more acidic fluids into the stomachs of rats stressed by immobilization had disparate effects on gastric erosive disease despite their producing a stepwise fall in venous pH. At the highest concentration infused, disease was exacerbated. However, at lower concentrations, disease was ameliorated. The acidity of the infusate altered the incidence but not the magnitude of the duodenal disease that accompanies stress. When bicarbonate was given parenterally, systemic pH was normalized but gastric disease still developed. Thus the level of mucosal pH does not reliably predict whether or not gastric disease will develop. When a series of progressively more basic fluids was infused into the stomachs of stressed rats, gastric disease was lessened in only those rats infused with the highest concentration of bicarbonate. Increasing the pH of the infusate in a stepwise fashion produced a stepwise diminution of duodenal disease incidence with no effect on duodenal disease severity. When the stressed rat's mucosa was stimulated to secret acid by the parenteral injection of secretagogues, gastric disease severity was the same as in control animals given saline. Although secretagogue infusion did not affect the incidence of stress-induced duodenal disease, it significantly exacerbated the magnitude of the elicited disease. These experiments suggest that luminal acid plays a negligible role in the onset of stress-induced gastric disease but may be important in determining the severity of the gastric disease once it has begun. Conversely the amount of luminal acid correlates with the incidence of stress-induced duodenal disease but does not seem to play a role in determining the severity of the duodenal disease after it has begun.

Animals↗
PubMed1983

Duodenal prostaglandin synthesis and acid load in health and in duodenal ulcer disease.

We sought to test the hypothesis that duodenal ulcer disease results from an imbalance between duodenal acid load, an injurious force, and mucosal prostaglandin generation, a protective factor. Ten patients with duodenal ulcer and 8 healthy controls were studied. The duodenal acid load after an amino acid soup was quantified by a double-marker technique. Mucosal biopsy specimens were taken endoscopically from the duodenal bulb before and after the test meal. Prostaglandin synthesis activity was measured by incubating biopsy homogenates in excess [14C]arachidonic acid. Although mean duodenal acid load was higher in duodenal ulcer, ranges overlapped. Neither the qualitative nor quantitative profile of mucosal prostaglandin synthesis activities differed significantly between test groups. Prostaglandin synthesis activities, however, tended to increase post cibum in controls, but change little or decrease in duodenal ulcer. Only by comparing the responses with a meal of both parameters together (duodenal acid load and the change in prostaglandin synthesis activities) was there complete or nearly complete separation of duodenal ulcer from controls. Greatest discrimination was observed with prostacyclin (6-keto-PGF1 alpha). We conclude that in health, mucosal prostaglandin generation in the duodenum is induced post cibum in relation to duodenal acid load; this may be a physiologic example of adaptive cytoprotection. In duodenal ulcer there may be a defect in such a mechanism.

Adult↗
PubMed1981

Abnormal gastric emptying response to pentagastrin in duodenal ulcer disease.

The effect of pentagastrin on gastric emptying in duodenal ulcer disease (DU) is unknown. The evaluation of this effect is complicated by the simultaneous action of the hormone on gastric secretion. We compared gastric emptying and net gastric output in 17 patients with active DU to that of 11 healthy controls. A dye-dilution technique was used to determine net acid output, fractional emptying rate, and acid emptying rate during a basal period and after pentagastrin (6 microgram/kg/hr, intravenously). Net basal acid output observed in controls (54 +/- 10 microEq/min; mean +/- SE) was used as the primary criterion for separating DU patients into 12 normosecretor (30 +/- 10 microEq/min) and 5 hypersecretor patient groups (163 +/- 40 microEq/min). The pentagastrin-stimulated net acid output was significantly greater in hypersecretor patients than in controls (P less than 0.01) but was normal in normosecretor patients. Basal fractional emptying and acid emptying rates were significantly greater in hypersecretors than in controls (P less than 0.05) but were normal in normosecretors. In contrast, both normo- and hypersecretor patients had significantly greater fractional emptying (P less than 0.01) and acid emptying rates than controls (P less than 0.05) during pentagastrin infusion. Thus, a greater load of acid transiently enters the duodenum in duodenal ulcer disease following pentagastrin stimulation, even in the absence of gastric hypersecretion.

Adult↗
PubMed1992

Nine years of maintenance treatment with ranitidine for patients with duodenal ulcer disease.

Four hundred and sixty-four patients with duodenal ulcer disease received continuous maintenance treatment with ranitidine for up to 9 years. Treatment failure was defined as either the first symptomatic recurrence of ulcer or the first ulcer recurrence accompanied by haemorrhage. Life tables were constructed using the Kaplan-Meier product-limit method; comparisons of survival curves were performed using the log-rank test; and multivariate analysis was carried out using the Cox proportional hazards model. Results. The proportion of patients remaining free from symptomatic recurrence of ulcer during maintenance treatment with either 150 mg/day or 300 mg/day ranitidine was: 95% at 1 year; 88% at 3 years; 86% at 5 years; and 81% at 7 and 9 years (95% C.I. 76-86%). Young age and the absence of exposure to non-steroidal anti-inflammatory drugs (NSAIDs) at the time of diagnosis of ulcer were shown to increase the likelihood of developing ulcer recurrence. The rate of ulcer recurrence after 9 years of maintenance treatment (17%) was significantly less than that after 5 years without active anti-ulcer therapy (80%), P = 0.0001. The proportion of patients who remained free from ulcer haemorrhage during maintenance treatment was: 99.1% at 1 year and 98.1% at 5 and 9 years (95% C.I. 96.7-99.6%). The risk of haemorrhage was significantly greater in patients who were not receiving active treatment (12.4% at 5 years) than in patients receiving maintenance treatment (less than 2% at 9 years), P = 0.0001 (log-rank test). Patients who had originally presented with haemorrhage had an increased risk of further ulcer bleeding compared with patients who presented with pain (P = 0.0013). A significantly greater proportion of patients with NSAID-associated duodenal ulcers remained free from ulcer recurrence during maintenance treatment compared with patients suffering from 'idiopathic' ulcers (P = 0.0238), although there was no difference between the two groups in respect of haemorrhage during maintenance treatment. Conclusions. (a) Continuous maintenance treatment with ranitidine for up to nine years successfully prevents ulcer recurrence in more than 80% of patients with duodenal ulcer disease. (b) Young age increases the risk of ulcer recurrence during maintenance treatment with ranitidine. Ulcers associated with NSAID-intake at the time of diagnosis have a lesser risk of recurrence during maintenance treatment. (c) The risk of haemorrhage in patients with ulcer disease receiving maintenance treatment with ranitidine for nine years was less than 2% compared with greater than 12% in untreated patients observed for 5 years.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1998

Relationship between fundic endocrine cells and gastric acid secretion in hypersecretory duodenal ulcer diseases.

BACKGROUND: Acid hypersecretion is associated with duodenal ulcer disease in the following conditions: Zollinger-Ellison syndrome (ZES) and antral gastrin cell hyperfunction (AGCH) due to hypergastrinaemia, or hypersecretory duodenal ulcer (HDU) without hypergastrinaemia. AIM: To evaluate whether quantitative changes in fundic ECL and D cells may be involved in acid hypersecretion. PATIENTS AND METHODS: Seven ZES, six AGCH and six HDU Helicobacter pylori-positive patients were compared. Basal (BAO) and pentagastrin-stimulated gastric acid secretions (PAO), and morphometry of fundic ECL and D cells were performed. The six AGCH and six HDU patients were investigated again using the same tests 1 year after H. pylori eradication. RESULTS: Median PAO values were no different in all the hypersecretory conditions studied. The median volume density of ECL cells in ZES was significantly higher than in controls (2.75, range 1.74-5.8 vs. 0.73, 0.52-1.11: P < 0.05), whereas it was in the control range in AGCH and HDU patients (0.77, range 0.20-1.39 and 0.99, range 0.42-1.51; respectively). The count of fundic D cells was significantly lower in AGCH patients than in all other investigated groups (median 0.16, range 0.1-0.52; P < 0.05). Cure of infection in AGCH and HDU patients did not modify the ECL cell volume density, whereas a significant increase in the count of fundic D cells was observed in AGCH patients. Thus, the ECL/D cell index was significantly affected in AGCH patients (P < 0.05), being higher during H. pylori infection (median 6, range 0.7-9.25) than after the cure (median 2.12, range 1.10-3.5). BAO and PAO were not affected by H. pylori eradication in either group. CONCLUSIONS: The study provides evidence, for the first time, that quantitative alterations in the fundic endocrine cells are not involved in acid hypersecretion of patients with hypersecretory states, and that eradication of H. pylori does not restore normal acid secretion values.

Adult↗
PubMed1976

Gastric acid secretion and acute gastroduodenal disease after burns.

Total titratable acidity of fasting gastric secretion was determined in 34 hemodynamically stable patients within five days after burn. Acid output was not predictive of disease; acute duodenal ulcers, however, were not discovered in patients with acid secretion of less than 3.11 mEq/hr. Patients with both gastric and duodenal disease secreted significantly (P less than .05) more acid than patients without duodenal involvement and complications were more likely to develop, especially from acute ulcerations. Hemorrhage or perforation occurred in nine patients whose acid output was significantly (P less than .05) greater than that of asymptomatic patients. Duodenal regulation and neutralization of acid secretion may be impaired in patients with early duodenal injury, resulting in a relative increase in acid output and enhanced potential for complications. A controlled evaluation of antacid therapy in the prevention of disease complications seems justified in these patients.

Antacids↗
PubMed1989

Irradiation-induced duodenal ulcer disease refractory to ranitidine: healing by omeprazole.

In two patients duodenal ulcer refractory to high dose H2-blocker treatment started several months after irradiation therapy following right nephrectomy because of renal adenocarcinoma. Established antiulcer drugs like ranitidine, famotidine, sucralfate, pirenzepine, and antacids alone or in combination were unable to control ulcer pain and failed to induce ulcer healing. Initiation of omeprazole treatment at dosages to produce complete achlorhydria were necessary for ulcer healing and maintenance therapy. We suggest that (a) irradiation may cause duodenal ulcer disease indistinguishable from idiopathic duodenal ulcer; (b) radiation-induced ulcers in the duodenal bulb are refractory to various antiulcer drugs but may heal after administration of omeprazole in dosages that completely suppress acid secretion.

Aged↗
PubMed1989

Gastric metaplasia and Campylobacter pylori in duodenal ulcer disease: an ultrastructural analysis.

An ultrastructural analysis was carried out on duodenal mucosa specimens, obtained during duodenoscopy from the edge of ulcers and distal duodenal cap mucosa in 42 patients with active duodenal ulcer disease, and in 12 controls. In 18 of 42 patients (43 p. 100), Campylobacter pylori was found in duodenal mucosa but not in controls (chi 2 = 5.91, p less than 0.05). In all 42 cases, gastric-type surface mucus cells were seen at the edge of the ulcer crater, and in 38 of the patients (90 p. 100) these metaplastic cells were also seen in the distal duodenal cap. C. pylori was always localized within the mucus layer, frequently in the intercellular spaces and, in 4 of 18 cases (22 p. 100), within the cytoplasm. C. pylori was detected exclusively in the proximity of gastric type metaplastic surface mucus cells with apparent fusion of membranes. It is suggested that the metaplastic surface mucus cell in the duodenal epithelium of patients with active duodenal ulcer disease is the target cell for colonization by C. pylori.

Adult↗
PubMed2000

[Morphological changes of gastric mucosa in duodenal ulcer disease in elderly and senile patients].

Morphological investigation of gastric mucosa was done in 85 patients of various age with duodenal ulcer disease using visual-analogue scale of the modified classification of the Sidney system (1996). In all the patients there was revealed chronic gastritis, possessing age morphological peculiarities. The frequency of infectionizing with Helicobacter pylori is reduced with the age increased.

Aged↗
PubMed1992

Mucosal reactive oxygen metabolite production in duodenal ulcer disease.

To investigate the hypothesis that reactive oxygen metabolites are important in the pathophysiology of duodenal ulcer disease, their production by duodenal mucosal biopsy specimens was measured using luminol and lucigenin amplified chemiluminescence. Luminol chemiluminescence, expressed as background corrected median photon emission/mg/min x 10(3) (95% confidence intervals), was increased in duodenal inflammation as assessed macroscopically: ulcers 20.3 (4.8 to 51.3), n = 29; severe duodenitis 13.9 (6.6 to 75.3), n = 16; mild duodenitis 0.0 (-0.5 to 0.8), n = 56; controls -0.8 (-1.3 to -0.1), n = 41; p = 0.0001, Kruskal-Wallis) and microscopically: severe 17.0 (9.3 to 51.3), n = 12; moderate 0.3 (-2.8 to 5.8), n = 17; mild -0.1 (-1.8 to 1.0), n = 17; controls -0.8 (-1.6 to 0.0), n = 15; (p = 0.0001). Luminol chemiluminescence was directly related to both the macroscopic and microscopic severity of duodenal damage (Spearman's R = + 0.53, + 0.55 respectively, both p = 0.0001), to histochemical assessment (myeloperoxidase activity) of neutrophil infiltration (R = + 0.63; p = 0.04), and to lucigenin chemiluminescence (R = + 0.56, p = 0.0002). Luminol chemiluminescence was inhibited by sodium azide (-80%), catalase (-73%), and dimethyl sulphoxide (-24%). Superoxide dismutase inhibited lucigenin more than luminol dependent chemiluminescence (-61% and -7% respectively, p < 0.05). Within disease groups, Helicobacter pylori antral infection was associated with increased duodenal chemiluminescence, whereas smoking, alcohol, and use of NSAIDs or H2 blockers had no influence. Their disease related generation in duodenal mucosa supports a role for reactive oxygen metabolites in the pathogenesis of duodenitis and duodenal ulcer. These metabolites might include superoxide, hydrogen peroxide, hydroxyl, and products of myeloperoxidase activity.

Adult↗
PubMed1994

Do clinicians accept the role of Helicobacter pylori in duodenal ulcer disease: a survey of European gastroenterologists and general practitioners.

OBJECTIVES: To examine to what extent clinicians in Europe accepted the theory of the casual role of Helicobacter pylori (H.pylori) in duodenal ulcer disease in the year 1992, and to what extent the theory had influenced their diagnostic and therapeutic habits in the management of duodenal ulcer patients at that time. DESIGN: Postal questionnaire. SETTING: Three European countries: the UK, the Netherlands, and Denmark. SUBJECTS: Three hundred and three gastroenterologists, 250 general practitioners, 83 junior hospital doctors. MAIN OUTCOME MEASURES: Number of doctors believing H. pylori to be a significant cause of duodenal ulcer disease, use of diagnostic tests for detection of H. pylori and therapeutic regimens for eradicating H. pylori. RESULTS: Four hundred and forty-two doctors replied. Eighty-four per cent of the British doctors, 73% of the Dutch doctors, and 47% of the Danish doctors accepted the role of H. pylori in duodenal ulcer disease. The rates were higher among gastroenterologists than among general practitioners. Eighty-four per cent of the British doctors, 80% of the Dutch doctors, and 48% of the Danish doctors used diagnostic tests for H. pylori, most frequently histological examination (64%). In patients with duodenal ulcer disease, H. pylori eradication was undertaken by 93% of the British doctors, 89% of the Dutch doctors, and 60% of the Danish doctors. A triple therapy (a bismuth salt, metronidazole, and either amoxicillin or tetracycline) was used by 57% (181/315) of the doctors. CONCLUSIONS: H.pylori treatment is frequently used in some countries. However, the role of H. pylori in duodenal ulcer disease has not been accepted to the same extent in different European countries.

Denmark↗