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PubMed1999

Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer.

BACKGROUND: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer. METHODS: Duodenal and gastric biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer, gastric ulcer or chronic gastritis. The extent of gastric metaplasia was evaluated histologically and endoscopically using the methylene blue test. In this study, we performed competitive polymerase chain reaction, a highly sensitive and quantitative method for determining the amount of H. pylori gastric and duodenal mucosa. The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in the three patient groups were compared. The correlation between the amount of H. pylori in the duodenum and gastric antrum and extent of gastric metaplasia were also determined. RESULTS: The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in patients with duodenal ulcer were much higher than in patients with gastric ulcer or chronic gastritis. A positive correlation was found between the amount of H. pylori in the duodenum and the extent of gastric bulb and that in the antrum. CONCLUSIONS: The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.

Adult↗
PubMed1987

Impaired proximal duodenal mucosal bicarbonate secretion in patients with duodenal ulcer.

The defensive factors that prevent the human duodenal mucosa from acidic and peptic damage have not been fully evaluated. To determine whether duodenal mucosal bicarbonate production was altered in patients with inactive duodenal ulcer, we measured basal and acid-stimulated bicarbonate output from the duodenal bulb and the distal duodenum in healthy subjects and patients with inactive duodenal ulcer. As compared with 16 normal subjects, the 12 patients had significantly less mean (+/- SE) basal proximal duodenal mucosal bicarbonate secretion (185 +/- 13 vs. 107 +/- 18 mumol per centimeter per hour; P less than 0.001). Moreover, in response to a physiologic amount of hydrochloric acid (2 mmol per five minutes) instilled directly into the duodenal bulb, peak proximal duodenal bicarbonate output in the patients was 41 percent of the normal response (263 +/- 65 vs. 642 +/- 77 mumol per centimeter per hour; P less than 0.01). There was little overlap between groups. In contrast, bicarbonate outputs in the distal duodenum were similar in the two groups. We conclude that most patients with duodenal ulcer disease have decreased proximal duodenal mucosal bicarbonate production at rest, in response to hydrochloric acid, and in relation to peak gastric acid secretion. Impaired proximal duodenal mucosal bicarbonate secretion may be an important factor in the development and natural history of duodenal ulcer.

Adult↗
PubMed1982

Cholecystokinin-like activity in the duodenal mucosa of duodenal ulcer patients.

Cholecystokinin-like activity in the duodenal mucosa was measured by the bioassay method described by Ljungberg to elucidate its significance in 14 duodenal ulcer patients as well as in 13 normal subjects with no evidence of gastrointestinal diseases. The stage of duodenal ulceration was determined endoscopically according to the criterion of the Japanese Gastroenterological Endoscopic Society. The cholecystokinin-like activity in the duodenal mucosa of duodenal ulcer patients in active stage 1, which was considered as an early stage of active open duodenal ulceration, did not differ statistically from that of normal subjects, whereas that of duodenal ulcer patients in active stage 2 began to show a significant increase (p less than 0.05), and the cholecystokinin-like activity in the duodenal mucosa of duodenal ulcer patients in healing stage 1 or healing stage 2 was significantly higher than that in normal subjects (p less than 0.01). The cholecystokinin-like activity in the duodenal mucosa of duodenal ulcer patients in the scarring stage, however, returned to the normal range. It is concluded that cholecystokinin may act physiologically in the cure of duodenal ulcer.

Adolescent↗
PubMed2002

Duodenal Helicobacter pylori associated duodenal ulcer depend on gastric Helicobacter pylori status.

Gastric Helicobacter pylori (H. pylon) plays an important role in the pathogenesis of duodenal ulcer (DU), although not all H. pylori infected persons will develop disease. Duodenal H. pylori was supposed to be one of the factors related with DU. The aim of this study was to investigate whether H. pylori in the duodenum of patients with DU plays a critical role in the pathogenesis of DU regarding the gastric H. pylori status. Furthermore, it was to determine the prevalence of duodenal H. pylori infection in Thailand. Ninety three patients were included in the study. They underwent gastroscopic evaluation for dyspeptic symptoms and none of them had previous H. pylori eradication therapy. An upper gastrointestinal endoscopy was performed and two specimens were collected each form the antrum, midcorpus and duodenal bulb in order to diagnose H. pylori infection. The gold standard for H. pylori detection is a positive specimen culture or polymerase chain reaction (PCR) assay for the vac A gene or positive urease test plus H. pylori seen in the pathology. Ninety three dyspeptic patients (43 males and 50 females; mean age 48.2 years; range 22 to 79 years) were included in the study. Duodenal H. pylori was detected in 31/93 (33.33%) patients which included 15 (48.38%) patients with duodenal ulcer, 2 (6.45%) patients with gastric ulcer and 14 (45.16%) patients with NUD. Five of thirty one (16.21%) patients with duodenal H. pylori infection had negative gastric H. pylori. These five patients included 1 with DU, 1 with DU and 3 with NUD. Duodenal H. pylori was associated with DU dependent of the presence of gastric H. pylori (p<0.05) and there was no association between duodenal H. pylori with negative gastric H. pylori and duodenal ulcer (p>0.05). Duodenal H. pylori is associated with duodenal ulcer dependent on the presence of gastric H. pylori. These results suggest that transmission of gastric H. pylori to the duodenum was prerequisited for the formation of DU.

Adult↗
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

Mucosal cell proliferation in duodenal ulcer and duodenitis.

Mucosal cell proliferation in the first part of the duodenum was studied in 24 patients using a tissue culture technique in which endoscopic biopsies were subjected to autoradiography after exposure to tritiated thymidine. Eight patients had a normal duodenum, eight had duodenal ulcer, and eight had symptomatic chronic non-specific duodenitis. The mean crypt labelling index (LI) in normal duodenum was 8.8 0.4% (SEM). Increased labelling indices of 15.6 +/- 1.7% were found near the edge of duodenal ulcers and 17.8 1.8% in duodenitis. Treatment with cimetidine reduced both the severity of duodenitis and the mean crypt LI. The LI of histologically normal duodenal mucosa distal to ulcer of duodenitis was similar to that of the control subjects' mucosa. The increased mucosal cell proliferation seen in severe duodenitis, either alone or associated with duodenal ulceration, suggested that erosions and ulcers arose when the crypts passed into 'high output failure' and were unable to compensate for further epithelial cell loss. There was no evidence in out study for a generalised failure of mucosal cell proliferation in duodenal ulcer or duodenitis.

Adult↗
PubMed2003

Diagnostic yield of duodenal aspirate for G. lamblia and comparison to duodenal mucosal biopsies.

Our objective was to examine the diagnostic yield of duodenal aspirates for Giardia in children and compare it to results of duodenal mucosal biopsies. The results of all duodenal aspirates submitted for direct parasite examinations over a 31-month period were reviewed, as were the histological results of duodenal mucosal biopsies from these patients. In all, 161 children (89 boys; age range 0.33-18 years) were included in the study. Giardia was identified in the duodenal aspirate of 5.6% (9/161) patients and on duodenal mucosal biopsies from all nine patients. In conclusion, the 5.6% diagnostic yield of duodenal aspirates for Giardia is higher than reported in a previous study of adult patients from a similar geographical region (0.7%). The detection of Giardia on duodenal mucosal biopsies from all patients with positive duodenal aspirates brings into question the utility and cost of the latter test. Duodenal aspirates for Giardia may be unnecessary if duodenal mucosal biopsies are obtained for histological examination.

Adolescent↗
PubMed2002

Induction of duodenal motility activates the sphincter of Oddi (SO)-duodenal reflex in the Australian possum in vitro.

1 The aim of this study was to determine if stimulation of duodenal motility by duodenal fluid distension or by administration of carbachol, activates the sphincter of Oddi-duodenal reflex, in an in vitro preparation from the Australian possum. 2 Duodenal distension was achieved by infusion of Krebs solution (0-8 cm H2O). In separate experiments, the sphincter of Oddi (SO) was partitioned from the duodenum and carbachol (10(-7) - 5 x 10(-6) M) added to the duodenal compartment. 3 Fluid distension increased duodenal motility to 120-600% of control activity. These treatments induced increased SO motility (to 120-390% of control) in six preparations, reduced activity (to 60% of control) in one and no response in another. 4 Addition of carbachol to the duodenal compartment resulted in increased duodenal motility. SO motility was increased in seven preparations, reduced in another two and no response were evoked in two others. All SO responses were blocked by tetrodotoxin pretreatment. 5 These data suggest that the SO receives inputs from duodenal mechano and/or stretch receptors resulting in excitatory or inhibitory responses, with the excitatory response dominating. These findings support the role for the SO-duodenal reflex in preventing duodenobiliary/pancreatic reflux during periods of elevated duodenal activity.

Animals↗
PubMed1996

The influence of Helicobacter pylori infection on postprandial duodenal acid load and duodenal bulb pH in humans.

BACKGROUND & AIMS: Recently, we postulated a new concept of duodenal ulcer pathogenesis suggesting that antral Helicobacter pylori infection blocks inhibitory pathways to the gastrin and parietal cells, resulting in an increased and prolonged postprandial acid secretion. the aim of this study was to examine duodenal acid load and duodenal bulb pH after a meal before and after eradication of H. pylori. METHODS: Using a marker-dilution method and a pH electrode in the duodenal bulb, gastric emptying, acid secretion, gastrin release, duodenal acid load, and duodenal bulb pH were studied during 2 hours after peptone meals of pH 7.0 and 2.0 in 8 H. pylori-negative controls and 8 H. pylori-infected subjects before and 6 months after eradication. RESULTS: The H. pylori-infected subjects had an increased gastric emptying, gastrin release, and acid secretion, higher duodenal acid load, and lower duodenal bulb pH after the meals. These responses were normalized after eradication. CONCLUSIONS: H. pylori-infected subjects have an increased and prolonged postprandial acid secretion, partly caused by an impaired low pH inhibition of acid secretion, gastrin release, and gastric emptying, resulting in an increased duodenal acid load and a prolongation of low pH in the duodenal bulb, as a general prerequisite for the development of duodenal ulcer disease.

Adult↗
PubMed1985

Duodenal gamma-glutamyltransferase activity in human biopsies: effect of chronic ethanol consumption and duodenal morphology.

Gamma-glutamyltransferase activity was determined in duodenal biopsies, and in the sera of forty-six non-alcoholic and eighteen alcoholic patients with a daily alcohol consumption of more than 80 g. Additionally, duodenal morphology was examined in biopsy material obtained at the same time. In both alcoholics (P less than 0.05) and in non-alcoholics (P less than 0.001) the duodenal gamma-glutamyltransferase activity revealed a significant positive correlation with duodenal villus length. In addition, alcoholics exhibited a significant decrease in duodenal villus length (338 +/- 13 vs. 363 +/- 13 microns, P less than 0.01), and a significant increase in duodenal gamma-glutamyltransferase activity (13.0 +/- 1.4 vs. 8.4 +/- 0.6 mU mg-1 protein, P less than 0.01) when compared to controls. No significant correlation was found between duodenal and serum gamma-glutamyltransferase activity in alcoholics and non-alcoholics. During follow up of two patients, duodenal gamma-glutamyltransferase activity decreased and duodenal villus length increased after withdrawing alcohol. These data underline the damaging effect of alcohol on the duodenal mucosa and demonstrate that chronic alcohol intake reversibly effects duodenal gamma-glutamyltransferase. In addition, the small intestine appears of minor importance as an origin for the elevated serum gamma-glutamyltransferase activities seen in the alcoholic.

Adult↗
PubMed1991

Helicobacter-associated duodenitis and gastric metaplasia in duodenal ulcer patients.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.

Antacids↗
PubMed1997

[Is active autonomous duodenitis a precursor of duodenal ulcer?].

Up to today, the relationship between autonomous nonspecific duodenitis (ANSD) has not yet been defined. ANSD has been noticed in about 26% of dyspeptic population. With reference to the presence of active inflammation, ANSD has been divided into chronic duodenitis (CD) (77.7%) and in active duodenitis (AD) (22.3%). The two duodenitis groups have been compared with a group of patients with duodenal ulcer (DU) in relation with the presence of duodenal gastric metaplasia (GM), of duodenal Helicobacter pylori (Hp) infection, of antral chronic gastritis (AG), of antral Hp infection, and in relation with the gastric secretion behaviour. The data concerning AD are superimposable to those of DU with presence of high percentage of duodenal GM, of duodenal Hp infection and of Hp positive AG. Furthermore, they present a gastric secretory profile similar to DU with prevalence of hyperchlorhydria and hyperpepsia. CD without activity, on the contrary, present values superimposable to dyspeptic population without duodenitis and DU. It is, therefore, that Hp positive AD can be considered as a possible precursor of DU. In periulcerous site, in fact, AD is present in more than 90% of cases.

Duodenal Ulcer↗
PubMed1989

Refractory duodenal ulcers (nonhealing duodenal ulcers with standard doses of antisecretory medication).

To evaluate possible differences between patients with refractory duodenal ulcers and those with duodenal ulcers that respond to standard doses of antisecretory medications, we determined basal acid outputs by nasogastric suction and daily smoking histories in 75 patients with endoscopically documented active duodenal ulcers. Patients were treated for at least eight weeks with standard doses of antisecretory medications and endoscopic healing or nonhealing was documented. Fifty-five patients that had complete healing of their duodenal ulcers had a mean basal acid output of 6.6 +/- 5.3 meq/hr, and 18/55 had daily cigarette smoking histories, whereas 20 patients that had nonhealing duodenal ulcers had a mean basal acid output of 20.0 +/- 9.6 meq/hr, and 8/20 had daily cigarette smoking histories. There were no significant differences between the two groups with regard to age, duodenal ulcer size, or cigarette smoking history. However, there were significant differences in male-female ratio (P less than 0.02) and in mean basal acid output (P less than 0.001), and all patients with nonhealing duodenal ulcers had basal acid outputs of greater than 10.0 meq/hr. Patients with nonhealing duodenal ulcers were treated with increased doses of ranitidine, mean 675 mg/day (range 600-1200 mg/day), and all had complete healing endoscopically documented. These results indicate that patients treated with standard doses of antisecretory medications with nonhealing duodenal ulcers have increased basal acid outputs of greater than 10.0 meq/hr, and the duodenal ulcers heal with increased doses of antisecretory medication.

Adult↗
PubMed1990

Proximal duodenal prostaglandin E2 release and mucosal bicarbonate secretion are altered in patients with duodenal ulcer.

Proximal duodenal mucosal bicarbonate production is impaired in patients with duodenal ulcer disease. Because prostaglandins of the E class increase human proximal duodenal bicarbonate secretion, this study tested the hypothesis that endogenous prostaglandin E2 production is defective in patients with duodenal ulcer. Ten patients, five with active and five with inactive duodenal ulcer disease, were studied along with 10 normal volunteers. The proximal 4 cm of duodenum, the bulb, was isolated and continuously perfused with 154 mmol/L NaCl. Basal bicarbonate secretion was measured for 30 minutes. The test segment was then acidified with a physiological amount of HCl (2 mmol over 5 minutes), and acid-stimulated bicarbonate secretion was measured by pH/PCO2 and back-titration for 55 more minutes. Prostaglandin E2 was measured in the effluents by a radioimmunologic assay validated by gas chromatography-mass spectrometry. Compared with the normal subjects after luminal acidification, the duodenal ulcer patients had significantly greater PGE2 release and decreased total 1-hour bicarbonate output. The peak 5-minute acid-stimulated bicarbonate responses were not significantly different between the duodenal ulcer patients and normal subjects. After luminal acidification, PGE2 output remained elevated in the duodenal ulcer patients but returned promptly to basal in the normal subjects. Furthermore, the ratio of bicarbonate secreted to the amount of PGE2 released was significantly less in the ulcer patients. These findings suggest that patients with duodenal ulcer disease have an impaired mucosal bicarbonate response to endogenous PGE2. The increased acid-stimulated PGE2 response in duodenal ulcer patients suggests a compensatory phenomenon in response to the diminished mucosal bicarbonate production.

Bicarbonates↗
PubMed1990

Nodular duodenitis and single duodenal nodules.

Duodenal nodules are an uncommon endoscopic finding generally thought to indicate duodenal inflammation. This study examines the incidence and histologic correlates of multiple and single duodenal nodules in 2,966 consecutive male patients who underwent esophagogastroduodenoscopy during the past five years. Five per cent had duodenal nodules. When two or more discrete nodules, with or without apical ulceration, were present, the finding was termed nodular duodenitis, which was seen five and one-half times more frequently than single nodules. There were 127 patients with nodular duodenitis (4.3%); seven had chronic renal disease and 33 (26%) had concomitant peptic ulcer disease. Biopsies showed either normal mucosa or histologic aberrations typical of nonspecific duodenitis. Single nodules were seen in only 23 patients (0.8%). Biopsies of these nodules revealed benign or malignant tumors in five instances and infrequently showed only normal mucosa. It is concluded that nodular duodenitis is a visually distinct, morphologic variant of nonspecific duodenitis bearing some yet-to-be-defined relationship to peptic ulcer disease. Single nodules are much less likely to represent duodenitis and, in fact, they have significant neoplastic potential, mandating biopsy whenever they are found.

Aged↗
PubMed1987

Persistence of Campylobacter pyloridis despite healing of duodenal ulcer and improvement of accompanying duodenitis and gastritis.

Campylobacter pyloridis has been associated with antral gastritis and duodenal ulcer. To study the pathogenetic role of these organisms in duodenal ulcer, endoscopic biopsies, two from the first part of duodenum, four from antrum, and four from body and fundus, were taken before and after four weeks of cimetidine treatment (1.2 g/day) from 67 patients with active duodenal ulcer. The biopsies were examined for the presence and severity of any inflammation by two independent pathologists in the absence of any clinical information and for the occurrence and density of Campylobacter pyloridis by culture and Warthin-Starry stain. Before treatment, inflammation was present in 71.1, 100, and 25.8%, while the organisms were present in 34.3, 91.0, and 79.1% of the duodenal, antral, and fundal biopsies, respectively. With complete healing of duodenal ulcer, inflammation was present in 48.9, 98.2, and 30.2%, while the organisms were present in 25, 76.7, and 63.3% of the respective mucosae. With ulcer healing, duodenitis became significantly milder (P less than 0.05). With improvement of gastritis and duodenitis, there was no significant change in the occurrence and density of Campylobacter pyloridis. These findings indicate that healing of duodenal ulcer is not influenced by the presence of Campylobacter pyloridis, which is frequently found in the gastroduodenal mucosa of patients with duodenal ulcer, but does not appear to be associated with mucosal inflammation except in the antrum.

Adult↗
PubMed1976

Gastritis duodenitis, and circulating levels of gastrin in duodenal ulcer before and after vagotomy.

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.

Biopsy↗
PubMed1981

Duodenal mucosal architecture in non-specific and ulcer-associated duodenitis.

This study was done to determine the severity and extent of abnormalities of duodenal mucosal architecture in non-specific (non-ulcerative) and ulcer-associated duodenitis. The effect of successful treatment with cimetidine on these changes has also been assessed. A method of microdissection and measurement of villus height, crypt depth, and mitotic figure count per crypt was applied to endoscopic biopsies from the duodenum. Five groups of patients were studied: untreated ulcer-associated duodenitis, untreated non-specific duodenitis, healed ulcer-associated and non-specific duodenitis after cimetidine treatment, and controls. Significant reduction in villus height, increase in crypt length, and increase in mitotic figure count per crypt were all found in both ulcer-associated and severe non-specific duodenitis as compared with controls. These changes were localised to visually inflamed areas and regressed after healing of these lesions with cimetidine. This is the first quantitative comparison of the architectural features between diseased states in the duodenum and control in the same study. Identical morphological changes in the form of crypt hyperplasia and villus atrophy were demonstrated in areas of non-specific and ulcer-associated duodenitis. No evidence could be found from this study that non-specific duodenitis constitutes a different disease from ulcer-associated duodenitis.

Cimetidine↗