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PubMed1986

Induction of duodenal ulcers in rats under water-immersion stress conditions. Influence of stress on gastric acid and duodenal alkaline secretion.

We investigated the influence of stress on gastric acid and duodenal HCO3- secretion in rats, and examined whether duodenal ulcers develop in rats under stress conditions in the absence or presence of acid hypersecretion caused by histamine. Either restraint alone or restraint plus water-immersion stress induced lesions in the stomach but not in the duodenum. However, subcutaneous administration of histamine dihydrochloride (40 mg/kg every 2.5 h for a total of three times) to stressed rats produced macroscopically visible damage in the proximal duodenum as well as in the stomach within 8 h of exposure to stress, and the incidence of duodenal lesions was 100% in the water-immersion group (24.8 +/- 3.8 mm2, n = 8). Histamine alone had no effect on either region. These lesions in the duodenum caused by water immersion plus histamine were prevented by subcutaneously administered cimetidine (30, 100 mg/kg) or 16,16-dimethyl prostaglandin E2 (10, 30 micrograms/kg) in a dose-related manner, but not by atropine (1, 3 mg/kg). Restraint decreased acid secretion by 40%, and additional water immersion restored the decreased acid secretion to normal levels. Basal duodenal HCO3- secretion was decreased to about 70% of normal values (5-6 microEq/15 min) in the restraint group, and after additional water immersion further declined to the values of 1.5-2 microEq/15 min. An increase of HCO3- secretion caused by acid was significantly inhibited by water immersion but not by restraint. Histamine significantly increased acid secretion but did not affect duodenal HCO3- secretion. In the rats treated with both water immersion and histamine, acid secretion was significantly reduced by either cimetidine (100 mg/kg) or 16,16-dimethyl prostaglandin E2 (30 micrograms/kg), whereas duodenal HCO3- secretion was significantly increased by 16,16-dimethyl prostaglandin E2. Atropine had little effect on either acid or HCO3- secretion. These results suggest that exposure of rats to stress decreases duodenal HCO3- secretion and increases the susceptibility of the mucosa to acid emptied from the stomach, thereby inducing duodenal ulcers if acid hypersecretion is concomitantly present.

Animals↗
PubMed1987

pH of the microclimate lining human gastric and duodenal mucosa in vivo. Studies in control subjects and in duodenal ulcer patients.

Measurements of pH in the microclimate on gastric and duodenal mucosa were made during gastrointestinal endoscopy in 21 normal subjects and 9 duodenal ulcer patients. In controls luminal and juxtamucosal mean pH (+/- SEM) of 3.29 +/- 0.3 and 4.48 +/- 0.25 were recorded respectively in distal esophagus, 2.01 +/- 0.17 and 4.84 +/- 0.37 in gastric fundus, 1.82 +/- 0.12 and 5.5 +/- 0.15 in body, 3.52 +/- 0.34 and 5.42 +/- 0.29 in antrum, 6.89 +/- 0.21 and 7.16 +/- 0.13 in duodenal cap, and 6.84 +/- 0.19 and 7.03 +/- 0.19 in proximal duodenal loop. When the lumen of esophagus and duodenum were perfused with acid (pH 2) luminal and mucosal pH values were 2.18 +/- 0.11 and 4.08 +/- 0.41 in esophagus, 2.57 +/- 0.15 and 6.74 +/- 0.13 in duodenal bulb, and 2.44 +/- 0.14 and 6.39 +/- 0.2 in duodenal loop. Juxtamucosal pH in fundus, body, and duodenum remained near neutral when luminal pH was 1.5, but in distal esophagus and antrum it fell sharply at luminal pH values below 3. In duodenal ulcer patients juxtamucosal pH in the cap was significantly lower than that in normals at luminal pH values below 3. These studies support the hypothesis that a "mucus-bicarbonate" barrier inhibits mucosal acidification in humans and that duodenal mucosa in ulcer patients is less able to maintain a neutral zone adjacent to it in the face of luminal acid.

Adult↗
PubMed2002

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS: . Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS: . The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.

Adult↗
PubMed2000

Gastric metaplasia in the duodenal bulb shows increased mucosal interleukin-8 activity in Helicobacter pylori-positive duodenal ulcer patients.

BACKGROUND: Although increased levels of interleukin (IL)-8 are known to be associated with infiltration of neutrophils in the gastric mucosa with Helicobacter pylori infection, no study has investigated the relationship between local IL-8 levels and neutrophil infiltration in the duodenal mucosa of patients with duodenal ulcer (DU). METHODS: Duodenal mucosal biopsy specimens with and without gastric metaplasia (GM) were obtained from patients with DU and controls with an endoscopic methylene blue (MB) staining method. Levels of IL-8 secreted in the organ cultures of biopsy specimens were measured with an enzyme-linked immunosorbent assay. The number of myeloperoxidase-positive neutrophils infiltrating the lamina propria was determined in immunohistochemically stained tissue sections. RESULTS: Histologic assessment showed that there was a strong correlation between the absence of endoscopic MB staining and the extent of GM. The levels of IL-8 in both duodenal and antral mucosal tissues were significantly higher in patients with H. pylori infection than in those without infection. In patients with DU the duodenal mucosal tissues with GM (MB-unstained mucosa) showed significantly higher levels of IL-8 than those without GM (MB-stained mucosa) or the antral mucosa. The number of neutrophils showed similar variations among DU and control patients with a positive correlation with IL-8 activity. The levels of IL-8 and the number of neutrophils decreased after H. pylori eradication in both duodenal and antral mucosal tissues, and these changes were more remarkable in the duodenal mucosal tissues with GM. CONCLUSIONS: Increased IL-8 activity in the duodenal mucosa with GM may be important for ulcerogenesis in H. pylori-positive DU patients.

Adult↗
PubMed1989

Duodenal and antral mucosal prostaglandin E2 synthesis in a study of normal subjects and all stages of duodenal ulcer disease treated by H2 receptor antagonists.

We tested the hypothesis that the production of prostaglandin E2 (PGE2) is impaired in duodenal ulcer disease and affected by treatment and healing. This was investigated by a study of maximal PGE2 synthesis rates in duodenal and antral mucosal biopsies obtained at endoscopy. The patients were divided into three groups. Group (a): endoscopically normal controls (n = 56); group (b): treatment controls (non-DU disease: gastric ulcer or oesophagitis treated by histamine H2 receptor antagonists) (n = 41); and group (c): patients with DU disease (n = 183) further subdivided into group (c1) active ulcer not on treatment (n = 47), (c2) treated active ulcer (n = 35), (c3) healed ulcer on treatment (n = 86), and (c4) healed ulcer not on treatment (n = 15). Group (a) synthesised (mean (SD] 106.6 (39.0) pg PGE2/mg wt of tissue from the duodenal bulb and 129.9 (56.9) from the second part of the duodenum. No difference was found between group (a) and (b) at either site. Group (c1) ulcer rim made 49.8 (22.7) and at all stages ulcer rim and scar made less than the control duodenal bulb (p less than 0.02). Uninvolved duodenal bulb form groups (c1) (63.4 (31.0], (c2) (83.6 (38.5], and (c3) (81.5 (31.1], however, also made significantly less than controls (p less than 0.02) and a similar though non-significant trend was seen in group (c4). Biopsies from the second part of the duodenum did not synthesise significantly less than the control group but a similar trend was noticed at each stage of ulcer treatment. Biopsies of control antrum synthesised 124.5 (32.2) but only 93.7 (44.2) in group (cl) (p < 0.005). All stages of duodenal ulcer healing were associated with a decreased capacity to synthesise the major prostaglandin PGE2 at the ulcer site and the uninvolved duodenal bulb and, in acute untreated duodenal ulcer, the uninvolved antrum. This decreased capacity may be the consequence of the disease process itself and not secondary to the treatment, indicating a basic pathophysiological abnormality which may explain the characteristic tendency of the disease to relapse.

Adult↗
PubMed2006

Gastric duodenal metaplasia in duodenal adenomas.

BACKGROUND: In cases of known aetiology, gastric duodenal metaplasia (GMD) is a reversible lesion. In cases of unknown aetiology, the fate of GMD remains elusive. GMD was recently found in a duodenal adenoma. AIM: To audit the frequency of GMD occurring in a cohort of duodenal adenomas. METHODS: Filed H&E-stained sections from 306 consecutive duodenal adenomas were investigated for the presence of GMD. RESULTS: 68% of the adenomas (n = 208) were from patients with familial adenomatous polyposis (FAP), and the remaining 32% (n = 98) were sporadic. GMD was found in 31.7% (66/208) of the duodenal FAP adenomas and in 59.2% (58/98) of the duodenal sporadic adenomas (p<0.05). The causes for this difference are elusive. CONCLUSIONS: As for other metaplasias of the gastrointestinal tract (intestinal metaplasia of the oesophagus and of the stomach, and metaplastic-hyperplastic polyposis of the colon, known to antedate neoplastic transformation), a subset of GMDs of unknown cause might be present in the duodenal mucosa before adenomatous changes ensue. That subset of GMD might have neoplastic proclivity similar to the metaplastic epithelium in other organs of the gastrointestinal tract. The known carcinogenic effect of high concentrations of bile acids and pancreatic juices bathing the duodenal mucosa carrying an irreversible subset of GDM might set aflame the adenomatous neoplastic transformation in these patients.

Adenoma↗
PubMed1976

Defective bicarbonate secretion in response to duodenal acidification in patients with chronic gastric or duodenal ulceration.

Histamine infusion studies were performed in 54 healthy persons, in 58 patients with duodenal ulcers and in 29 patients with gastric ulcers. The acid load entering the duodenum was estimated by measuring the loss of an intragastric marker, phenol red. The volume of duodenal juice that had refluxed into the stomach and which was aspirated with the gastric juice was estimated by the sodium content of the aspirate. The bicarbonate concentration of the refluxed duodenal juice was calculated from the relationship between neutralisation and total electrolyte concentration, since the reaction of one bicarbonate ion removes two ions from the resultant mixture. The mean bicarbonate concentration of the refluxed duodenal juice in the control group was 116,4 (+/- 9) mEq/1, and the individual bicarbonate concentrations showed the expected dependence on the magnitude of the intraduodenal acid load. The mean bicarbonate concentration in patients with duodenal ulcers was 84,6 (+/- 9) mEq/1, which was significantly lower than in healthy persons. In patients with duodenal ulcers and in those with gastric ulcers, the reflux bicarbonate concentrations were independent of acid load. These results confirm previous reports of an impaired pancreatic bicarbonate secretion in response to duodenal acid load in patients with duodenal ulcers, and indicate a similar response in patients with gastric ulcers.

Bicarbonates↗
PubMed1988

Duodenal exclusion for management of lateral duodenal fistulas.

The first clinical application of pyloric occlusion with gastrojejunostomy (duodenal exclusion) for management of lateral duodenal fistulas was reported by Berg in 1907. More recently Berne et al. applied this procedure to treat patients with complex pancreaticoduodenal trauma and modified it to include antrectomy with Billroth II reconstruction and tube duodenostomy. Over time the indications for duodenal exclusion have gradually been expanded to include management of actual or anticipated duodenal fistulas arising from operative injury or as a complication of inflammatory or neoplastic diseases. Our recent success using duodenal exclusion and/or diverticularization to manage one patient with duodenal trauma and two patients with nontraumatic forms of duodenal injury resulting in lateral duodenal fistulas caused us to reevaluate the efficacy of this procedure and forms the basis for this report.

Aged↗
PubMed2000

Relationship of gastric metaplasia and age, sex, smoking and Helicobacter pylori infection in patients with duodenal ulcer and duodenitis.

Gastric metaplasia is one of the factors in duodenal ulcer appearance. The aim of this study was to investigate the frequency of gastric metaplasia and its connection with age, sex, cigarette smoking and H. pylori infection. In the study 216 patients were included. There were 98 patients with duodenal ulcer, 60 with duodenitis, and 58 healthy control subjects. There was no statistically significant difference in gastric metaplasia frequency according to age and sex. Gastric metaplasia was statistically more significant in patients with duodenal ulcer (p < 0.01). In all the subjects cigarette smoking did not significantly influence gastric metaplasia. In smokers with duodenal ulcer, and those who besides duodenal ulcer and smoking had H. pylori infection gastric metaplasia was more frequent (p < 0.01). However, in patients with duodenal ulcer, there was no statistically significant difference of gastric metaplasia related to H. pylori presence. It may be suggested that H. pylori infection is not of indispensable significance for gastric metaplasia appearance.

Adult↗
PubMed2004

[The duodenal epithelium in duodenal diseases].

The purpose of the study was to define duodenal epithelial function in duodenal diseases and to assess the potentialities of correction of detected dysfunctions. The electrical properties (EPs) of the duodenal epithelium were explored in patients with primary chronic duodenitis, duodenal peptic ulcer (DPU) on an exacerbation and in the late postoperative period after selective proximal vagotomy. Mucosal biopsy specimens were obtained at fibrogastroduodenoscopy with biopsy forceps and placed in a sign-alternating field with the parameters, adequate bioelectric epitheliocytic characteristics: 28 V at a voltage sign change rate of 1 Hz, and a current strength of 200 microA. Bioelectrical cell reactions (nuclear fluctuation amplitude) were recorded by light microscopy using a MOB-1A ocular micrometer at minutes 10, 30, and 60 of the onset of electrical field action. A significant reduction was found in the amplitude of duodenal epithelial nuclear fluctuations in the examinees, which was most pronounced in DPU on an exacerbation. Duodenal epithelial EPs were shown to undergo regular changes during therapy and may serve as an additional test in evaluating the efficiency of therapy.

Chronic Disease↗
PubMed1984

Progression of antral and body gastritis in patients with active and healed duodenal ulcer and duodenitis.

The dynamics of the antral and body mucosa has been studied in biopsy specimens obtained during endoscopy of patients with duodenal ulcer (103 cases), patients with duodenal ulcer scars (108 cases), and patients with duodenitis (44 cases). A representative Finnish population sample consisting of 434 subjects was used as reference material. The antral mucosa of all patient series showed an increase in the severity and prevalence of gastritis similar to that of the general population, whereas virtually no progression of gastritis with age was seen in the body mucosa, which remained normal or at the stage of superficial gastritis up to geriatric age. In contrast, in the present controls and in all earlier population samples studied by us so far, there was a significant and steady increase in the severity and prevalence of body gastritis with age. It is concluded that the age behavior of the antral and body mucosa was in duodenal ulcer scars and duodenitis similar to that of patients with active duodenal ulcer. The persistence of normal conditions in the acid-secreting area may serve as one explanation of the strong tendency of the disease to recur. In addition, it is tentatively concluded that in duodenal ulcer disease there are factors that have a 'protecting' influence on the body glands and which are abolished by antrectomy, according to our earlier studies.

Duodenal Ulcer↗
PubMed1991

Decrease of duodenal calcitonin gene-related peptide- and substance P-like immunoreactivity in rat duodenal ulcers.

We have investigated the endogenous levels of duodenal calcitonin gene-related peptide- (CGRP) and Substance P- (SP) like immunoreactivity (li) following the induction of duodenal ulcers in rats. Using three duodenal ulcerogens, namely cysteamine, dulcerozine or mepirizole given in a single oral dose, a decrease of duodenal CGRP-li and SP-li was observed. Time-relationship studies of this phenomenon show that CGRP-li and SP-li were decreased concomitantly to the formation of gastroduodenal ulcers after the administration of cysteamine (900 mg/kg p.o.). Pretreatment with the selective sensory neurotoxin capsaicin induced CGRP-li decrease in the duodenum, which was not further decreased by an ulcerogenic dose of cysteamine, indicating that cysteamine induced a release of CGRP-li of capsaicin-sensitive origin. Otherwise duodenal SP-li was not sensitive to capsaicin pretreatment and its duodenal content decreased by cysteamine originates from an intrinsic source. Our observations indicate that CGRP and SP may play an important local role in duodenal ulcerogenesis.

Animals↗
PubMed1977

Effects of parenteral secretin--cholecystokinin and of duodenal acid perfusion on gastric secretion in duodenal ulcer patients.

The effect of parenteral secretin-cholecystokinin and duodenal acid perfusion on broth-stimulated gastric acid secretion was studied in 11 duodenal ulcer patients. Statistically significant inhibition occurred in both experimental conditions. The effect of secretin-cholecystokinin was more marked than the effect of duodenal acid perfusion. A poorly responsive subgroup of patients appeared to be responsible for the diminished inhibitory effect of duodenal acid perfusion. In this poorly responsive group there was a diminished duodenal volume response as well as diminished duodenal acid clearing. We conclude that there may exist a diminished release of gastrointestinal hormones such as secretin and cholecystokinin in certain duodenal ulcer patients.

Adult↗
PubMed1983

Duodenal ulcerogens cysteamine and propionitrile decrease duodenal neutralization of acid in the rat.

Neutralization of acid was evaluated in rat proximal duodenal segments isolated from biliary and pancreatic secretions. Duodenal ulcerogenic doses of cysteamine produced a significant decrease in acid disposal 0.5-2 hr after treatment. Oral or subcutaneous administration of the duodenal ulcerogen was effective. The potent ulcerogen cysteamine produced a more pronounced decrease than propionitrile (a weak duodenal ulcerogen). The failure of ethanolamine, a nonulcerogenic structural analog of cysteamine to significantly alter acid disposal suggests that the effect is not due to the toxic properties of the duodenal ulcerogen. The results reinforce the concept that the duodenum is able to dispose of significant quantities of acid. The decrease in acid-handling may contribute to duodenal susceptibility to acid after treatment with ulcerogens and possibly reflects pathophysiologic changes early in duodenal ulceration.

Animals↗
PubMed1992

Radiological assessment of duodenal calibre in congenital duodenal obstruction.

A review of barium meal studies in 32 cases of congenital intrinsic duodenal obstruction (CDO) from the Adelaide Children's Hospital was performed to assess and measure pre and post operative duodenal dilatation. Comparisons were made with a group of 153 normal barium studies from the same Hospital with a view to quantifying normal and abnormal proximal duodenal calibre. Duodenal size was expressed as a ratio D1/L1, (diameter of 1st part of duodenum/height of first lumbar vertebra). In this study a normal range of duodenal diameter was found to be 0.90 to 1.62 (+/- 2 SD from mean), with a mean of 1.26. The CDO patients recorded a range of postoperative ratios on first follow-up barium studies of between 1.2 and 4.5 with a mean of 2.28. Where serial studies had been performed, duodenal diameter was found to show some decrease in size postoperatively. In patients who underwent surgery for membrane obstruction there was a trend towards normalisation of duodenal diameter over time, compared with the atresia group. However, this difference did not reach statistical significance.

Barium Sulfate↗
PubMed1989

Effects of sham feeding and a meal on plasma gastrin and duodenal pH in normal and duodenal ulcer patients.

The roles of plasma gastrin and duodenal acidity in duodenal ulcer disease remain unclear. In this pathophysiologic study, plasma gastrin and dual gastro-duodenal pH were measured before, during, and after cephalic stimulation (modified sham feeding) and the ingestion of a meal in 16 duodenal ulcer (DU) patients and twelve healthy subjects. Gastrin levels were significantly higher in DU patients both in the fasting state (42.5 ng/l vs. 22.5 ng/l, p less than 0.001) and after the meal (130 vs. 60, p less than 0.02). Two separate patient subsets were identified: a "hypergastrinemic" (HRG) group exhibiting exaggerated gastrin responses and a "Normogastrinemic" (NOG) group comprised of patients with gastrin levels similar to those of controls. Only the HRG group exhibited a significant gastrin response to sham feeding. Both patient groups exhibited a delayed onset of duodenal acidity and delayed peak acid response after feeding indicative of delayed gastric emptying of the acid load. The HRG group exhibited a longer duodenal acid exposure and a prolonged return to premeal pH levels, suggesting a defective switch-off mechanism of acid secretion after duodenal acidification.

Adult↗
PubMed1996

Gastric metaplasia of regenerating duodenal mucosa and deformity of duodenal bulb: a correlative study.

The correlation between the presence and degree of gastric metaplasia of regenerating duodenal mucosa and the deformity of duodenal bulb was studied. Based on the endoscopically morphological patterns of bulb, the duodenal ulcers were divided into three types: type I, with a normal-shaped bulb; type II, with mildly deformed bulb; and type III, with a markedly deformed bulb. A total of 159 patients with active duodenal ulcers were scheduled to be treated with H2-receptor antagonists. Of these patients, 124 proved to have a healed duodenal ulcer 4 weeks after initial treatment upon follow-up endoscopic examinations. Two biopsies were taken from the centre of the ulcer scar when the ulcer was found to be healed for light microscopic study. Histologically, the degree of gastric metaplasia was divided into three grades: grades 0, 1 and 2. The results show that a healed duodenal ulcer with a normal-shaped bulb is not frequently accompanied by gastric metaplasia. However, a healed ulcer with a markedly deformed bulb has a high incidence and degree of gastric metaplasia, which may be easily colonized by Helicobacter pylori and thus develop an environment of easy recurrence. Therefore, a cycle of healing and recurrence may exist in patients with a duodenal ulcer and a markedly deformed bulb. Eradication of H. pylori may be the best way to break this cycle.

Adult↗
PubMed2003

Decreased epithelial cytokine responses in the duodenal mucosa of Helicobacter pylori-infected duodenal ulcer patients.

Helicobacter pylori colonizes the human stomach and areas of gastric metaplasia in the duodenum, but only a minority of those that are infected develop symptoms, e.g., peptic ulcers. Although most ulcers occur in the duodenum, almost all studies of mucosal immune responses against the infection have been limited to responses in the stomach. In the present study we evaluated whether there are differences in the levels of proinflammatory cytokines as well as immunoregulatory cytokines in the duodenal mucosa of duodenal ulcer (DU) patients and asymptomatic (AS) carriers which may be related to the development of duodenal ulcers. Duodenal biopsy specimens collected from normal mucosa as well as metaplastic mucosa of DU patients, AS carriers, and uninfected controls were analyzed for a number of cytokines by immunohistochemistry. Interestingly, the level of epithelial staining for several cytokines, e.g., interleukin-8 (IL-8), transforming growth factor beta (TGF-beta), and gamma interferon (IFN-gamma), was found to be significantly lower in DU patients than in AS carriers and uninfected individuals. No differences were observed when cytokine staining in normal and metaplastic biopsy specimens was compared. However, larger numbers of IL-8-, IL-6-, TGF-beta-, and IFN-gamma-positive mononuclear cells were observed in the duodenal lamina propria of both DU patients and AS carriers than in that of the uninfected controls. Our finding that a number of cytokines that may be important for the mucosal host defense against H. pylori are strongly decreased in the duodenal epithelium of ulcer patients suggests that a down-regulated immune response plays a role in the development of duodenal ulcers.

Adult↗