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At least 19 recordsLinked to original sources
PubMed1990

Cell renewal in non-specific duodenitis, ulcer-related duodenitis and duodenal ulcer. Experiments in Mastomys (Praomys natalensis).

Cell renewal in the duodenal mucosa of Mastomys was studied by autoradiography 1 and 24 h after intraperitoneal injection of tritiated thymidine. Non-specific duodenitis and duodenal ulceration were produced with a continuous infusion of histamine. Mucosal renewal in the duodenum of 30 control Mastomys was compared with 30 which received histamine dihydrochloride for 5 days. No abnormality developed in the controls, but 11 of the experimental group developed non-specific duodenitis and 12 duodenal ulcers. The size of the proliferative zone was increased in the Mastomys sacrificed 1 h after injection of tritiated thymidine which received histamine, compared with controls (p = 0.004). The number of labelled nuclei (p = 0.0003) and the size of the columns of labelled nuclei (p = 0.001) were increased in the Mastomys receiving histamine and sacrificed 24 h after injection of tritiated thymidine, compared with controls. The number of labelled nuclei (p = 0.004) and the size of the columns of labelled nuclei (p = 0.01) were increased in the Mastomys with ulcers compared with the other Mastomys which had received histamine. Cimetidine prevented duodenitis and ulceration, normalising the pattern of cell renewal. There was correlation between the severity of non-specific and ulcer-related duodenitis as judged by Lance's system and the number of labelled nuclei (Spearman rank correlation coefficient 0.771, p less than 0.002). Cell renewal increased as duodenitis became more severe and duodenal ulcers were found in duodenal mucosa where cell renewal was fastest.

Animals↗
PubMed1989

Abnormalities in the duodenal transit and motility in duodenal ulcer patients: studies with a new isotopic technique.

Abnormalities of duodenal motility have been described in patients with duodenal ulcer and in experimental ulcers in rats and it has been postulated that they could be pathogenic in peptic ulcer disease. We have investigated with an isotopic technique whether duodenal bulb clearance or duodenal transit are abnormal in duodenal ulcer. Six patients with inactive and six with active duodenal ulcers, all men, and six healthy male controls were studied. Motility of the duodenum was simultaneously monitored. A bolus of 99mTcDTPA was injected into the duodenum while water or acid were perfused on different occasions. Duodenal bulb clearance and transit to the ligament of Treitz were calculated. Duodenal transit in duodenal ulcer patients 108.8 (23) sec was faster than in controls, 194.9 (5.1) sec (p less than 0.05) during the quiescent period of the motility cycle. The frequency of duodenal bulb contractions during acid perfusion was higher in duodenal ulcer patients 1.7 (0.4) cont/min, than in controls 0.8 (0.1) cont/min (p less than 0.05). No other significant differences were observed between ulcer patients and controls. These data suggest that patients with duodenal ulcers do not have major abnormalities of duodenal bulb clearance, nor of duodenal transit and that duodenal motility does not play a primary role in the pathogenesis of the ulcer.

Adolescent↗
PubMed1989

Effect of duodenal ulcerogens cysteamine, mepirizole, and MPTP on duodenal myoelectric activity in rats.

Increased gastric acid secretion, enhanced acid delivery to the duodenum, and reduced alkaline secretion in the proximal duodenum are relatively well-established pathophysiologic abnormalities in duodenal ulcer. Impaired duodenal motility, however, may also contribute to duodenal ulceration by altering the distribution of acid and alkaline secretions along the upper digestive tract. We tested the hypothesis that the duodenal ulcerogens cysteamine, MPTP, and mepirizole modify duodenal motility in the rat and that motility changes might be a common and early alteration in experimental duodenal ulceration. All three duodenal ulcerogens rapidly produced extensive changes in duodenal myoelectric activity and reduced the frequency of myoelectric slow waves. Cysteamine induced marked hypermotility for at least 6 hr; MPTP rapidly decreased motility and fragmented the myoelectric migrating pattern. Mepirizole induced biphasic changes: an early hypermotility phase of about 30 min was followed by profound hypomotility. These results indicate that marked alterations of duodenal motility are common during experimental duodenal ulceration. In light of the differential effect of the ulcerogens on duodenal motility, it remains to be determined how these changes influence acid neutralization in the proximal duodenum. Nevertheless, our results suggest that all three duodenal ulcerogens, which are different in structure, alter duodenal motility.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
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↗
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↗
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↗
PubMed1992

Helicobacter pylori, gastritis and duodenitis in the healing process of duodenal ulcer.

The occurrence of antral gastritis, duodenitis, gastric metaplasia and Helicobacter pylori (H. pylori) were compared between 63 endoscopically proven duodenal ulcer (DU) patients and 34 non-ulcer dyspepsia (NUD) patients with no ulcer history and no ulcer present as documented by endoscopy. The DU group showed a significantly higher rate of active antral gastritis (89% vs 41% p less than 0.05), a higher antral H. pylori carrying rate (76% vs 27% p less than 0.01), a higher rate of active chronic duodenitis (75% vs 32% p less than 0.05), and a higher rate of gastric metaplasia in the duodenal bulb (68% vs 27% p less than 0.05) than the NUD group. The H. pylori carrying rate in the bulb was 16% in the DU group and 0% in the NUD group. The difference is evident, although it is statistically insignificant. All 10 cases carrying H. pylori in the duodenum in the DU group had active chronic duodenitis with gastric metaplasia. Further evaluation of the variables (rate of active antral gastritis and duodenitis and the carrying rate of H. pylori in the antrum and bulb) showed no difference between different ulcer stages (active, healing, or scarred). The above findings strongly suggest a close relation between H. pylori and duodenal ulcer. However, the low occurrence rate of the bacteria in the bulb can only indicate a partial etiologic role of the bacteria in DU. No improvement in antral gastritis, duodenitis and H. pylori occurrence, despite the healing of an ulcer, is in agreement with the naturally high recurrence rate of duodenal ulcers.

Duodenal Ulcer↗
PubMed1991

Serotonin-induced decrease of duodenal mucosal blood flow plus acid load produces duodenal mucosal lesion in rats.

To clarify the role of duodenal mucosal blood flow in the genesis of duodenal mucosal lesions, a single dose of serotonin, 20 mg/kg, was administered subcutaneously to rats. Serotonin significantly decreased both the duodenal mucosal blood flow and the output of gastric acid and pepsin. However, mild duodenal erosions were observed in only 2 of the 9 rats receiving that agent. The repeated intragastric administration of 1 ml of 0.1 N HCl hourly for 6 h failed to induce duodenal mucosal lesions. On the other hand, the administration of both serotonin and repeated doses of HCl produced marked duodenal mucosal lesions in all rats. It is concluded, therefore, that one of the factors responsible for the genesis of duodenal mucosal lesions is a decrease of duodenal mucosal blood flow combined with an acid load against the duodenal mucosa.

Animals↗
PubMed1989

Chronic nonspecific duodenitis. A multiple biopsy study of the duodenal bulb in health and disease.

A clinical, endoscopic and histopathologic study on chronic nonspecific duodenitis was performed in 174 subjects, 124 patients (control patients, patients with gastric or duodenal ulcer and nonulcer dyspepsia) and 50 healthy volunteers without clinical history of gastro-intestinal disease. Chronic nonspecific duodenitis was found in 6 healthy volunteers (12%), 5 control patients (7%), one gastric ulcer patient (7%), all duodenal ulcer patients and in 15 patients with nonulcer dyspepsia (83%). Chronic non-specific duodenitis is a focal process affecting the duodenal bulb. It can be missed when only one biopsy is studied. Superficial gastric metaplasia was directly correlated to gastric acid secretion and was found in 32 healthy volunteers (64%), 23 control patients (34%), six gastric ulcer patients (43%), 20 duodenal ulcer patients (20%) and in 17 patients with nonulcer dyspepsia (94%). This study suggests that chronic nonspecific duodenitis is a stage of duodenal ulcer disease.

Adult↗
PubMed1990

[The morphofunctional characteristics of the duodenal mucosa in patients with a duodenal ulcer at different phases of the disease].

Endoscopic, morphological, histochemical and biophysical properties of the duodenal mucosa as well as secretory activity of the stomach and pancreas were studied and compared in 398 patients with duodenal ulcer in different phases (active ulcer, healing ulcer, red and white scars). Sixteen patients were observed over time. Analogous studies were conducted in 88 patients with chronic diseases of the biliary and duodenopancreatic zone (with non-ulcerous duodenitis) and in 32 normal persons. The duodenal mucosa was established to undergo consistent morphofunctional reorganization related to the disease phase. Active duodenal ulcer was marked by duodenitis with thickening of the mucosa, shortening of the villi, reduction of the depth of the cryptae, gastric metaplasia, impairment of histochemical properties of epitheliocytes and decrease of the transmural potential difference, overproduction of acid and pepsin in the basal period, high sensitivity of the chief cells to stimulation, and insufficient output of bicarbonates by the pancreas. Gastric metaplasia of the duodenal epithelium, appreciable histochemical and morphometric alterations may be regarded as relatively specific traits of peptic duodenitis. As ulcer heals, a well-defined tendency may be noted towards normalization of all the parameters mentioned. However, they only correspond to normal in 25% of patients in the phase of a white scar. The conclusion is made that there is also a necessity of correcting morphofunctional abnormalities after duodenal ulcer healing.

Adolescent↗
PubMed1976

A comparison of basal and stimulated gastric acid and duodenal bicarbonate in patients with and without duodenal ulcer disease.

Basal gastric secretion and the maximum response to pentagastrin and basal secretion into the duodenumand its near-maximum response to secretin were measured in 20 control subjects and ten patients with duodenal ulcer disease. In control subjects the volumes of stimulated gastric and duodenal secretions were significantly correlated. In patients with duodenal ulcer, there were no significant correlations between basal gastric and duodenal secretion but after stimulation both volumes and outputs (but not concnetrations) of gastric and duodenal secretions were significantly correlated. The bicarbonate secretory capacity in patients with duodenal ulcer was not only normal but was also comparable to the gastric acid secretory capacity. The basal bicarbonate content of the duodenal aspirate, however, in patients with duodenal ulcer was only half that in control subjects, perhaps another example of inadequate entry of bicarbonate into the duodenum in patients with duodenal ulcer in spite of the normal bicarbonate secretory capacity.

Adolescent↗
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↗
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↗