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At least 19 recordsLinked to original sources
PubMed1983

Duodenal epithelial thymidine uptake in patients with duodenal ulcer or endoscopic duodenitis.

To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [3H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [3H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [3H]thymidine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [3H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation.

Adolescent↗
PubMed1985

Duodenal bulb plasma cells in duodenitis and duodenal ulceration.

Using an immunoperoxidase technique IgA, IgM, IgE and IgG plasma cells were studied in endoscopic duodenal bulb biopsies taken from 14 controls, 25 patients with grade 1 duodenitis (Whitehead classification), 12 patients with grade 2 duodenitis and three with grade 3 duodenitis. The control counts were compared with those in the jejunum and rectum. In addition cell counts were compared in 16 pairs of patients, with and without duodenal ulcer, exactly matched for grade of duodenitis. The control counts were not significantly different from counts in jejunum or rectum except for IgG which were higher in the jejunum (p = 0.03). IgA plasma cell counts were significantly increased in both grade 1 and grade 2 duodenitis compared with controls (p less than 0.05 and p less than 0.01). There was no significant difference for the other plasma cells. All plasma cell counts were decreased in the small group of grade 3 duodenitis compared with the other groups. There was no significant difference between counts in duodenitis whether or not there was associated duodenal ulceration. The isolated IgA plasma cell response of the duodenal bulb mucosa in duodenitis is very different from that of the jejunal mucosa in coeliac disease, and the rectal mucosa in inflammatory bowel disease and bacterial colitis and probably represents the basic response to any mucosal damage.

Cell Count↗
PubMed1997

Effects of smoking and Helicobacter pylori on prostaglandin concentrations in gastric and duodenal mucosa of patients with duodenal ulcer and duodenitis.

The aim of this study was to determine the level of endogenous prostaglandin E2 (PGE2), prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) in the gastric and duodenal mucosa of patients with duodenal ulcer and duodenitis. Besides, the investigation aimed at determining the effect of smoking and infection by Helicobater pylori on prostaglandin synthesis. The investigation comprised 62 patients with duodenal ulcer, 46 patients with duodenitis and 44 controls. The results of our investigation indicate that the decreased prostaglandin synthesis in gastric and duodenal mucosa determined in patients with duodenal ulcer may have a considerable role in development of duodenal ulcer. Furthermore, the harmful effects of smoking on the gastric and duodenal mucosa may be mediated by the decreased prostaglandin synthesis in the gastric and duodenal mucosa. However, Helicobacter pylori seems to affect the development of duodenal ulcer through other mechanisms.

Analysis of Variance↗
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↗
PubMed2001

Relationship of duodenal ulcer recurrence to gastric metaplasia of the duodenal mucosa and duodenal bulb deformity.

BACKGROUND AND PURPOSE: This study investigated changes in the severity of gastric metaplasia (GM) of the duodenal mucosa before and after ulcer healing and Helicobacter pylori eradication. It also investigated whether deformity of the duodenal bulb affects the severity of GM and the likelihood of ulcer recurrence. METHODS: Eleven patients were consecutively enrolled in this study. They all had duodenal ulcer(s) and H. pylori infection, for which they had received anti-H. pylori triple therapy during the active ulcer stage, and had all undergone serial endoscopic examinations during both the active ulcer and scarring ulcer stages, and at 1 year after ulcer healing. Duodenal biopsies were obtained at each endoscopy to identify the severity of GM. Duodenal ulcers were divided into three types by bulbar shape and GM was classified into four grades of severity. RESULTS: All 11 patients had increased GM severity just after ulcer healing. The 1-year follow-up study revealed that the GM was unchanged in six of eight patients with grade 3 GM severity at the scarring stage, while in the other two it regressed to grade 1 or 2; these two patients suffered ulcer recurrence. A markedly deformed bulb (type III) was found in three patients, of whom two had ulcer recurrence. CONCLUSION: Two characteristic conditions were found in patients with duodenal ulcer recurrence after H. pylori eradication: a markedly deformed bulb with grade 3 GM at the scarring stage, and a change in GM from high to low grade at or around the previous ulcer site after ulcer healing.

Adult↗
PubMed1996

Duodenal mucosal histology and histochemistry in active, treated and healed duodenal ulcer: correlation with duodenal prostaglandin E2 production.

We investigated whether impaired duodenal mucosal prostaglandin E2 (PGE2) production previously observed in duodenal ulcer (DU) was a primary pathophysiological abnormality or secondary to mucosal architectural changes that accompany ulceration. One hundred patients were studied: at endoscopy, paired duodenal biopsies were taken in patients with normal endoscopies and from the ulcer edge or scar and background mucosa in active or healed DU. One of the pair of biopsies was used to estimate PGE2 synthesis ability, the other was processed for histology and histochemistry. The following features graded: goblet cell numbers and staining with Periodic acid-Schiff reagent (PAS), epithelial staining with PAS, villous atrophy, columnar cell height, inflammatory cell infiltrate and micro-erosions and gastric metaplasia taken as a whole. Patients were found to have normal endoscopy (n = 31), active untreated DU (n = 20) active DU on treatment with either cimetidine or ranitidine (n = 13), healed DU on maintenance treatment (n = 27) and healed DU off treatment (n = 9). Active duodenal ulceration was found to be associated with decreased numbers of goblet cells, loss and blunting of villi, increased columnar cell height, increased epithelial cell PAS staining and with gastric metaplasia. After healing, only villous blunting remained. These changes were present, but less marked, at sites removed from the ulcer and were not apparent in the patient groups with healed ulcers. A strong correlation between overall gastric metaplasia and epithelial cell PAS staining and the reduced ability to synthesize PGE2 (P < 0.001) was only apparent when biopsies from all patients were grouped together, but not within individual patient subgroups. There was no consistent correlation between PGE2 generation and individual parameters of pathological change in duodenum. We conclude that, although inflammatory and mucosal changes may contribute, the evidence suggests that the impaired PGE2 generation in DU disease is, to a large extent, independent of histological and histochemical features.

Analysis of Variance↗
PubMed1997

Duodenal gastric metaplasia, gastric anatomic-functional correlations (parietal cell mass and hydrochloric acid secretion) and Helicobacter pylori. Any differences between chronic autonomous non-specific duodenitis ("non active") and duodenal ulcer?

BACKGROUND AND METHODS: Aim of the present experience was to carry out a study on a dyspeptic population in order to verify the role of Helicobacter Pylori (HP), duodenal gastric metaplasia (GM), hydrochloric acid secretion in the genesis of chronic autonomous non-specific duodenitis (ANSD). A comparison with duodenal ulcer (DU) was effected. RESULTS: Histology showed the presence of ANSD in 24.6% of dyspeptic population. GM was present in 15.1% of ANSD, in 12.8% of dyspepsia without ANSD and in 78.1% of DU. HP in duodenum was present in 12.1% of ANSD, in 10.8% of cases of dyspepsia and in 75% of DU. Concerning parietal cell mass and acid secretion in ANSD and in dyspepsia was found a prevalence of normoparietalism with normochlorhydria, while in DU was found a prevalence of hyperparietalism with hyperchlorhydria. This study shows that the role of HP has not a well defined etiologic weight in ANSD. CONCLUSIONS: The observations of the present experience, which differentiate ANSD and DU, lead to exclude a pathogenetic relation between ANSD and DU.

Adult↗
PubMed1996

[Relationship between duodenal diverticuli, gallstones and duodenal and pancreaticobiliary disorders].

OBJECTIVE: To determine the relationship between duodenal diverticula and the prevalence of bile duct stones, and between duodenal diverticula and pancreatic pathology and/or duodenal inflammation. DESIGN: Retrospective descriptive study. SETTING: Department of Internal medicine, Division of Gastroenterology/Hepatology, University Hospital Maastricht. METHODS: The medical records were reviewed of 273 consecutive patients in whom an endoscopic retrograde cholangiopancreatography (ERCP) had been performed for the first time during the period 1991-1992. Clinical data such as previous history of cholecystectomy and ERCP findings such as presence of a duodenal diverticulum, its location (juxtapapillary or circumpapilary), and possible concomitant pancreaticobiliary disorders and/or duodenal inflammation were evaluated. RESULTS: Duodenal diverticula were present in 49 out of 273 patients (18%(: 30 patients with a juxtapapillary, 18 patients with a circumpapillary duodenal diverticulum and one patient with both types. A history of cholecystectomy was not reported more frequently in patients with a diverticulum than in those without. At the time of ERCP investigation, gallbladder stones were not diagnosed more frequently in diverticulum patients. A significantly higher prevalence of common bile duct stones was found in diverticulum patients than in those without (53% versus 22%, p = 0.001). Pancreatic pathology was not related to the presence of duodenal diverticula (p = 0.441). Furthermore. duodenitis and duodenal ulcers were significantly more prevalent in diverticulum patients than in those without (18% versus 7% for duodenitis, p = -0.049; 14% versus 2% for duodenal ulcers, p = 0.001). CONCLUSIONS: Duodenal diverticula were not only associated with common bile duct stones, but were also related to duodenitis and duodenal ulcers. Pancreatic pathology appeared not to be related to duodenal diverticula.

Adult↗
PubMed1984

Duodenal pH in health and duodenal ulcer disease: effect of a meal, Coca-Cola, smoking, and cimetidine.

Intraluminal duodenal pH was recorded using a combined miniature electrode and logged digitally every 10 or 20 seconds for five hours (basal/meal/drink) in eight control subjects and 11 patients with duodenal ulcer (five on and off treatment with cimetidine). Over the whole test there were no significant differences in duodenal mean pH or log mean hydrogen ion activity (LMHa) between control subjects and patients with duodenal ulcer, but there were significantly longer periods of duodenal acidification (pH less than 4) and paradoxically more periods of duodenal alkalinisation (pH greater than 6) in the duodenal ulcer group compared with controls. After a meal duodenal mean pH and LMHa fell significantly in both controls and patients with duodenal ulcer, with more periods of duodenal acidification and alkalinisation in the duodenal ulcer group. An exogenous acid load (Coca-Cola) significantly increased the periods of duodenal acidification, and reduced alkalinisation, in both groups. Cimetidine significantly increased mean pH and LMHa and abolished the brief spikes of acidification in four of five patients with duodenal ulcer. Peak acid output (but not basal acid output) was significantly correlated with duodenal mean pH and LMHa but not with the periods of duodenal acidification. Smoking did not affect duodenal pH in either group.

Adult↗
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↗
PubMed2002

Effect of Helicobacter pylori eradication on duodenal ulcer scar in patients with no clinical history of duodenal ulcer.

BACKGROUND: Helicobacter pylori eradication has become the standard treatment for duodenal ulcer. However, there is no relevant evidence for antibacterial treatment of the white scar stage of duodenal ulcer (duodenal ulcer scar) in patients with no past history of duodenal ulcer. AIM: To investigate whether H. pylori eradication could decrease duodenal ulcer recurrence in patients with duodenal ulcer scar and no past history of duodenal ulcer. PATIENTS AND METHODS: We prospectively enrolled 66 patients with duodenal ulcer scar: 53 were H. pylori-positive and 13 were H. pylori-negative. H. pylori-positive patients were randomly assigned into two groups (two-to-one allocation): 36 patients were assigned to the treatment group and 17 to the follow-up group. Thirteen H. pylori-negative patients were followed up according to the study protocol. Follow-up endoscopy was performed to evaluate ulcer scar changes and H. pylori status 6 weeks after anti-H. pylori treatment and then every 6 months for up to 30 months. RESULTS: Active duodenal ulcer recurrence was identified in seven of 23 H. pylori-positive/non-cured patients (30%). There was no duodenal ulcer recurrence in 43 H. pylori-negative/cured patients (0%), which was significantly different in terms of duodenal ulcer recurrence (P=0.001). CONCLUSIONS: H. pylori eradication is effective at preventing active duodenal ulcer recurrence in patients with duodenal ulcer scar and no past history of duodenal ulcer.

Amoxicillin↗
PubMed1996

Duodenal bicarbonate secretion: eradication of Helicobacter pylori and duodenal structure and function in humans.

BACKGROUND & AIMS: Eradication of Helicobacter pylori expedites duodenal ulcer healing and prevents recurrences. Most patients with duodenal ulcers have impaired proximal duodenal mucosal bicarbonate secretion (DMBS). In patients with inactive, healed duodenal ulcers and normal subjects, the effect of H. pylori infection on DMBS and proximal duodenal secretory function and structure were examined. METHODS: DMBS was quantitated before and after eradication of H. pylori. Mucosal structure (duodenal bulb histopathology) and function (DMBS at rest and stimulated, effect of active vs. healed ulcer and of age) were determined in patients with duodenal ulcers and normal subjects. RESULTS: In patients with duodenal ulcers, H. pylori eradication normalized proximal DMBS. Histological examination of duodenal biopsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent relationship between inflammation and DMBS. Significantly impaired DMBS occurred in response to all agonists tested (luminal acid, prostaglandin E2, and cephalic-vagal stimulation) in patients with duodenal ulcers, suggesting a generalized secretory defect. Neither the presence of active (vs.inactive) ulcer nor age significantly affected bicarbonate secretion. CONCLUSIONS: In patients with duodenal ulcers, eradication of H. pylori normalized proximal DMBS and may thereby reduce ulcer recurrences. Altered DMBS in patients with duodenal ulcers was unrelated to histopathologic abnormalities. Impaired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or physiological regulatory transport defect possibly related to H. pylori.

Adult↗
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↗
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↗