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At least 127 records · Page 7Linked to original sources
PubMed1994

Seven-year follow-up of patients with duodenal ulcer disease.

BACKGROUND: The activity of duodenal ulcer disease varies not only between patients but also from time to time within patients, and earlier studies have concluded that the disease 'burns out' in many cases. It was the aim of this study to examine duodenal ulcer disease activity over a long period, to determine whether the degree of activity is stable within the individual patient. METHODS: A cohort of 145 patients with a first-time duodenal ulcer diagnosed in our department between 1980 and 1985 were followed up for 7 years. The patients' self-reported use of acid-inhibitory drugs was taken as a measure of disease activity. RESULTS: Twenty-eight per cent of the patients had no or minimal ulcer symptoms during the 7 years after healing of the index ulcer, whereas 13% had maximal activity with frequent or continuous use of acid-inhibitory drugs every year or ulcer surgery. A total of 11 patients were operated on because of severe ulcer symptoms or complications to the ulcer disease. The disease activity during the first 2 years after diagnosis did not change much during the following 5 years in most of the patients. CONCLUSIONS: The course of duodenal ulcer disease during the first 2 years after diagnosis was a predictor of the long-term prognosis with a predictive value of approximately 70%, which may be considered satisfactory for decision-making in some clinical situations.

Duodenal Ulcer↗
PubMed1999

Strictureplasty is an effective option in the operative management of duodenal Crohn's disease.

INTRODUCTION: Duodenal Crohn's disease requiring surgery has traditionally been managed with a bypass procedure. We compared our experience with duodenal strictureplasty with this traditional approach. METHODS: Records of patients operated on for duodenal Crohn's disease since 1980 were retrospectively reviewed. Patients having strictureplasty or bypass were compared with regard to demographics, indications, complications, and outcome. RESULTS: Since 1980, 34 patients were operated on for duodenal Crohn's disease. Mean age was 38.9 (range, 16-68) years, and 20 of 34 patients were females, with no significant differences between operative groups. Obstruction was the presenting symptom in 33 of 34 patients, and all had strictures. The basis for diagnosis of duodenal Crohn's disease was macroscopic appearance and the presence of Crohn's elsewhere in 29 of 34 patients, with only 5 of 34 having either duodenal or contiguous antral granulomas. Thirty-seven strictures were present in the 34 patients; 24 were in the proximal duodenum (8 strictureplasty, 16 bypass), 9 were in the midduodenum (4 strictureplasty, 5 bypass), and 4 were in the distal duodenum (3 strictureplasty, 1 bypass). Bypass was performed in 21 patients, with two operative complications, and at a mean follow-up of 8 years, 1 of 21 patients required reoperation for recurrent disease. Strictureplasty was performed in 13 patients, with two operative complication, and at a mean follow-up of 3.6 years, 1 patient required reoperation for recurrence also. Vagotomy was performed in 16 of 21 bypasses and 7 of 13 strictureplasties. CONCLUSIONS: Although follow-up is shorter, strictureplasty is a safe and effective operation for duodenal Crohn's disease and should be considered when feasible.

Adolescent↗
PubMed1990

[Duodenal ulcer disease. A controlled study of aggressiveness and other personality factors].

We study the aggressivity level and its direction in the context of personality, in 36 patients with DUD (23 males and 13 females). We employed 30 patients with chronic disease (15 men with COPD and 15 female with arthrosis) as control groups, in addition to the normal population. The purpose of this investigation is to determinate if suffering or chronicity could determinate psychopathological findings similar to those described in the literature about patients with DUD. The results point out that we can not consider a specific ulcerous personality, but a psychophysiological reaction or psychopathological alterations resulting from a somatic disease, on the other hand the autoaggressivity factor pulsion-inhibition, is the most reliable variable when compared with control groups (p less than 0.05-0.01).

Adult↗
PubMed1998

Histamine and tissue fibrinolytic activity in duodenal ulcer disease.

Patients with duodenal ulcer have lower gastroduodenal mucosal histamine and a reduced tissue fibrinolysis at the ulcer edge. In the duodenal mucosa fibrinolysis is regulated by the tissue-type and urokinase-type plasminogen activators; and inhibitors type 1 and type 2. Trends across ordered groups leading from mucosa of nonulcer control subjects, "normal" mucosa of ulcer patients, to ulcer edge were found in tissue-type plasminogen activator concentration, histamine concentration, and histamine methyltransferase activity. Concentrations of tissue-type activator, inhibitor type 1, and histamine were significantly lower at ulcer edge than at normal. An inverse correlation was found between histamine methyltransferase and plasminogen activator activities, methyltransferase and tissue-type activator, and methyltransferase and histamine. These results support the hypothesis that in active ulceration, reduction in tissue fibrinolytic activity is closely associated with enhanced release and metabolism of histamine.

Duodenal Ulcer↗
PubMed1986

Evidence for the involvement of dopamine agonists and antagonists in duodenal ulcer disease.

In experimental duodenal ulceration, dopamine levels, turnover, and binding sites are influenced. Dopamine agonists and antagonists exert anti- and proulcerogenic effect, respectively, probably by influencing duodenal hyper- or hypomotility, rather than effecting gastric secretion. The duodenal ulcerogenic effect of the dopamine neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) given to rats in multiple daily doses (p.o. or s.c.) also induced in a dose-dependent manner duodenal ulcers. Duodenal ulcers were prevented by pretreatment with dopamine agonists (e.g. bromocriptine, lergotrile) or monoamine oxidase inhibitors (e.g. pargyline or 1-deprenyl). Our hypothesis suggests that duodenal ulcerogens may interfere with the action of dopamine resulting in loss of the inhibitory function of dopamine, and producing tissue damage from the accumulated auto-oxidation products of dopamine. Alternatively a motility disorder induced by cysteamine, propionitrile or MPTP may contribute to the pathogenesis probably by involving localized hyperacidity in the duodenal bulb because of decreased neutralization and impaired duodenal emptying of acid.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1993

Rationale for eradication of Helicobacter pylori infection in duodenal ulcer disease.

Helicobacter pylori is presently considered a major factor predisposing to the development of duodenal ulceration. The risk of duodenal disease is increased up to 15-fold in patients with H pylori-associated gastritis compared with individuals without H pylori infection. This magnitude of risk with H pylori infection is higher than that of any other known or postulated factor contributing to duodenal ulcer formation. To reclassify duodenal ulcer disease from simply being an acid-related disease to being an infectious disease may appear radical, but no questions remain concerning the essential role of H pylori in this disease. The sequence of events in the development of duodenal ulceration is based on strong circumstantial evidence. The steps by which H pylori interacts with the duodenal mucosa in forming duodenal ulcers may be as follows: 1) H pylori infection of the antral mucosa alters gastric physiology, with an increase in gastrin release and a consequent increase in gastric acid secretion. 2) The increased acid load of the bulbar-duodenal mucosa is responsible for the induction of gastric metaplasia. 3) Gastric metaplasia in the duodenal mucosa can be colonized by H pylori resulting in chronic duodenitis. 4) The interaction of H pylori with the metaplastic gastric epithelium leads to weakening of the normal mucosal integrity. At this point, a variety of factors related to H pylori itself, the host response, or the superimposition of factors such as smoking or stress may ultimately lead to ulcer formation. 5) From clinical observations, it is well established that treatment of H pylori infection without concomitant effects on acid secretion is effective in healing duodenal ulcers. More importantly, eradication of H pylori significantly reduces duodenal ulcer relapse rates. Data from clinical trials strongly suggest that H pylori eradication may cure duodenal ulcer disease.

Clinical Trials as Topic↗
PubMed1984

Abnormally processed gastrins in active duodenal ulcer disease.

In contrast to healthy subjects, duodenal ulcer patients in the active phase contain large amounts of a peptide in serum and antrum which react with antiserum specific for the N-terminus, but not the C-terminus of gastrin-17. The immunochemical and chromatographic properties were similar to that of the N-terminal tridecapeptide sequence of gastrin-17. The peptide follows the clinical course of duodenal ulcer disease, as it disappears when the ulcer heals. The N-terminal tridecapeptide - lacking the bioactive tetrapeptide of gastrin-17 - is a potent inhibitor of gastric acid secretion, presumably by way of competitive antagonism to gastrin. It is suggested to participate in the regulation of gastric acid secretion in patients with active duodenal ulcer disease. To confirm the chemical structure of the peptide, antral and gastrinoma extracts were used for isolation, purification and amino acid analysis. We found two different peptides with the same N-terminus as gastrin-17, namely the previously known N-terminal tridecapeptide fragment of gastrin-17 and a new gastrin component, identical with a C-terminal glycine extended gastrin-17. Furthermore, a C-terminal glycine extended component, corresponding to each of the other molecular forms of gastrin were present. Thus, a variety of abnormally processed gastrins are synthesized and released to the circulation during the active period of duodenal ulcer disease.

Amino Acid Sequence↗
PubMed1996

Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori.

BACKGROUND: Helicobacter pylori infection of the gastric mucosa is vital in the pathogenesis of duodenal ulcer disease. H pylori will only colonise gastric epithelium and its association with duodenal disease is therefore not easily explained. AIMS: To determine if gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected with H pylori. PATIENTS: All children undergoing upper endoscopy over a 20 month period in a children's hospital in Ireland. METHODS: Two biopsy specimens were obtained from the antral mucosa and two from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identification of H pylori. Periodic acid Schiff (PAS) stain was performed to identify areas of gastric metaplasia. RESULTS: Gastric and duodenal biopsy specimens were obtained from 148 patients (M:F 1:2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of children under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p < 0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) children with duodenal ulcer disease compared with 28 of 141 (20%) without ulceration (p < 0.001). While both H pylori and gastric metaplasia were each significant risk factors for duodenal ulcer disease, the combined presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50% of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when both were absent. CONCLUSION: The presence of gastric metaplasia in the duodenum is the major risk factor for duodenal ulcer disease in patients colonised by H pylori.

Adolescent↗
PubMed1989

Duodenal ulcer disease: what role does Campylobacter pylori play?

Duodenal ulcer is a chronic relapsing condition which only became common early this century. Many pathogenic factors have been identified including excess gastric acid secretion, cigarette smoking, non-steroidal anti-inflammatory drugs and reduced mucosal defence. There is a strong association of duodenal ulceration, gastric Campylobacter pylori and antral (type-B) gastritis. The link between ulceration in the duodenum and C. pylori-associated antral gastritis may lie in the formation of gastric-type epithelium in the duodenum (gastric metaplasia). This metaplastic tissue is susceptible to C. pylori colonization and therefore to the local effects of these bacteria. Several reports suggest that duodenal ulcer relapse is more frequent in patients infected with C. pylori. These data are reviewed and a brief history of duodenal ulcer disease is presented.

Campylobacter Infections↗
PubMedDate not supplied

Maintenance treatment with H2 receptor antagonists for duodenal ulcer disease: toward a rational use.

Duodenal ulcer disease is a heterogenous condition characterized by episodes of recurrence and remission. Recurrences are often painful and may result in gross duodenal scarring and pyloric stenosis; bleeding and perforation can complicate the disease, requiring operative treatment and increasing mortality. Treatment should therefore maintain remission after ulcer healing, prevent possibly lethal complications, be safe and maintain efficacy over time. Maintenance treatment with H2 receptor antagonists reduces the rate of symptomatic relapse, but there is no evidence that it affects the complication rate. Tolerance develops in a subgroup of patients and seems to contribute to their poor response to long-term H2 antagonist therapy. It seems wise to prescribe maintenance treatment for 3 years following initial healing in patients with severe relapsing disease, or smokers with recurrent symptoms, and to continue it for life in selected individuals at increased risk of acute complications or of complication-related mortality.

Drug Tolerance↗
PubMed1992

Evidence of clonal variants of Helicobacter pylori in three generations of a duodenal ulcer disease family.

Nine members of a family with a high incidence of duodenal ulcer disease were studied by interview, examination of hospital records, endoscopy, and antral biopsy. Helicobacter pylori was confirmed by CLO test, histology and culture. DNA extraction from pure isolates of H pylori was possible in six family members and strain typing was performed by restriction fragment length polymorphism. DNA restriction digestion was followed by vacublotting and then DNA hybridisation, using a cDNA probe complimentary to H pylori rRNA cistrons. Eight of the nine family members were H pylori positive by CLO test and histology. Five had duodenal ulcer disease. Three family members (one from each generation) harboured clonal variants of a single parent strain of H pylori but only two had duodenal disease. The other three members harboured different strains. Intrafamilial clustering of clonal variants of H pylori occurs in some duodenal ulcer disease families. Family members however, may develop duodenal disease irrespective of the colonising strain.

Adolescent↗
PubMed1975

The effect of the site of lesion and extent of resection on duodenal bile acid concentration and vitamin B12 absorption in Crohn's disease.

Duodenal bile acid concentration following a standard meal, glycine/taurine (G/T) ratio, vitamin B12 absorption, and faecal fat were determined in 79 patients with Crohn's disease. Intestinal resection had been made in 50 patients before the study, and no evidence of recurrence was present at the time of the study. Among 46 patients subjected to ileal resection of 10-180 cm, a reduced duodenal bile acid concentration and vitamin B12 malabsorption was almost invariably present when 50 cm or more of ileum had been removed. Patients with smaller resections and unoperated patients did not show a consistent pattern. Vitamin B12 absorption and duodenal bile acids were of equal value as indicators of ileal dysfunction with the exception that, in 10 ileostomy patients, duodenal bile acids were decreased in every case, but vitamin B12 absorption only when 80 cm of ileum or more had been resected. G/T-ratio was related to the extent of ileal resection-being elevated after large resections (80 cm or more)-but not to the presence of an abnormal flora. Faecal fat was much more elevated in ileostomy patients with large ileal resection (80 cm or more) than in unoperated patients and patients without an ileostomy.

Bile Acids and Salts↗