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PubMed1980

The prevalence of duodenal lesions in patients with rheumatic diseases on chronic aspirin therapy.

Peroral endoscopy was performed in 56 patients with rheumatic disease who had been taking 8 or more aspirin tablets daily for more than 3 months yet who had no major gastrointestinal symptoms or history of peptic ulcer disease. Duodenal mucosal lesions were observed in 16 patients; 15 (27%) had erythema, 7 (13%) had erosions, and 2 (4%) had ulcers. The prevalence of duodenal lesions was the same in patients taking regular, buffered, or enteric-coated aspirin preparations. Patients with duodenal lesions were more likely to have associated gastric lesions.

Adult↗
PubMed1994

How does Helicobacter pylori cause duodenal ulcer disease: the bug, the host, or both?

Helicobacter pylori infection is the most common cause of duodenal ulcer disease, yet duodenal ulcer is an uncommon outcome of H. pylori infection. We reviewed the possible explanations such as differences in the host or in the strain of H. pylori. Host factors reviewed included genetic susceptibility to H. pylori infection and excess gastric acid secretion. The role of potential H. pylori virulence factors not present in all strains such as the cagA gene and the results of other molecular methods to identify disease-specific differences among isolates was also reviewed. Although cure of H. pylori infection resolves gastrin releasing peptide stimulated acid secretion there was no change in parietal cell mass. Twin studies have shown genetic differences in H. pylori susceptibility. There was no difference in the prevalence of the cagA gene between H. pylori infected asymptomatic volunteers and duodenal ulcer patients (P = 1.0). DNA-DNA hybridization of whole genomic DNA in solution and cluster analysis of rep-PCR genomic DNA fingerprints suggest that isolates from patients with duodenal ulcer disease are different from those obtained from individuals with asymptomatic gastritis. Cluster analysis of the rep-PCR DNA fingerprints revealed two major groups of the strains; one set consisted of strains from patients with duodenal ulcer disease and the second cluster consisted largely of strains from individuals with asymptomatic gastritis. Recent molecular studies suggest that disease-specific cell lineages or strains may exist among H. pylori isolates leading to the various outcomes observed in patients with H. pylori infection.

DNA Fingerprinting↗
PubMed1997

Improving management of duodenal ulcer disease.

Audit of treatment of duodenal ulcer disease has allowed management to improve and keep abreast of rapid advances in care. Eradication of Helicobacter pylori was assessed by 14C urea breath test one to two months after anti-Helicobacter therapy. The old triple therapy regime of bismuth, tetracycline and metronidazole for two weeks was found to be toxic and of low effectiveness (82%). Regimes with lansoprazole for one month and antibiotics for one week gave 90-98% success rates. The best success has been with regimes containing both clarithromycin and a nitro-imidazole. There was complete success in 98% of 109 patients given quadruple therapy with lansoprazole 30 mg daily for one month plus tetracycline 500 mg twice daily, clarithromycin 250 mg twice daily and metronidazole 400 mg twice daily for one week.

Adult↗
PubMed1998

Partial or complete circular duodenectomy with highly selective vagotomy for severe obstructing duodenal ulcer disease: an initial experience.

OBJECTIVE: To evaluate partial and complete circular duodenectomy combined with highly selective vagotomy (HSV) for relief of gastric retention. DESIGN: A retrospective, case-comparison study. SETTING: University hospital referral center. PATIENTS: Eighteen patients with severe obstructing duodenal ulcer disease defined by failure of a saline load test and endoscopic narrowing of the gastric outlet to 5 mm or less. METHODS: In patients with severe obstructing ulcer the diseased duodenal segment was excised with electrocautery (partial excision, 10 patients; complete excision, 8 patients). An HSV was then done. Postoperative fasting gastric residuum measurement and measurement of the emptying of liquids and solids was done at 3 months and patients were weighed at 3 and 12 months. RESULTS: No patient experienced postoperative gastric retention or required reoperation in a 2-year follow up. The early emptying of liquid (20 minutes) in complete circular duodenectomy plus HSV was more rapid than in normal subjects and duodenal ulcer patients. The emptying of solids was slightly delayed in partial duodenectomy plus HSV compared with duodenal ulcer patients but not with normal controls. The emptying of solids in duodenal ulcer patients was more rapid than in normal controls. Weight gain was excellent at 3 and 12 months. CONCLUSION: Partial duodenectomy and complete circular duodenectomy plus HSV are more efficacious than alternative nonresective procedures in restoring gastric emptying to near normal and restoring weight in patients with obstructing duodenal ulcer.

Duodenal Obstruction↗
PubMed1997

Evolving therapy for Helicobacter pylori infection: efficacy and economic impact in the treatment of patients with duodenal ulcer disease.

Helicobacter pylori infection is present in most patients with duodenal ulcer disease, and cure of H pylori infection has been shown to dramatically reduce ulcer recurrence. Therapeutic strategies for duodenal ulcer disease have rapidly evolved over the past several years in an effort to consistently cure H pylori infection in a safe, cost-efficient manner. This paper reviews the effectiveness of treatments for H pylori infection in patients assessed with duodenal ulcer disease. The impact of clinical success on economic effectiveness has been determined in a recent prospective outcomes trial. Treatments with clarithromycin plus omeprazole or clarithromycin plus ranitidine-bismuth-citrate (RBC) provide consistent cure of H pylori infection, with eradication rates of 70% to 80%. Recent studies suggest that higher rates of eradication are possible with triple combination therapy (e.g., clarithromycin plus a second antibiotic and a proton pump inhibitor or RBC), but the optimal triple therapy regimen (including the combination of drugs, dosage, and duration of treatment) has not yet been defined. A recent 1-year prospective outcomes trial has demonstrated that eradication therapy with clarithromycin and omeprazole, compared with standard antisecretory therapy, provides measurable savings in utilization of ulcer-related health-care resources. Combination therapy with clarithromycin plus omeprazole, clarithromycin plus RBC, or clarithromycin plus lansoprazole and amoxicillin have been approved for the treatment of H pylori infection in patients with duodenal ulcer disease. Economic analysis has confirmed that cure of H pylori infection not only contributes to the clinical resolution of duodenal ulcer disease, but also provides economic advantages by reducing costs associated with recurrence.

Anti-Bacterial Agents↗
PubMed1997

Co-existing gastric cancer and duodenal ulcer disease: role of Helicobacter pylori infection.

BACKGROUND: The association of gastric cancer and chronic duodenal ulcer disease is considered rare. In fact duodenal ulcer disease is believed to somehow "protect" against the development of gastric cancer. Helicobacter pylori infection is an important factor in the development of gastric cancer. No detailed investigation on the prevalence of H. pylori in coexistence of gastric cancer and duodenal ulcer disease has been performed. We evaluated the frequency of H. pylori infection in the patients with co-existence of gastric cancer and duodenal ulcer disease. MATERIALS AND METHODS: During the period March 1994 to February 1995, we collected data from 3,652 patients in whom esophagogastroduodenoscopy was done. During this period, when the cancerous or ulcerative lesions in stomach or duodenum were found, rapid urease tests were performed. RESULTS: Six patients had concurrent gastric carcinoma and duodenal ulcer disease. Three of the cases had early gastric carcinoma; 2 had active duodenal ulcers and one had a duodenal ulcer scar; all 3 had positive rapid urease tests. The patients with early gastric cancer were younger than the individuals with advanced gastric cancer. CONCLUSIONS: The co-existence of both diseases may be higher than reported from Western countries or from Peru which may either reflect the high prevalence of circulation of H. pylori ulcer and cancer strains in Korea and the co-infection with both types of organism in some individuals.

Adult↗
PubMed2000

[The Helicobacter pylori role in origination of hemorrhage in elderly and senile patients with duodenal ulcer disease].

During examination of 37 patients with duodenal ulcer disease aging more than 60 years it was established that while presence of the ulcer complicated by bleeding the revelation frequency of Helicobacter pylori (HP) in gastric antrum is increasing up to 74% and in cases of noncomplicated ulcer--70%. HP was revealed most frequently in patients with "senile" ulcer. For an "inveterate" ulcer the presence of S-like forms is typical. The absence of HP in 41.6% patients with "senile" ulcer testifies the presence of other mechanisms of occurrence and support of bleeding.

Aged↗
PubMed1981

Morphological and morphometric assessment of human duodenal biopsies maintained in organ culture. In vitro influences of gluten in coeliac disease.

Duodenal biopsy specimens from 51 coeliac patients (children and young adults) and 13 non-coeliac controls were maintained in organ culture for 24 h. Morphometric determinants were compared after culture in the presence of different gluten fractions, after culture on gluten-free medium, and in non-cultured specimens. Biopsies from patients with untreated coeliac disease were susceptible to gluten fractions, which provoked disorganization of crypt architecture, reduced height and irregularities of enterocytes and crypt cells, together with detrition of surface epithelial cells and even tissue necrosis. In latent coeliac disease (silent relapse) biopsies were more resistant to gluten, and higher concentrations were required to induce signs of morphological deterioration. Remission mucosa and biopsies from non-coeliac controls showed no signs of impairment after gluten exposure in vitro.

Adolescent↗
PubMed2001

[Causal relationship between Helicobacter pylori infection and upper gastroduodenal diseases].

Helicobacter pylori infection causes chronic gastritis (nonatrophic gastritis), which progresses to atrophic gastritis and intestinal metaplasia over a period of decades. Atrophy may result from inflammation and apoptosis caused by H. pylori infection. H. pylori is an important risk factor for peptic ulcer disease. Duodenitis in the gastric metaplasia of the duodenum, hypergastrinemia, and impaired proximal duodenal mucosal bicarbonate secretion are considered causal factors for duodenal ulcer disease. Low-grade B-cell gastric lymphoma of mucosa-associated lymphoid tissue (MALT) develops in response to H. pylori infection. Studies of Mongolian gerbil model demonstrated that H. pylori had an initiator or promoter effect on gastric carcinogenesis.

Chronic Disease↗
PubMed1993

Helicobacter pylori in the pediatric patient.

H. pylori is the major cause of gastritis in children and adults. Studies in children have demonstrated a specific association between H. pylori and primary gastritis. H. pylori colonization of the gastric mucosa is also important in relation to the natural history of duodenal ulcer disease. Duodenal ulcers do not appear to relapse if H. pylori is cleared from the gastric mucosa. Because of the low incidence of duodenal ulcer disease in children, a multicenter study is required to demonstrate whether this finding is true in children. To date, no specific symptoms have been associated with the presence of H. pylori gastritis in children. H. pylori gastritis may therefore be an asymptomatic condition in the majority of infected children. Further studies in relation to H. pylori gastritis and symptoms in children will be important because it should be easier to identify specific symptoms in children than in adults. H. pylori gastritis in children can be diagnosed by obtaining antral biopsy specimens for culture and histologic study during upper gastrointestinal endoscopy. Serologic study is also a sensitive and specific indicator of H. pylori infection, provided that children's sera are used to standardize the assay. Noninvasive tests such as 13C urea breath tests are very attractive for use in children but are expensive. H. pylori can be cleared from the gastric mucosa in as many as 70% of children by using a combination of metronidazole or amoxicillin with colloidal bismuth subcitrate or bismuth subsalicylate. Studies in children are important in determining the epidemiology of H. pylori. Children in Western societies are not usually colonized. Infection becomes more common with increasing age. Children in underdeveloped countries and those living in poor social conditions in Western countries are much more likely to be infected at a young age. The reason for the increased prevalence of infection among these groups is not known. There is also significant intrafamilial clustering of H. pylori infection. Again, it is unclear why the organism is clustered within households and institutions. Future studies on children will be of importance in determining whether H. pylori gastritis is a cause of specific symptoms, the epidemiology of H. pylori infection, and the possible role of the organism in the natural history of gastric cancer.

Child↗
PubMed1986

Psychological correlates of gastric and duodenal ulcer disease.

Psychological correlates of gastric and duodenal ulcer disease were assessed in a group of somewhat older patients with ulcer disease identified by endoscopy. Associations between both ulcer types and symptom measures (anxiety and depression) seemed only to reflect severity or chronicity of gastrointestinal symptoms or the impending endoscopy procedure. Associations with 'trait' psychological indices may be of causal significance. Duodenal ulcer patients had higher 'introversion' and 'psychoticism' scores (on the EPQ) than controls, while gastric ulcer patients had higher psychoticism scores and 'trait anxiety' scores. These findings could not be attributed to confounding variables. When the two ulcer groups were compared, the gastric ulcer group had significantly higher neuroticism, psychoticism and hostility scores which were not attributable to confounding variables. The higher depression scores in gastric ulcer patients, however, simply reflected the greater chronicity of their physical symptoms. The groups did not differ significantly on measures of trait anxiety, tension, introversion or Type A behaviour.

Anxiety Disorders↗
PubMed1990

[Seasonal variation in duodenal ulcer disease in the Upper Galilee].

Active duodenal ulcer disease was diagnosed in 179 of 748 patients presenting with onset of symptoms of the peptic syndrome in the course of 3 years. The diagnosis was made on the basis of either endoscopy or X-ray. The highest average annual incidence was in kibbutzim and the lowest in moshavim (98.9 and 49.2 new cases/year/100,000, respectively). A peak in the diagnosis of new cases of active duodenal ulcer was demonstrated in November, December and January, compared with an equal distribution among other months. There was a diagnostic peak in the winter, and a seasonal decrease in the fall (56 +/- 4 vs 38 +/- 4, M +/- SE, respectively). These findings were statistically significant when proportions of total visits to the Gastroenterology Clinic were compared (Z = 1.976; p less than 0.05).

Duodenal Ulcer↗
PubMed1993

Treatment and long-term follow-up of Helicobacter pylori-associated duodenal ulcer disease in children.

In a 7-year period, 33 children had endoscopically documented duodenal ulcer disease. Of the 33 children, 29 had Helicobacter pylori antral gastritis. All children with H. pylori-associated duodenal ulcer disease were treated with antibiotics but no H2-receptor blocking agents. For the first 3 years of the study, initial treatment was with bismuth subsalicylate or amoxicillin for 6 weeks. For the latter 4 years, therapy with both bismuth subsalicylate and amoxicillin for 6 weeks was used initially; those in whom treatment failed received bismuth subsalicylate and amoxicillin for 6 weeks, and metronidazole for 4 weeks. Follow-up with endoscopic biopsies was performed immediately after each treatment course and at a mean of 6.5 months after clearance of H. pylori from antral biopsy specimens. Data for noncompliant patients and those receiving nonsteroidal antiinflammatory drugs were analyzed separately. For compliant patients, the rates of H. pylori clearance from antral biopsy specimens immediately after each treatment were as follows: bismuth subsalicylate, 6 of 12 children; amoxicillin, 1 of 5 children; double therapy, 9 of 9 children; and triple therapy, 3 of 3 children. At long-term follow-up, the number of children with no H. pylori in antral biopsy specimens were as follows: monotherapy, 1 of 5; double therapy, 4 of 4; and triple therapy, 3 of 3. Of the noncompliant patients, only 1 of 5 had H. pylori eradication with combination therapy and none had H. pylori eradication with monotherapy. Duodenal ulcer disease had healed in all children with H. pylori-negative antral biopsy specimens at follow-up; duodenal ulcers recurred in all children with persistent or recurrent H. pylori infection. We conclude that therapy with two drugs for 6 weeks is the treatment of choice for endoscopically proved duodenal ulcer and histologically proved H. pylori antral gastritis, and that poor patient compliance reduces the rate of success. Our data strongly support a causal relationship between H. pylori and duodenal ulcer disease.

Adolescent↗
PubMed2000

Pathogenesis of duodenal ulcer disease: the rest of the story.

Although several duodenal ulcer disease-specific abnormalities in gastric function have been described (e.g. exaggerated gastrin releasing peptide-stimulated acid secretion and an abnormal sensitivity of the parietal cells to gastrin), none has withstood careful examination. We describe here the critical nature of the duodenal acid load in precipitating and washing out bile salts, which inhibit the growth of Helicobacter pylori (H. pylori) in the development of duodenal ulcer disease. The risk of duodenal ulcer is enhanced by infection with proinflammatory H. pylori (e.g. with an intact cag pathogenicity island). Progressive damage to the duodenum promotes gastric metaplasia, resulting in sites for H. pylori growth and more inflammation. This cycle results in an increasing inability of the duodenal bulb to neutralize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. Cure of the H. pylori infection results in a sustained fall in duodenal acid load as well as a marked (and continuing) reduction in inflammation, which results in the cure of chronic ulcer disease.

Duodenal Ulcer↗
PubMed1991

Duodenal ulcer dyspepsia in the first degree relatives of subjects with duodenal ulcer disease.

In a population survey, the point prevalence of duodenal ulcer disease (DUD) was found to be 11.98 percent which is the highest prevalence rate so far reported in the literature. The prevalence of duodenal ulcer dyspepsia in the first degree relatives of groups of subjects with proven duodenal ulcer, non ulcer dyspepsia (NUD) (duodenal ulcer dyspepsia but without evidence of ulcer at endoscopy) and normal healthy control (HC), all matched by age and sex and all from the population with the high prevalence of duodenal ulcer disease, were studied. Both DUD and NUD subjects had a significantly higher family history of duodenal ulcer dyspepsia than the control subjects.

Adult↗
PubMed1989

Operations for duodenal ulcer disease.

Operative treatment of duodenal ulcer has been restricted to the small proportion of ulcer patients who have complications of ulcers or to those patients who do not respond to medical treatment. The principal surgical procedures that have been used include different types of gastric drainage, gastric resection, gastric denervation, or various combinations of these principles. Initially, the primary objective of ulcer surgery was to prevent recurrent ulcer. Currently, the objectives of operation are to cure an ulcer without a recurrent ulcer or any undesirable sequelae developing as a result of altered gastric physiology. Perhaps no operation will satisfy each of these conditions for every patient. Parietal cell vagotomy without a drainage procedure, the latest contribution to ulcer surgery, has been intensively studied for 19 years. The operative mortality of 0.26%, the recurrence rate of 4 to 11%, and virtually no significant side effects have caused the operation to become the procedure of choice for an increasingly large number of gastric surgeons.

Duodenal Ulcer↗
PubMed2001

Gastric acid secretory response in Helicobacter pylori-positive patients with duodenal ulcer disease.

BACKGROUND: Patients with duodenal ulcer (DU) have an increased parietal cell mass and sensitivity to secretagogues, with increased acid output. AIM: To determine the effect of Helicobacter pylori eradication on parietal cell sensitivity and gastric acid secretion. SUBJECTS AND METHODS: Twenty-five H pylori-positive DU patients and 18 H pylori-negative healthy volunteers were studied. Serum H pylori immunoglobulin G, basal acid output and acid secretory response to graded doses of pentagastrin were determined before and after treatment, at six months and at one year. Subjects were randomly assigned to ranitidine or sucralfate treatment for six weeks, and all DU patients received bismuth subsalicylate, metronidazole and tetracycline for the first two weeks. RESULTS: H pylori was eradicated in 66% of patients receiving sucralfate and 92% receiving ranitidine. Compared with healthy volunteers, DU patients demonstrated a 2.7-fold greater basal acid output, a 1.3-fold greater peak acid output, significantly higher acid output for each dose of pentagastrin and a 1.38-fold increase in the area under the pentagastrin dose acid response curve. Cure of H pylori, irrespective of ulcer healing regimen, resulted in a gradual decrease in acid secretory capacity with basal acid output, peak acid output and area under the pentagastrin dose acid response curve returning to healthy volunteer levels by one year. No demonstrable differences were observed in parietal cell sensitivity in all subjects before or after treatment. These data suggest that disturbances in acid secretion in H pylori-positive DU patients are not due to an increased parietal cell sensitivity to pentagastrin but rather due to an increased parietal cell mass with increased capacity to secrete acid, which gradually resolves following cure.

Adult↗