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PubMed1968

Recent history of ischaemic heart disease and duodenal ulcer in doctors.

Data are presented on the incidence of ischaemic (coronary) heart disease and duodenal ulcer among the several thousand male medical practitioners aged 35-64 holding immediate sickness benefit policies with the Medical Sickness Annuity and Life Assurance Society Limited. Three periods are considered: 1947-50, 1957-60, and 1961-5.The incidence of first clinical episodes of ischaemic heart disease in the doctors altered little between 1947-50 and 1957-60 but increased in 1961-5. Comparison of the late 1940s with the early 1960s shows a 60% rise of incidence at ages 45-54 but little change at other ages. Cases first presenting as "sudden" death increased between 1947-50 and 1961-5 by 111% at 45-54, and again changed little at 55-64. In two other occupational groups that have been studied-bus conductors and insurance salesmen-the increase of incidence was greater than for the doctors at 45-54 and it occurred also over 55 years of age. The increase from 1947-50 to 1961-5 in mortality during all episodes of ischaemic heart disease was the same in the doctors as in the male population of England and Wales at 45-54, but at 55-64 it was less.The results in the doctors are not due to alterations over the period in length of sickness absence, or underwriting policy, or of the nomenclature used on the certificates.Well-documented changes in the smoking habits of doctors may be partly responsible for what appears to have been a relatively favourable experience of ischaemic heart disease from 1947-50 to 1961-5, especially at ages 55-64.Incidence of duodenal ulcer at ages 35-64 declined steadily in this population of doctors from 1947-50 to 1961-5. The decline is very likely to be real.

Adult↗
PubMed1995

The economic and quality-of-life benefits of Helicobacter pylori eradication in chronic duodenal ulcer disease--a community-based study.

A policy of Helicobacter pylori eradication in patients with duodenal ulceration on long-term acid-suppressing therapy was evaluated in a prospective study amongst a general practice population, with particular reference to economic and quality-of-life benefits. One hundred and sixty-eight patients on long-term acid-suppressing therapy had chronic duodenal ulcer disease of whom 88 were eligible for the study; 45 patients attended for review, with 42 testing positive for H pylori (as assessed by 13C-urea breath test). The median duration of acid-suppressing therapy was six years (maximum 15 years); 47.6% of the patients were using additional antacids and 80.9% still experienced epigastric discomfort. Two-thirds (28/42) of the patients eradicated H pylori. Successful eradication was associated with a highly significant reduction in all symptoms. At 12 months follow-up, heartburn had decreased from 28.7% to 7.1%, epigastric discomfort from 75% to 3.6%, nausea from 32.1% to 0% and wind from 50% to 0%. Of the patients that eradicated H pylori 96.4% reported an improvement in their general health compared to none of those that remained H pylori positive. Successful H pylori eradication therapy scored higher on satisfaction ratings than long-term acid-suppressing therapy. Eradication of H pylori resulted in 27/28 patients being able to discontinue acid-suppressing therapy, representing a 5.8% reduction in the use of such drugs per year in the local general practice population. A policy of H pylori eradication in chronic duodenal ulcer disease reduces the use of long-term acid-suppression therapy in general practice. This has important financial implications as well as offering considerable symptomatic benefits to the patients and improving their quality of life.

Adult↗
PubMed1995

The Helicobacter pylori theory and duodenal ulcer disease. A case study of the research process.

OBJECTIVES: To describe the medical research process from the time of the generation of a new theory to its implementation in clinical practice. The Helicobacter pylori (H. pylori) theory, i.e. the theory that H. pylori plays a significant causal role in duodenal ulcer disease was chosen as a case. MATERIAL: Abstracts from 1984 to 1993, identified in the CD-Rom, Medline system, ("Silverplatter"), using the search terms Campylobacter pylori and Helicobacter pylori, and reviews and editorials about H. pylori in some of the most widespread clinical journals. RESULTS: 2204 papers on H. pylori were published, of which 64% (1,403) were original articles. Of these, 30% (415/1,403) were descriptive clinical studies, 5% (64) were epidemiological studies, 33% (459) were laboratory studies of disease mechanisms, 8% (112) were therapeutic intervention studies, and 24% (336) concerned diagnostic and therapeutic techniques. A total of 204 of the clinical studies addressed duodenal ulcer disease. Of these, 72% (147) were cross-sectional studies, 3% (7) were observational cohort studies and 25% (50) were therapeutic intervention studies. Thirty-one editorials and reviews concerning the etiological role of H. pylori in duodenal ulcer disease had been published in some of the most widespread clinical journals. In half of the papers the authors were convinced of the causal role of H. pylori in duodenal ulcer disease, while in the remainder they were sceptical. In seven cases the authors stated which patients should be selected for H. pylori eradication treatment. CONCLUSION: Descriptive clinical studies and laboratory studies of disease mechanisms were the prevailing types of research about H. pylori. Comparatively few therapeutic intervention studies were done; this fact may have hampered the acceptance of the H. pylori theory and the introduction of eradication therapy in clinical practice.

Animals↗
PubMed1985

Gastroduodenal mucosal hormone content in duodenal ulcer disease.

To further elucidate the pathophysiological role of peptide hormones in duodenal ulcer (DU) disease, several endocrine, paracrine and neurocrine peptides were determined radioimmunologically in biopsies of gastroduodenal mucosa obtained endoscopically in 8 subjects without upper gastrointestinal disease, and in 8 duodenal ulcer patients. The DU patients had a BAO of 6.6 +/- 1.9 and a PAO of 41.8 +/- 6.1 mEq/h. In DU patients, a lack of the acid and gastrin-release inhibiting agent somatostatin was found neither in antral nor in fundic mucosa (185 +/- 60 vs 83 +/- 19 pmol/g tissue wet weight in controls). Basal and peak acid outputs of DU patients were positively correlated with fundic somatostatin concentrations (p less than 0.01). While gastrin levels were not significantly elevated in the antrum of DU patients, the mucosal content of potentially releasable gastrin of the duodenal bulb and the descending duodenum was higher than in controls (p less than 0.01). In the whole duodenum, CCK-like immunoreactivity was also more abundant in DU patients than in controls, whereas GIP and motilin did not exhibit characteristic profiles. Presumably as a reactive phenomenon, the mucosal levels of the peptidergic neurotransmitters VIP and substance P were markedly increased in the proximal duodenum of DU patients.

Adult↗
PubMed1980

Duodenal ulcer disease in chidren.

Eleven cases of chronic duodenal ulcer in children were subjected to surgical treatment in a period of 7 years. The diagnosis was based on typical peptic ulcer symptoms, hyperchlorhydria, and barium meal x-ray studies delineating a duodenal bulb deformity with an ulcer crater in 8 patients. Three cases of duodenal ulcer perforation in infants were diagnosed at aparotomy for peritonitis with pneumoperitoneum. All the patients hailed from the rgion of Assam, India, where peptic ulcer is prevalent. A positive family history of peptic ulcer in 5 patients, blood group O in 7 patients, and the regional diet were considered to be predisposing factors. Medical treatment consisting of a bland diet, sedatives, antispasmodics, and a brief hospital stay failed to provide permanent relief of symptoms. Truncal vagotomy with a drainage procedure was done in 8 patients with no deaths. However, simple closure of the perforation in the 3 infants resulted in fatalities due to fulminant septicemia. The patients were followed up for 1-8 years. Six patients had permanent relief of symptoms. Two patients occasionally complained of epigastric fullness and eructation. They showed normal growth, gain in weight and hemoglobin levels, and had no recurrence. We believe that operative treatment is preferable to medical management of chronic duodenal ulcer in children.

ABO Blood-Group System↗
PubMed1997

Two omeprazole-based Helicobacter pylori eradication regimens for the treatment of duodenal ulcer disease in general practice.

BACKGROUND: Helicobacter pylori is the main acquired factor in the pathogenesis of duodenal ulcer disease. METHODS: This multicentre study conducted in 32 general practice centres in the UK and Ireland was a double-blind, placebo-controlled, randomized, parallel-group comparison of triple therapy (n = 98: omeprazole 40 mg once daily and amoxycillin 1 g b.d. for 2 weeks, and metronidazole 400 mg t.d.s. for the first week) and dual therapy (n = 85: omeprazole 40 mg once daily and amoxycillin 1 g b.d. for 2 weeks, with placebo during the first week) for the eradication of H. pylori in patients with symptomatic duodenal ulcer disease. Patients who were successfully treated entered a follow-up phase for 12 months to assess symptomatic relapse and use of health-care resources. RESULTS: Eradication of H. pylori based on a second 13C-urea breath test was successful in 95% (95% confidence interval (CI) = 90-100%) of patients receiving omeprazole triple therapy and 53% (95% CI = 41-65%) of those receiving omeprazole dual therapy (P < 0.0001 between groups, all data available analysis). The all-patients-treated analysis gave eradication rates of 80 and 44% for omeprazole triple therapy and omeprazole dual therapy, respectively. Symptomatic relapse occurred in 16% (18/116) of the H. pylori-negative patients who entered the 12-month follow-up period, and there were significant reductions in the number of consultations, investigations and prescriptions relating to upper gastrointestinal symptoms compared with the 12 months prior to the eradication therapies (all P < 0.0001). The two treatment strategies were comparable in terms of the number of adverse events reported. CONCLUSIONS: Omeprazole triple therapy provides a highly effective treatment for the eradication of H. pylori infection in patients in general practice, with an adverse event profile similar to that seen with omeprazole dual therapy. The successful eradication of H. pylori with these omeprazole regimens results in a significant decrease in the use of health-care resources in the 12 months following treatment.

Adult↗
PubMed2000

One-week triple therapy with esomeprazole provides effective eradication of Helicobacter pylori in duodenal ulcer disease.

BACKGROUND: Esomeprazole is the first proton pump inhibitor to be developed as an optical isomer for the treatment of acid-related diseases. METHODS: Four hundred and forty eight duodenal ulcer patients with Helicobacter pylori infection, confirmed by 13C-urea breath test (UBT), and no current ulcer, were randomised to double-blind treatment with esomeprazole 20 mg twice daily (b.d.) (n=224) or omeprazole 20 mg b.d. (n=224), in combination with amoxicillin 1 g b.d. and clarithromycin 500 mg b.d. for 1 week (EAC and OAC, respectively). A negative UBT at both 4 and 8 weeks after completing therapy indicated successful H. pylori eradication. RESULTS: Intention-to-treat (ITT) analysis comprised 400 patients (EAC, n=204; OAC, n=196) and per protocol (PP) analysis 377 patients (EAC, n=192; OAC, n=185). Eradication rates (95% confidence intervals) for ITT and PP populations were: EAC, 90% (85-94%) and 91% (86-94%); OAC, 88% (82-92%) and 91% (86-95%). Between-group differences in eradication rates were not statistically significant. Both regimens were well tolerated, with an adverse event profile and frequency typical of proton pump inhibitor plus antibiotic combination therapy. CONCLUSIONS: Esomeprazole-based triple therapy for 1 week is highly effective in eradicating H. pylori infection in duodenal ulcer disease, offers comparable efficacy to omeprazole-based therapy, and is well tolerated.

Adult↗
PubMed1976

Sleep patterns and gastric acid secretion in duodenal ucler disease.

Five normal volunteers and five patients with duodenal ulcer (DU) disease were studied for five consecutive nights. All subjects underwent placement of a nasogastric tube, continuous collection of gastric juice, and continuous electroencephalographic monitoring of sleep. Gastric juice was collected in 20-minute samples by remote suction (Gomco). Blood samples were drawn every 20 minutes on the third night via an indwelling venous needle. Results showed no significant correlations between the sleep variables and the gastric acid secretion measures or between the sleep variables and serum gastrin levels. Acid secretion decreased from hour 1 to hour 2 in controls and in patients with inactive DU disease, while it increased in patients with active DU disease. Each subject had at least one night of recording in which continuous gastric secretion was less than 0.1 mEq per 20-minute sample. It appears unlikely that the gastric discomfort of DU patients can be attributed to acid hypersecretion triggered by rapid eye movement sleep.

Duodenal Ulcer↗
PubMed1997

Pathophysiology of duodenal ulcer disease.

Before the discovery of Helicobacter pylori infection some 12 years ago, three major disturbances in gastric physiology had been identified in patients with duodenal ulcer disease. These abnormalities were: impaired acid inhibition of gastrin release from the antral mucosa, increased basal and stimulated acid secretion by the body of the stomach and increased acid load in the duodenum. Some of these abnormalities in gastric function can now be explained by the effects of H. pylori infection. The increased release of gastrin by the antral mucosa in duodenal ulcer patients, for example, can be entirely explained by the effects of this organism. Other abnormalities, however, appear to have a genetic basis or may be due to environmental factors. Much work has been conducted on the relationship between H. pylori and the development of duodenal ulcer disease and this paper aims to review recent studies in the field and to give an overview of the latest understanding of the pathophysiology of this disease.

Duodenal Ulcer↗
PubMed1991

[Changes in serotonin-containing EC-cells in the lamina epithelialis mucosae of the small intestine in young children with growth disorders caused by intestinal diseases].

Duodenal jejunal biopsy material from children with growth retardation due to enteric disease was investigated. The disease dependent mucosa types were classified into three groups according to Shmerling (1970). 5-hydroxytryptamine was demonstrated with an impregnation technique and histochemically, as well, in EC-cells in the crypt epithelium. The EC-cell content in specimens with subtotal villus atrophy (type III) was higher significantly compared to normal mucosa (type I). The findings were discussed with regard to the possible role of 5-hydroxytryptamine in the pathogenesis of the growth retardation due to enteric disease in children.

Biopsy↗
PubMed1986

Lack of specific binding of prostaglandin E2, prostaglandin F2 alpha, and 6-keto prostaglandin F1 alpha to serum in patients with peptic ulcer disease and in healthy subjects.

Rabbits immunized against prostaglandins develop antibodies to prostaglandins and peptic ulcer disease (duodenal and gastric ulcers). We have evaluated the hypothesis that idiopathic gastric or duodenal ulcer disease in humans may be associated with the spontaneous occurrence of serum antibodies directed against endogenous prostaglandins. We found that serum from 45 ulcer patients (34 duodenal, 11 gastric) had a low degree of binding of radiolabeled prostaglandin E2, prostaglandin F2 alpha, or 6-keto prostaglandin F1 alpha. The extent to which prostaglandins were bound to serum of ulcer patients was not statistically different from prostaglandin binding to serum from 25 normal subjects. Therefore, we conclude that spontaneous occurrence of circulating antibodies against endogenous prostaglandins is an unlikely cause of gastroduodenal ulceration in humans.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Smoking and duodenal ulcer disease.

Cigarette smoking has long been thought to be associated with duodenal ulcer disease, there being an increased incidence and an adverse outcome in both healing and relapse. This review evaluates this evidence and the possible mechanisms that might account for a poor outcome in smokers.

Animals↗
PubMed1988

Diagnostic strategy in suspected duodenal ulcer disease. A questionnaire study.

In a questionnaire study of 89 Danish gastroenterologists the current diagnostic strategy in patients suspected of having duodenal ulcer disease was elucidated. A case summary concerning a patient with upper abdominal pain was presented. It was assumed that the patient had had a double-contrast barium meal examination or an upper gastrointestinal endoscopy performed. If the X-ray had revealed a deformity of the duodenal bulb, 30% of the gastroenterologists would offer the patient specific medical treatment (H2-blocking agent etc.), but a significantly higher number of gastroenterologists, 45%, (p less than 0.05) would offer specific medical treatment if a deformity was revealed at endoscopy. There was also a significant difference (p less than 0.01) between those who would offer specific treatment if X-ray (84%) or if endoscopy (100%) had revealed an ulcer. Considerable variation was found among experts in their decisions on the basis of X-ray and endoscopy in patients with suspected duodenal ulcer disease. Gastroenterologists generally rely more on endoscopic than on radiographic findings.

Barium↗
PubMed2000

Rabeprazole is superior to ranitidine in the management of active duodenal ulcer disease: results of a double-blind, randomized North American study.

OBJECTIVE: The primary purpose of this study was to compare the efficacy and tolerability of rabeprazole versus ranitidine in the treatment of patients with active duodenal ulcer disease. METHODS: This multicenter, double-blind, randomized, parallel-group study enrolled 376 patients. Patients were randomly assigned to receive rabeprazole 20 mg administered once daily in the morning (q.a.m.) with matching ranitidine placebo twice daily (b.i.d.) (n = 188), or ranitidine 150 mg b.i.d. with matching rabeprazole placebo q.a.m. (n = 188). Three visits were scheduled: wk 0 (baseline; days -3 to -1), wk 2 (day 15+/-3 days), and wk 4 (day 29+/-3 days). The primary efficacy response variable was defined as complete regeneration of the mucosa at the site of all ulcers identified during the study. Secondary efficacy variables included patients' ratings of frequency and severity of ulcer pain, frequency of antacid use, and improvement of overall physical well-being. Tolerability was evaluated with analyses of adverse events, laboratory evaluations, fasting serum gastrin levels, vital signs, body weight, and electrocardiograms. RESULTS: Up to 4 wk of treatment with rabeprazole 20 mg q.a.m. produced significantly greater healing rates, compared to treatment with ranitidine 150 mg b.i.d. (83% vs 73%; p = 0.017). Significant differences between treatment groups were also observed for secondary efficacy indices. At wk 2, rabeprazole was more likely than ranitidine to produce complete resolution of duodenal ulcer pain (39% vs 25%; p = 0.006), improvement in duodenal ulcer nighttime pain severity (76% vs 65%; p = 0.044), and improvement in overall well-being (55% vs 41%; p = 0.009). At wk 4, the proportion of patients with normalization of overall well-being was significantly higher in the rabeprazole group than in the ranitidine group (45% vs 29%; p = 0.003). Rabeprazole was safe and well tolerated in this study. CONCLUSIONS: In patients with active duodenal ulcer disease, rabeprazole 20 mg q.a.m. is superior to ranitidine 150 mg b.i.d. in healing, resolving ulcer pain frequency, improving nighttime pain severity, and improving overall well-being. Rabeprazole is an effective and well-tolerated alternative treatment for patients with active duodenal ulcer disease.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1977

Inflammatory cell count and identification in specific duodenitis. (Celiac disease, Whipple's disease and Crohn's disease). Comparison with jejunal findings.

The authors studied the count and identification of inflammatory cells in duodenal biopsies of specific duodenitis. In celiac disease there is an increase of lymphocytes in the epithelial layer, and rich population of plasmacells in the lamina propria of duodenal mucosa. In Whipple's disease the reticulum cell component of lamina propria is increased, while total inflammatory cells are within normal limits, and both lymphocytes and plasmacells are decreased. The comparison between duodenal and jejunal findings shows similar data in celiac and Whipple's disease. In Crohn's disease the inflammatory cell count differs from controls only in presence of radiological or endoscopical features of duodenal involvement.

Adult↗
PubMed1990

Gastric histology and plasma gastrin response to a meal in patients with duodenal ulcer disease after five years treatment with ranitidine.

Fifty asymptomatic patients with duodenal ulcer disease, aged 31-82 years, who had received ranitidine maintenance therapy continuously for five or more years without a symptomatic recurrence, were studied. Fasting plasma gastrin concentrations were normal (mean 24 pmol/L, S.D. +/- 22) while the post-prandial gastrin response was variable with maximum plasma concentrations ranging from 16 to 309 pmol/L. Endoscopy revealed six asymptomatic peptic ulcers. Histological examination of gastric biopsies showed mild, superficial inflammatory cell infiltration of the fundic mucosa, but more extensive inflammatory cell infiltration with some atrophy of the mucosal glands in the antral mucosa. Patchy intestinal metaplasia was evident in the antral mucosa of 18 patients. No fundic ECL cell hyperplasia was seen. Helicobacter pylori were detected in the corpus and antrum of most patients. These results suggest that maintenance treatment with ranitidine for 5 years is not associated with either significant hypergastrinaemia or with changes in the fundic mucosa which could be interpreted as pre-malignant.

Adult↗