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Laparoscopic vagotomy for chronic duodenal ulcer disease.

Two laparoscopic procedures for treatment of chronic duodenal ulcer are described: bilateral truncal vagotomy with balloon pyloric dilatation and posterior truncal vagotomy with anterior lesser curve seromyotomy. The first procedure is simple to perform and easily reproducible, but the latter is preferred because it respects the physiology of the stomach. Thirty-six patients were operated on over a period of 18 months with good results comparable to those with open surgery. The indications for surgery were intractable chronic duodenal ulcers resistant to optimal medical therapy. There was no perioperative morbidity or mortality, and recurrent ulcers have not been demonstrated during early postoperative follow-up. The proper role of laparoscopic surgery in the arsenal of treatment of duodenal ulcers is unclear. The method of laparoscopic vagotomy requires rigorous experimental evaluation in specialized centers before widespread clinical application. Future multicentric prospective studies with long-term follow-up are necessary to assess the results of this innovative therapy of acid-peptic disease.

Adult↗
PubMed1992

Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease.

Infection of the gastric antrum by Helicobacter pylori is associated with recurrent duodenal ulcer disease but the mechanism of ulcerogenesis is unclear. Since pathways inhibiting gastric secretion are defective in patients with duodenal ulcers, we investigated whether H pylori interferes with the normal gastric inhibition that is mediated by somatostatin. We studied 28 patients with active duodenal ulcers in whom H pylori was eradicated successfully. In 18 patients, we measured the density of antral somatostatin-immunoreactive cells and in a further 10 subjects, the amount of somatostatin mRNA before and after eradication of H pylori was determined. After eradication, the median density of somatostatin-immunoreactive cells increased significantly from 9 (range 3-47) to 19 (6-57) cells per mm muscularis mucosa (p = 0.025). The median somatostatin mRNA/rRNA ratio increased from 50 (25-160) to 95 (40-180) (p = 0.01). The number of gastrin cells and quantity of gastrin mRNA did not change significantly. Our results suggest that in duodenal ulcer disease, gastric secretory function is disinhibited through the suppression of mucosal somatostatin.

Adult↗
PubMed1972

Salivary secretion in duodenal ulcer disease.

Salivary response to stimulation with citric acid was higher in patients with duodenal ulcer disease than in patients with other diseases of the upper gastrointestinal tract. This increase was proportional to an increase of histamine-stimulated gastric acid secretion. In duodenal ulcer disease, the increase in parietal cell mass may therefore be associated with the growth of other exocrine organs such as the salivary glands.

Adult↗
PubMed1991

Pathogenetic role of Helicobacter pylori in duodenal ulcer disease. Multivariate analysis of factors affecting relapse.

The pathogenesis of duodenal ulcer disease is multifactorial and the contribution of Helicobacter pylori in relation to the other factors to the release of duodenal ulcer is unknown. To investigate this, we studied 147 patients with endoscopically proven healed ulcers. These patients were randomized to receive either placebo, misoprostol 200 micrograms or misoprostol 300 micrograms four times daily, and clinical, personal, physiological and endoscopic characteristics were obtained prospectively. Endoscopy was performed at the active phase of the ulcer and when the ulcer healed. Biopsies were taken from the antrum to assess histologically for: (1) the activity of gastritis as assessed by the degree of polymorph infiltration, (2) the degree of chronic inflammation by the degree of chronic inflammatory cells infiltration and degree of mucosal degeneration, and (3) bacteriologically for the presence of H. pylori. The severity of the gastritis and the bacterial density were graded independently by two pathologists. The patients were assessed at two-month intervals for 12 months or until the ulcer relapsed. The results demonstrated that the relapse rates of duodenal ulcer were similar in the three treatment groups. The relapse rate was higher in the group with higher density of the bacteria (P less than 0.05). The degree of gastritis did not affect the relapse rate of duodenal ulcer in either the placebo or misoprostol group or in all patients combined. Stepwise logistic regression analysis identified that increased duodenal inflammation, male sex, early-onset disease, and H. pylori adversely affected relapse of the ulcer. We conclude that multiple factors affect the relapse of duodenal ulcer and H. pylori is one of them.

Adult↗
PubMed1981

Serum gastrin and the family environment in duodenal ulcer disease.

The study investigated the relationships between specific demographic, psychosocial, and physiological variables and the severity of duodenal ulcer disease in a population of patients with proved duodenal ulcer. Intercorrelations between psychosocial and physiological variables were also studied. The study design was cross sectional and retrospectively assessed life change units and DUD severity during the previous 6 months in 39 male ulcer clinic outpatients. Anxiety, depression, life change units, the family environment, ABO blood type, secretor status, serum pepsinogen, and serum fasting gastrin were evaluated. A DUD severity score was calculated from self-reported ulcer pain symptoms and ulcer complications. Gastrin levels correlated significantly with three Family Environment Scale (FES) subscales, including: (a) independence, (b) achievement orientation, and (c) expressiveness. Duodenal ulcer disease severity scores correlated with Zung SDS scores, but not with state or trait anxiety, life change units, or the FES.

Achievement↗
PubMed1992

Spontaneous nonfistulous barium reflux into the biliary tract: association with duodenal ulcer disease. A report of four cases.

Reflux of barium into the bile duct system during a barium study of the upper gastrointestinal tract is rare in the absence of spontaneous or postoperative fistula. We report four patients, three men and one woman, who had such reflux, associated with active duodenal ulcer disease, shown at radiologic and endoscopic investigation. Reflux of gastrointestinal contents into the biliary tract can result from peptic ulcer disease with duodenal involvement. The finding does not necessarily imply fistulous communication, ulcer perforation, or surgical emergency.

Adult↗
PubMed1982

Duodenal ulcer disease in the hospitalized elderly patient.

The clinical presentation, hospital course, and outcome of duodenal ulcer disease in elderly patients were reviewed from the records of 168 patient admitted to a municipal hospital over a three-year period. All patients had an active duodenal ulcer confirmed by either endoscopy and/or surgery. Patients were separated into one of two groups: an elderly patients group (greater than or equal to 60) and a young group (less than 60). The demographics, past clinical history, symptomatology, physical examination features, admitting laboratory data, hospital course, and outcome of these groups were compared. The elderly group, while having the same duration of acid peptic disease, had significantly less complaints of epigastric pain just prior to admission (P = 0.01) and less alcohol usage (P = 0.03) when compared to the younger patient population. The older patient population on the other hand did have a more complicated course of acute disease characterized by a greater rebleeding (P = 0.004), larger transfusion requirement (P = 0.03), and a more prolonged stay of hospitalization with a higher mortality (P = 0.003).

Adult↗
PubMed1989

The potential impact of Campylobacter pylori on the treatment of duodenal ulcer disease.

In most studies the association between Campylobacter pylori infection, Type B gastritis and duodenal and gastric ulceration is extremely strong. The best evidence for it having an aetiological role is at present in Type B gastritis. It should be remembered, however, that serological studies show carriage of the organism to be common also in the general population. An attempt is made here to gain some idea of the clinical impact of C. pylori infection in duodenal ulcer disease by analysing clinical trials, and in particular relapse data, in which an agent which suppresses C. pylori is used (colloidal bismuth subcitrate) and compared with one which does not (an H2-receptor antagonist). A mathematical model based on the data from these studies predicts that the prevalence of active duodenal ulceration will be twice as common in a group of subjects treated repeatedly upon relapse with an H2-receptor antagonist as in a group treated with colloidal bismuth. Other possible mechanisms are discussed but the ability of bismuth to suppress C. pylori infection is perhaps the best available explanation at present. Early data from several centres suggest that patients who can be rendered C. pylori negative over a prolonged period of time are relatively immune from relapse of their duodenal ulcers. If confirmed this observation may well transform the long-term management of duodenal ulcer disease.

Anti-Ulcer Agents↗
PubMed1979

Genetic heterogeneity of hyperpepsinogenemic I and normopepsinogenemic I duodenal ulcer disease.

In a search for a genetic marker of duodenal ulcer, we measured serum pepsinogen I levels in 168 ulcer patients and 151 of their clinically normal siblings. The ulcer patients tended to have either hyperpepsinogenemia I (pepsinogen I, greater than or equal to 100 ng/mL) or a normal level on a familial basis. Further evidence supporting this separation was the finding that the mean serum pepsinogen I level in the clinically normal siblings of the hyperpepsinogenemic patients was 91.2 ng/mL, significantly higher than the mean level (63.1 ng/mL) in the normal siblings of the normopepsinogenemic I patients. In the hyperpepsinogenemic I families the results of segregation analysis of an elevated pepsinogen I were consistent with autosomal-dominant inheritance of this trait. The genetic basis of normopepsinogenemic I duodenal ulcer was also shown by the familial aggregation of this disorder. These data provide direct evidence for genetic heterogeneity of duodenal ulcer disease.

ABO Blood-Group System↗
PubMed1997

Clarification of the link between polyunsaturated fatty acids and Helicobacter pylori-associated duodenal ulcer disease: a dietary intervention study.

Epidemiological evidence has suggested that the declining prevalence of duodenal ulcer disease may be attributable to rising consumption of polyunsaturated fatty acids, a hypothesis supported by in vitro evidence of toxicity of such substances to Helicobacter pylori. The objective of the present study was to establish whether this association is causal. Forty patients with proven infection with H. pylori and endoscopic evidence of past or present duodenal ulcer disease were randomized to receive either polyunsaturated fatty acids (PUFA group), in the form of capsules and margarine, or a placebo (control). Both groups received concurrent H2 antagonist therapy. Efficacy of therapy was determined endoscopically by assessment of ulcer healing while H. pylori status was determined by antral biopsy, urease (EC 3.5.1.5) culture and histological assessment of the severity of H. pylori infection. Antral levels of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) were quantified. Compliance was monitored. Before treatment, both groups were comparable for severity of H. pylori infection, smoking status and levels of LTB4 and PGE2. Despite a significant difference in consumption of linoleic acid (19.9 (SE 1.6) g for PUFA group v. 6.7 (SE 0.8) g for controls (P < 0.01) and linolenic acid (2.6 (SE 0.2) g v. 0.6 (SE 0.03) g (P < 0.01) there was no significant change in either the severity of H. pylori infection or prostaglandin levels in either group at 6 weeks. Consumption of a considerable amount of PUFA does not inhibit the colonization of the stomach by H. pylori nor does this alter the inflammatory changes characteristic of H. pylori gastritis. We conclude that the association between duodenal ulceration and a low level of dietary PUFA is likely to be spurious, probably reflecting the effect of confounding factors such as affluence, social class or smoking.

Combined Modality Therapy↗
PubMed1993

[Oral triple therapy for eradication of Helicobacter pylori in duodenal ulcer disease].

25 patients with Helicobacter pylori-associated active duodenal ulcer disease (bleeding: n = 5, penetrating: n = 1, stenosis of the bulb: n = 4, frequent ulcer relapse: n = 18) were treated with 3 x 600 mg bismuth subsalicylate (BSS), 3 x 400 mg metronidazole and 3 x 500 mg tetracycline in addition to 300 mg ranitidine. 23 out of 25 patients (92%) proved to be Helicobacter pylori-negative four weeks after cessation of study medication as judged from negative urease test, specific culture and histology after modified Giemsa staining. 24/25 ulcers (96%) had healed after six weeks. In one patient on NSAIDs a small duodenal ulcer was detected on the final endoscopic examination despite successful Helicobacter pylori eradication. Twelve out of 25 (48%) patients complained side effects that did not lead to discontinuation of therapy. In conclusion, oral triple therapy with BSS, metronidazole and tetracycline is highly effective in Helicobacter pylori eradication, but there was a rather high rate of more or less serious side effects, diminishing the attractiveness of this therapeutic regimen.

Administration, Oral↗
PubMed1978

Prophylactic effect of cimetidine in duodenal ulcer disease.

Fifty-seven symptom-free patients with duodenal ulcer entered a double-blind trial to assess the prophylactic effect of cimetidine. Patients were randomly allocated to receive cimetidine 400 mg twice daily (29 patients) or placebo (28 patients). The trial was designed to imitate daily clinical practice, so duodenal ulcer disease was diagnosed by means of x-ray examination. Three patients from each group withdrew from the trial. All remaining patients continued to receive treatment for 12 months or until symptoms recurred. Three out of 26 patients suffered relapses during cimetidine treatment, compared with 20 out of 25 receiving placebo. No side effects were attributable to cimetidine. Long-term cimetidine treatment had no curative effect as relapses occurred soon after treatment was stopped. The estimated chance (cumulative remission rate +/- 2 SE) of remaining symptom-free 13 weeks after one year's cimetidine treatment had been completed was 47 +/- 21%. Maintenance treatment with cimetidine is a suitable alternative to elective in surgery in patients with duodenal ulcer subjects frequent relapses. Further study is needed to establish the optimal duration and safety of prolonged cimetidine treatment.

Adult↗
PubMed1979

Long-term cimetidine in duodenal ulcer disease.

Forty patients with chronic duodenal ulcer who had healed endoscopically with a 6-week course of cimetidine were randomized double blind to 1 year of either placebo or cimetidine tablets 400 mg bid (20 patients in each group). Patients were seen at monthly intervals, and endoscopy was performed at clinical relapse or on completion of 1 year. One of 20 patients on active cimetidine relapsed clinically and endoscopically at 3 months; 16 of 20 patients on placebo relapsed clinically and endoscopically within 9 months, the majority within 3 months, and 2 were shown to have asymptomatic chronic ulcers at routine 12-month endoscopy. None of the 19 patients on active cimetidine routinely endoscoped at 12 months showed evidence of ulceration. This study confirms a high relapse rate when short-term cimetidine is ceased and indicates that maintenance treatment with cimetidine prevents relapse.

Alcohol Drinking↗
PubMed1976

Vagal and hormonal influences on gastric secretion in duodenal ulcer disease.

Current concepts on the pathophysiology of gastric hypersecretion in duodenal ulcer disease have been presented and the role of vagal nerves and gastrointestinal hormones particularly gastrin has been discussed. Duodenal ulcer patients form a heterogenous group with regard to the gastric acid and pepsin secretion and gastrin release. They may differ from healthy subjects by several wall defined defects including an increased mass of parietal and peptic cells, increased capacity to secrete acid and pepsin, increased vagal drive to the parietal cells, hyperreactivity of antrum, decreased effectiveness of antral and duodenal autoregulatory mechanisms, defective release of secretin, increased gastric emptying and defective removal of gastric acid load from the duodenum. Very little is known what proportion of duodenal ulcer patients suffer from various pathologic disturbences and what are the mechanisms underlying these changes.

Animals↗
PubMed1994

Five-year maintenance treatment with ranitidine: effects on the natural history of duodenal ulcer disease.

In this study, we assessed the effect of a 5-yr maintenance program with ranitidine on the natural history of duodenal ulcer disease both during treatment and after drug withdrawal. Two groups of patients with duodenal ulcer were studied. In group A patients (n = 40), ranitidine (150 mg/day) was given continuously for 5 yr; group B patients (n = 40), received seasonal, 8-wk prophylactic treatment with ranitidine (300 mg/day), in spring and fall. Routine endoscopy was performed every year and whenever ulcer symptoms recurred. After the 5-yr study, the drug was discontinued in both groups, and patients underwent endoscopy after 3, 6, 12, and 18 months. The probability of duodenal ulcer recurrence was significantly lower in patients continuously receiving ranitidine (p < 0.001), and ulcer complications were significantly lesser in group A patients (p < 0.03). In the 18 months of follow-up after drug discontinuation, only 15% (4/26) of patients of group A relapsed, whereas ulcer recurrence was diagnosed in 84% (26/32) of group B patients (p < 0.001). We conclude that low-dose continuous treatment with ranitidine is preferable to seasonal prophylaxis for its ability to modify the natural history of duodenal ulcer disease.

Adult↗
PubMed2003

[Association between Helicobacter pylori virulence and duodenal ulcer disease in patients from Hong Kong in China].

OBJECTIVE: A number of putative virulence factors have been postulated to be relevant to the clinical outcome of Helicobacter pylori infection based on strains identified in the western countries. The aim of this study was to investigate the association between genotypes of vacA, cagA and iceA and duodenal ulcer disease in patients from Hong Kong. METHODS: Seventy-two dyspeptic patients with or without duodenal ulcer disease, with proven H.pylori infection, were studied. Gastric biopsy specimens were analyzed by specific polymerase chain reaction and Southern blot to determine the genotypes of these virulence factors. RESULTS: Except 6 (8.3%) cases with evidence of multiple infections, all of the remaining 66 cases had vacA signal sequence s1 type strains. Twenty-seven (90%) of the 30 cases with duodenal ulcers were infected with cagA-positive strains, compared with 32 (88.9%) of 36 with non-ulcer dyspepsia (P > 0.05). Similarly, vacA middle region sequences were detected with no significant difference in the two groups, 9 (30.0%) versus 13 (36.1%) for m1b and 21 (70.0%) versus 23 (63.9%) for m2 type. IceA1 subtype was detected in the same frequency in 42 (63.6%) of the 66 cases. Neither cagA nor vacA and iceA were associated with duodenal ulcer disease. CONCLUSION: No clear differences were found in the distribution of cagA, vacA and iceA genotypes among patients with duodenal ulcer or non-ulcer dyspepsia. The association of these virulence genes and duodenal ulcer disease needs reappraisal, particularly under geographic considerations.

Antigens, Bacterial↗
PubMed1994

Medium- and high-dose omeprazole plus amoxicillin for eradication of Helicobacter pylori in duodenal ulcer disease.

The purpose of the present study was to investigate the Helicobacter pylori eradication potency of combined amoxicillin-omeprazole treatment in patients with duodenal ulcer disease and to compare the efficacy of two omeprazole and amoxicillin doses concerning H. pylori eradication, ulcer healing, pain relief, and safety. Ninety patients with active H. pylori-positive (culture and/or histology) duodenal ulcer disease were randomly treated with either omeprazole 20 mg twice a day plus amoxicillin 1 g twice a day (group I, N = 30), omeprazole 40 mg twice a day plus amoxicillin 1 g twice a day (group II, N = 30), or omeprazole 40 mg twice a day plus amoxicillin 1 g three times a day (group III, N = 30) over two weeks, followed by ranitidine at bedtime for another four weeks. The overall proportion of H. pylori eradication was 83% and of ulcer healing 92% without statistically significant differences between the study groups. Complete pain relief occurred after a median of one day in all groups. Six patients complained of side effects during the therapy phase, which led to therapy discontinuation in one female patient. In conclusion, omeprazole plus amoxicillin is a highly effective and well-tolerated therapy regimen to eradicate H. pylori in duodenal ulcer disease. In addition, the results suggest that there is no clear dose-response relation between the dosages of omeprazole and amoxicillin used in this study on the one hand and the H. pylori eradication rates on the other.

Adult↗