Duodenal Ulcer Healing Research Articles

Clinical significance of Helicobacter infection in children.

Helicobacter pylori infection of the gastric mucosa causes chronic gastritis and is associated with peptic ulcer disease and gastric carcinoma. These are conditions which usually occur in adult life. However, H. pylori is an infection which is mainly acquired in childhood. The overall prevalence of H. pylori in children is 10% in developed countries but can be as high as 30-40% in children from lower socio-economic groups. In developing countries, the prevalence of H. pylori in children ranges from 80-100%. H. pylori gastritis does not appear to be associated with symptoms in children in the absence of duodenal ulcer disease. H. pylori infection is present in the vast majority of children with duodenal ulcer disease and, as in adults, eradication of the organism results in long-term healing of duodenal ulceration. H. pylori infection acquired in childhood is now considered to be a significant risk factor for the development of gastric carcinoma. The World Health Organization has classified H. pylori as a Group 1 carcinogen. Specific epidemiological questions which need to be answered in children include the age at which infection is acquired, specific risk factors for infection, the mode of transmission and the risk of reinfection following treatment. Recently, a one week treatment regimen using colloidal bismuth subcitrate, metronidazole and clarithromycin has been shown to be effective in treating children, but compliance is important. Currently there are no guidelines on the need to treat children and a consensus is urgently required on this issue.

DOES SMOKING INFLUENCE THE ERADICATION OF HELICOBACTER PYLORI AND DUODENAL ULCER HEALING WITH DIFFERENT REGIMENS?

SUMMARYTo determine the effect of smoking on Helicobacter pylori eradication and ulcer healing, we investigated 232 patients with H. pylori‐positive duodenal ulcer. Patients were given one of seven different treatment protocols and divided into three groups according to smoking habits. Group 1 (n=128) consisted of non‐smokers, group 2 (n=65) of mild smokers (5‐20 cigarettes/day) and group 3 (n=39) of heavy smokers (>20/day). The eradication of H. pylori and ulcer healing rate was controlled eight weeks later after ceasing the therapy. The overall eradication rate was 66% in all patients and 68%, 66%, 59% in each group, respectively. The eradication rates showed no statistical difference between groups. Complete ulcer healing was achieved in 84% of all patients and ulcer healing rate between groups did not show any significance (85%, 83% and 82% respectively). These results suggest that smoking status does not influence the eradication of H. pylori and duodenal ulcer healing rates at eight weeks in patients on different treatment schedules.

Prevention of ulcer recurrence after eradication of Helicobacter pylori: A prospective long-term follow-up study

BACKGROUND & AIMS: Short-term follow-up studies show lower relapse rates of duodenal and gastric ulcers after successful Helicobacter pylori eradication. The aim of this study was to determine the long- term outcome of ulcer disease after successful H. pylori eradication.METHODS: We prospectively studied the long-term effect of H. pylori eradication on ulcer recurrence rates in patients after endoscopically proven healing of duodenal or gastric ulcers between 1984 and 1995. Patients using nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, or maintenance antisecretory therapy were excluded. H. pylori infection was assessed by culture and histopathology of gastric biopsy specimens. After endoscopically proven ulcer healing and successful H. pylori eradication, 186 patients with ulcers underwent elective endoscopy every 3 months during the first year of follow-up and were advised to contact us at symptom recurrence. Thereafter, 96 patients were available for elective half-yearly endoscopies. The 89 patients who did not choose to undergo the repeated endoscopies were asked about symptom recurrence and to undergo elective endoscopy in 1995.RESULTS: Successful H. pylori eradication was achieved in 141 patients with duodenal ulcers and 45 patients with gastric ulcers. None of the 141 H. pylori-eradicated patients with duodenal ulcers had an ulcer relapse after follow-up of 367 patient-years. Ulcer relapses were also absent in the 45 H. pylori-eradicated patients with gastric ulcers after 113 patient-years of follow-up.CONCLUSIONS: Excluding patients taking aspirin or NSAIDs, recurrence of duodenal or gastric ulcers is completely prevented after successful H. pylori eradication for up to 9.8 years.(Gastroenterology 1997 Oct;113(4):1082-6)

High eradication rate of Helicobacter pylori using a four-drug regimen in patients previously treated unsuccessfully

The objective of this study was to assess the efficacy of a new regimen in eradicating Helicobacter pylori (Hp) in patients with duodenal ulcer (DU) who were previously treated unsuccessfully with standard triple therapy (tripotassium dicitratobismuthate [TDB] 120 mg QID, metronidazole 500 mg TID, and tetracycline 500 mg QID) or proton-pump inhibitor (PPI) dual therapy (omeprazole 20 mg BID and amoxicillin 500 mg QID). The study included 133 consecutive patients aged 17 to 83 years with endoscopically diagnosed DU (diameter ≥5 mm) in whom standard triple therapy or PPI dual therapy had failed to eradicate Hp. A rapid urease (CLO) test was performed on four biopsy specimens at study entry and at least 1 month after the end of treatment to confirm Hp colonization and eradication, respectively. Patients were considered to be Hp positive if any CLO test was positive within 2 hours, and Hp was considered to be eradicated if all CLO tests were still negative after 24 hours. In 31 randomly selected patients, Hp eradication was confirmed histologically as well. Patients were given omeprazole 60 mg/d (20 mg in the morning and 40 mg in the evening) plus amoxicillin 500 mg QID for 10 days and subsequently were given metronidazole 500 mg TID for 10 days plus TDB 120 mg QID for 6 weeks. One hundred and twenty-four patients were followed up; five (4%) withdrew because of side effects (protracted diarrhea, stomatitis, skin rashes). Per-protocol analysis showed Hp eradication in 113 of 119 patients (95%) and ulcer healing in 118 of 119 (99%). Intent-to-treat analysis showed an Hp eradication rate of 85% (113 of 133 patients) and an ulcer healing rate of 89% (118 of 133 patients). In per-therapy analysis, the Hp eradication rate was 91% (113 of 124 patients), and the ulcer healing rate was 95% (118 of 124 patients). Side effects were observed in 39 of 119 patients (33%) and were generally mild. The four-drug regimen used in this study, when given to patients previously treated unsuccessfully with standard triple therapy or PPI dual therapy, was highly effective in eradicating Hp and healing DUs and had no major side effects.

Ranitidine bismuth citrate with clarithromycin for the treatment of duodenal ulcer

Background/Aims—To investigate the effect of the new Helicobacter pylori eradication regimen, ranitidine bismuth citrate (RBC) and clarithromycin (CLAR) dual therapy, on duodenal ulcer healing and absence of ulcer recurrence during...

Does treatment of Helicobacter pylori with antibiotics alone heal duodenal ulcer? A randomised double blind placebo controlled study.

BACKGROUND: Treatment of Helicobacter pylori infection prevents duodenal ulcer relapse. It has not been established if treatment of the infection heals duodenal ulcer. AIM: To test the hypothesis that treatment...

Healing of duodenal ulcer after eradication of Helicobacter heilmannii

Helicobacter pylori is the main cause of duodenal ulcer, and eradication of this organism leads to ulcer healing and prevents relapse. We describe successful healing of duodenal ulcer after eradication of another Helicobacter spp, H heilmannii.

Unhealed Duodenal Ulcers despite Helicobacter pylori Eradication

Background: Our aims were 1) to study the influence of several factors (age, sex, smoking, previous ulcer disease, ulcer size, chronic gastritis, serum gastrin and pepsinogen I levels, therapy regimen and, especially, eradication of Helicobacter pylori) on duodenal ulcer healing; 2) to evaluate the frequency of duodenal ulcer healing failure despite eradication of H. pylori, to study why this failure occurs, and to verify its evolution without antisecretory therapy; and 3) to confirm whether a week's prescription of omeprazole is sufficient to obtain ulcer healing. Methods: Three-hundred and eight patients (mean age, 45 ± 13 years; 71% males) with duodenal ulcer and H. pylori infection were studied prospectively. Biopsy specimens were obtained at initial endoscopy, and serum gastrin and pepsinogen I levels were measured. A repeat endoscopy (with biopsies) was performed 1 month after eradication therapy had been completed, and a 3C-urea breath test was also carried out. Three eradication therapies were used: omeprazole plus amoxycillin for 2 weeks (OA group, n = 61); 'classic' triple therapy (with bismuth; CTT group, n = 65); and 'new' triple therapies for 1 week (NTT group, n = 182): omeprazole plus two of the following antibiotics: clarithromycin, metronidazole, and amoxycillin. When the ulcer did not heal despite successful H. pylori eradication, antacids were prescribed on an as-needed basis, and endoscopy was repeated 1 month later (2nd control endoscopy). If the ulcer was still present, the acid output (basal and pentagastrin-stimulated) was measured, a secretin test was performed, and a final endoscopy (3rd control endoscopy) was carried out after an additional month. The statistical method used was multiple logistic regression. Results: Overall eradication was achieved in 69% (n = 212) of the patients, and ulcer healing in 76% (n = 233): 57% in the OA group, 80% in the CTT group, and 81% in the NTT group (P < 0.01 when comparing the OA group with the others). Ulcer healing was achieved in 90% of H. py/o/v'-eradicated patients and in only 45% of patients with eradication therapy failure (P < 0.001). Similar results were obtained when only patients treated with NTT were considered: ulcer healing in 90% of patients with the organism eradicated. Eradication of H. pylori (odds ratio (OR), 11.8; 95% confidence interval (Cl), 6.3–22) and sex (OR, 2.5; 95% Cl, 1.2–5.1) were the only variables that correlated with ulcer healing in the multivariate analysis. The ulcer persisted despite successful eradication of H. pylori in 22 patients. The duodenal ulcer had healed spontaneously in 73% of these patients at the 2nd control endoscopy. Finally, by the 3rd control endoscopy, only three patients still had duodenal ulcer. Therefore, ulcer healing was finally achieved in 98.1% (95–99%) of patients in whom H. pylori was eradicated. Gastrin, pepsinogen I, acid output, and the secretin test had normal values in all patients. Conclusions: Eradication of H. pylori favours ulcer healing, which is achieved in most patients in whom the organism is eradicated. Just 1 week of omeprazole therapy (that is, the antibiotic administration period in the new triple therapies) is enough to obtain a high ulcer healing rate. Most duodenal ulcers that do not heal initially despite H. pylori eradication will ultimately do so after several weeks without additional therapy.

Effectiveness of ranitidine 150 mg at bedtime as maintenance therapy for healed gastric ulcers

As many as 89% of gastric ulcer patients experience ulcer recurrences within 1 year of successful healing with conventional antiulcer therapies. Because ranitidine is effective in the healing of gastric and duodenal ulcers and the maintenance of healed duodenal ulcers, we hypothesized that ranitidine would also be effective in the maintenance of healed gastric ulcers. A 48-week, placebo-controlled, randomized, double-blind, multicenter trial was conducted to compare ranitidine 150 mg administered at bedtime with placebo for the maintenance of healed gastric ulcers. Endoscopies were performed at baseline and repeated after 12, 24, 36, and 48 weeks of treatment. Gastric ulcer recurrence rates at each scheduled endoscopy were significantly lower in patients receiving ranitidine (5%, 13%, 16%, and 19%, respectively) compared with those receiving placebo (20%, 30%, 40%, and 50%, respectively). Compared with placebo, ranitidine was more effective in maintaining healed gastric ulcers regardless of previous gastric ulcer history, smoking status, age (<65 vs ≥ 65 years), or sex. There were no significant differences between the two treatment groups in the number of patients experiencing adverse events or laboratory abnormalities. Ranitidine 150 mg administered at bedtime provides safe and effective treatment for the maintenance of healed gastric ulcers.

Elisa and western blot studies with basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) in experimental duodenal ulceration and healing

Time-dependent changes of duodenal and gastric mucosal levels of bFGF and PDGF were examined in rats after oral administration of the duodenal ulcerogen cysteamine-HC1. The animals were killed at 12 h, 24 h, 48 h, 7 days or 14 days after the first dose of cysteamine and the duodenal ulcers were evaluated. The gastric and duodenal mucosa was scraped and homogenized for Western blot and ELISA studies. The ulcer formation was macroscopically detectable at 12 h while the largest ulcers were seen at 48 h. In parallel, the duodenal mucosal concentration of bFGF increased at 12 and 24 h and reached its maximum at 48 h, while the PDGF concentration was slightly elevated at 12 and 48 h, and a more than 3-fold peak was seen at 24 h. The gastric mucosal level of bFGF and PDGF did not change during the development and healing of duodenal ulcers.

Abundance of surfactant-like particles reflects mucosal integrity in patients with peptic ulcer disease.

Surfactant-like particles, normal products of the human enterocyte, are released into the lumen and secreted into blood. To assess their role as markers for mucosal functional integrity, this study examined their content in biopsy specimens and serum of patients with duodenal ulcer disease, compared with non-diseased control subjects. Endoscopic biopsy specimens were taken 1-2 cm from areas of active inflammation or ulcer (peptic ulcer patients) or just beyond the duodenal bulb (normals) in 35 consecutive subjects. After staining for phospholipid, extracellular and intracellular particles were counted on transmission electron micrographs of coded specimens. Serum was obtained from 24 patients, and densitometry of the 59 kDa band detected on western blot by antiserum against human jejunal particle was measured. Normal duodenum (n = 15) contained more particles (44 (4.7)) particles/block, mean (SD) than active duodenal ulcer (n = 13, 17 (3.9)) or gastritis/duodenitis patients (n = 4, 9 (2.7)). Three patients examined after healing of duodenal ulcers showed abundant particles (n = 3, 67 (2.2)). Similarly, the 59 kDa band was decreased in serum of patients with active peptic ulcer disease (n = 11, 0.25 (0.04) absorbance units) compared with normal patients (n = 10, 0.40 (0.03)) or healed ulcers (n = 3, 0.62 (0.04)). There was good correlation between morphological mucosal particle abundance and particle protein content of serum assayed from the same patients (r = 0.831). These changes were independent of Helicobacter pylori status. The mucosal and serum content of surfactant-like particles may reflect general mucosal integrity of the enterocytes from which they are derived.

Effect of Omeprazole Therapy on the Survival of Helicobacter pylori, Urease Activity, and Antral Gastric Histology in Patients with Duodenal Ulcer

Helicobacter pylori is associated with chronic active gastritis and peptic ulceration (PU). Omeprazole is a proton pump inhibitor that is effective in healing PU and reducing gastritis. Previously it has been found that omeprazole has some bacteriostatic activity against H. pylori both in vitro and in vivo and in inhibiting urease activity in vitro. Our aim was to evaluate the effect of omeprazole on H. pylori colonization of the gastric mucosa, urease activity in vivo, and the presence of associated gastritis in patients with duodenal ulcer (DU). We studied 12 patients (7 men and 5 women, ages 22-68 yr) with Du larger than 5 mm in diameter with a positive CLOtest (Delta West Ltd., Australia). Omeprazole, 20 mg bid, was given for 8 weeks to each patient, patients were endoscoped at the end of this period to check for healing of DU, and repeat biopsies were obtained from the gastric antrum for histological analysis, CLOtest, and culture. DU healed completely in all patients. Likewise in all patients there was significant reduction in the urease activity, from 22.1 +/- 4.17 to 1.58 +/- 0.92 units/ml (p < .001; 95% confidence interval of the difference between means, 32.7-14.1), and reduced H. pylori density, from 1,403.46 +/- 128.23 to 422.5 +/- 172.39 colony-forming units (CFU) per milligram of tissue biopsy (p < .001; 95% confidence interval of the difference between means, 1,486.1-590.5). The numbers of H. pylori were reduced on the gastric mucosa after omeprazole therapy and disappeared in six patients, a result that correlated with a negative CLOtest reading after 24 hours. Omeprazole, 20 mg bid, is capable of reducing H. pylori numbers and urease activity in vivo. There was no significant reduction in the severity of antral gastritis in DU patients studied.

Detection ofHelicobacter pylori by polymerase chain reaction assay using gastric biopsy specimens taken for CLOtest

The concordance rate between a rapid urease test (CLOtest) and polymerase chain reaction (PCR) assay for the detection of Helicobacter pylori in gastric biopsy samples was investigated. To avoid the bias produced by patchy distribution of the organism in the stomach, the samples used for these two tests were not obtained from two different sites of the antrum. Instead, the PCR assay was performed with the the same biopsy sample that was taken for the CLOtest. Among 82 biopsy samples included for this study, 56 were positive and 26 were negative by CLOtest. Of the 56 CLOtest-positive samples, 52 (93%) were also positive by PCR assay, and of the 26 CLOtest-negative samples, 20 (78%) were negative by PCR assay. The total concordance rate of these two tests was 87.6%. Of the 4 cases with CLOtest-positive and PCR-negative results, 3 had been treated with long-term H2 blockers. Of the 6 patients with CLOtest-negative and PCR-positive results, 4 suffered from recurrent or poorly healing duodenal ulcers. Interestingly, a significantly lower density of the PCR products was observed during electrophoresis analysis for all the 6 cases, presumably due to a small number of H. pylori in these samples. These results indicated that PCR might be used as a complementary assay for CLOtest. False negative results by CLOtest might occur when only a small amount of H. pylori was present in the samples, which could be detected by subsequent PCR assays using the same biopsy specimens. The clinical significance of such CLOtest-negative and PCR-positive cases requires further study.

Eradication of Helicobacter pylori infection.

Helicobacter pylori is probably the most common bacterial infection worldwide and the accepted cause of chronic active gastritis. It has a critical role in duodenal ulcer, where the prevalence of infection is 90-95%. There is a dramatic reduction in the rate of ulcer recurrence after successful eradication of the organism to about 4% per annum compared with up to 80% when the infection persists. What is true for duodenal ulcers is also true for patients with gastric ulcer who are infected with H. pylori. The risk of recurrent ulcer complications with bleeding is virtually abolished following successful eradication of H. pylori; in contrast, the risk of rebleeding is about 33% in patients still harboring the organism. The treatment of H. pylori infection in patients with confirmed peptic ulcer on first presentation or recurrence has been advocated by a Consensus Conference of the National Institutes of Health. The most evaluated regimens include dual therapy with a proton pump inhibitor and either amoxicillin or clarithromycin, and bismuth-based triple therapy with metronidazole and tetracycline. The use of a proton pump inhibitor-containing regimen offers the advantage of rapid symptom relief and the highest rates of duodenal ulcer healing. Moreover, combinations of a proton pump inhibitor and clarithromycin show more predictable and higher eradication rates than amoxicillin combinations. Newer triple therapies with a proton pump inhibitor plus two antibacterial agents given for 7-1O days are being increasingly described and may become the treatment of choice if initial results are confirmed. However, the optimum dosage regimen needs to be established. A new combination of ranitidine bismuth citrate and clarithromycin has also recently been shown to be effective. At this time it is reasonable to consider all patients with confirmed duodenal or gastric ulcer for eradication of H. pylori, and no patient should be considered for elective surgery without first being offered eradication therapy.

Treatment of patients with duodenal ulcer positive for helicobacter pylori infection: ranitidine or omeprazole associated with colloidal bismuth subcitrate plus amoxicillin

This study evaluated treatment of patients affected with duodenal ulcer positive for Helicobacter pylori. We compared patients treated with ranitidine plus amoxicillin plus colloidal bismuth subcitrate (n = 20) with patients treated with omeprazole plus amoxicillin plus colloidal bismuth subcitrate (n = 20) with regard to: (1) healing of duodenal ulcer; (2) eradication of H pylori; and (3) recurrence of ulcer. Baseline and follow-up for 24 months were performed through clinical, laboratory, and endoscopic tests. The ulcer healing rate was 95% in the ranitidine group and 100% in the omeprazole group; the H pylori eradication rate was 90% and 95%, respectively. During follow-up, only 3 patients (16%) in the ranitidine group and 2 patients (10%) in the omeprazole group had recurrence of duodenal ulcer; only 1 patient in each group showed reinfection with H pylori. In conclusion, there were no statistically significant differences between treatment with ranitidine or omeprazole, with regard to ulcer healing rate, eradication of H pylori, or recurrence of duodenal ulcer.

Basic fibroblast growth factor and PDGF in GI diseases

This chapter is focused on the relatively recent investigations demonstrating a pharmacological and pathophysiological role for bFGF and PDGF in ulcerative and inflammatory lesions in the upper and lower GI tract. Our initial animal model experiment revealed a potent healing of chronic cysteamine-induced duodenal ulcer in rats treated by intragastric administration of bFGF-w, the acid-resistant bFGF-CS23 or PDGF-BB without decreasing gastric acid secretion or concentration. Subsequently we and others have demonstrated that these peptides accelerate the healing of chronic gastric ulcers, chronic erosive gastritis and ulcerative colitis. Contrary to the potent ulcer healing properties of bFGF and PDGF, these growth factors exert no or modest acute gastroprotection. Nevertheless, new biochemical, molecular biological and immunohistochemical studies indicate that both bFGF and PDGF play a pathophysiological role in the natural history of ulcer healing.

Psychologic predictors of duodenal ulcer healing.

We investigated psychologic influences on duodenal ulcer by examining the effect of personality, stress, and mood, measured at diagnosis, on subsequent ulcer healing. Stressful life events, psychopathology (assessed using the Minnesota Multiphasic Personality Inventory), anxiety, depression, smoking, alcohol consumption, nonsteroidal antiinflammatory drug use, and serum pepsinogen I levels were determined immediately after endoscopy showed duodenal ulcer craters in 70 patients with recent onset of symptoms. Endoscopy was repeated following 6 weeks of ranitidine therapy. Six ulcers (8.6%) persisted, and the duodenum remained inflamed in an additional five cases, for a total of 16% with incomplete healing. The only baseline characteristic significantly associated with poor healing was anxiety (p = 0.03 for ulcer persistence, p = 0.02 for incomplete healing). Being in the highest anxiety tertile was associated with a more than fourfold elevation in the risk of incomplete healing (p = 0.02). The association between anxiety and poor healing was not changed by modification of the anxiety score to eliminate gastrointestinal symptom items or by adjustment for serum pepsinogen, sex, or cigarette smoking. Anxiety inhibits the healing of duodenal ulcers treated with adequate antisecretory therapy.

Sucralfate suppresses Helicobacter pylori infection and reduces gastric acid secretion by 50% in patients with duodenal ulcer

BACKGROUND & AIMS: The mechanism(s) by which sucralfate heals duodenal ulcers remains unclear. The aim of this study was to determine the effect of sucralfate on Helicobacter pylori infection and on the accompanying hypersecretion of gastric acid the infection induces in patients with duodenal ulcer. METHODS: Basal and gastrin-releasing peptide (GRP) stimulated gastrin release and acid secretion. H. pylori density, gastric urease activity, and severity of gastritis were studied in patients with duodenal ulcer who were positive for H. pylori before, during, and after 4 weeks' treatment with sucralfate (2 g twice daily). RESULTS: The density of H. pylori decreased by 70% during sucralfate treatment and returned to the pretreatment level after discontinuation of therapy. This suppression of H. pylori infection was accompanied by an 80% decrease in gastric urease activity. GRP- stimulated plasma gastrin concentrations, GRP-stimulated acid output, and basal acid output all decreased by approximately 50% during sucralfate therapy and returned to pretreatment levels after treatment was discontinued. CONCLUSIONS: These findings indicate that sucralfate markedly suppresses H. pylori infection and the accompanying hypersecretion of acid the infection induces in patients with duodenal ulcer. These effects are likely to be important mechanisms by which the drug promotes duodenal ulcer healing. (Gastroenterology 1996 Mar;110(3):717-24)

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. (Gastroenterology 1996 Mar;110(3):705-16)

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.