Gastric acid inhibits antral phase III activity in duodenal ulcer patients

Fourteen patients with duodenal ulcers and eight healthy volunteers were examined to measure interdigestive gastroduodenal motility and plasma motilin. In order to study the effects of gastric acid on the gastroduodenal motility, 20 mg of famotidine was administered intravenously. The motility index of the gastric antrum and the duodenum, as well as the pH in the duodenal bulb were calculated. The duodenal pH was significantly lower and the gastric motility index was significantly weaker before the duodenal interdigestive migrating complex (IMC) in the ulcer patients than in the controls. Motilin levels increased before the duodenal IMC and decreased afterwards in both groups. Famotidine significantly increased the duodenal pH and the gastric motility index before the IMC, but no changes in the motilin level were noted. We conclude that duodenal ulcer patients have duodenal hyperacidity that results from increased inflow from the antrum and antral hypomotility during the gastric IMC and that these changes are normalized by the administration of famotidine. These results suggest that gastric acid inhibits antral contraction during the gastric IMC.     

Expression of trefoil peptides pS2 and human spasmolytic polypeptide in gastric metaplasia at the margin of duodenal ulcers.

Duodenal ulcers are associated with gastric metaplasia in the duodenum, both at the ulcer margin and at more distant sites in the duodenal bulb. pS2 and human spasmolytic polypeptide (hSP) are secretory peptides expressed in gastric epithelial cells and in gastric metaplasia. As these peptides may be important in ulcer healing, this study investigated the possibility that the expression of pS2 and hSP is increased in gastric metaplasia at the margin of duodenal ulcers. Duodenal bulb biopsy specimens from 12 duodenal ulcer patients were assessed. Sections were immunostained with monoclonal antibodies for pS2 and hSP. Cytoplasmic stain intensities were measured by an image analysis system and expressed as integrated optical density (IOD) units, In situ hybridisation for pS2 and hSP mRNA was carried out on parallel sections. Duodenal sections were also stained with diatase periodic acid Schiff/alcian blue to localise areas of gastric metaplasia. pS2 antigen staining in the duodenum was restricted to surface epithelial cells, and hSP to acinar and ductular components of Brunner's gland. mRNA localisation corresponded to immunostaining cells. In gastric metaplasia, pS2 expression was greater at the ulcer margin than away from the ulcer, as judged by the intensity of antibody staining (mean IOD units (SEM), 20.6 (3.3) v 9.5 (3.0); p < 0.001). There was a trend towards greater hSP staining at the ulcer margin but this did not achieve statistical significance. These findings support the putative role of pS2 and possible hSP in mucosal healing and providy further evidence for an autocrine 'ulcer-gastric metaplasia-repair' loop involving these trefoil peptides.     

Disturbed gastroduodenal motility in patients with active and healed duodenal ulceration

Disordered gastroduodenal motility may promote duodenal ulceration by allowing prolonged acid contact with the duodenal mucosa. Using a multilumen perfused catheter incorporating 3 pH microelectrodes, antral and duodenal pH and antropyloroduodenal pressure activity were recorded in 36 subjects (10 with healed duodenal ulceration, 11 with active duodenal ulceration, and 15 healthy volunteers) during fasting and after a radiolabeled solid test meal. Correct pH probe/catheter position was continuously verified by recording transmucosal potential difference across the pylorus. Patients with active and healed duodenal ulcer had similarly disordered gastroduodenal motility. The chief abnormalities consisted of an increase in postprandial duodenal retroperistalsis (healed duodenal ulceration, 12 +/- 1 events per hour; active duodenal ulceration, 12 +/- 1; control, 6 +/- 1; mean +/- SEM: healed and active duodenal ulceration vs. control, P = 0.004 and P = 0.03, respectively), a reduction in pressure waves sweeping aborally through the duodenum after the meal (healed duodenal ulceration, 22 +/- 4 events per hour; active duodenal ulceration, 23 +/- 3; control, 34 +/- 4: healed and active duodenal ulceration vs. control, P = 0.04 and P less than 0.05, respectively), and an increased incidence of atypical, complex forms of coordinated duodenal motor activity throughout the study (postprandial data; healed duodenal ulceration, 8 +/- 1 events per hour; active duodenal ulceration, 10 +/- 1; control, 4 +/- 1: healed and active duodenal ulceration vs. control, P = 0.02 and P less than 0.02, respectively). In addition, gastric emptying of the solid test meal was significantly delayed in healed, but not active, duodenal ulceration [half-emptying time, healed duodenal ulceration 185 minutes (117-235); active duodenal ulceration 102 minutes (80-200); control 107 minutes (78-130): healed duodenal ulceration vs. control, P less than 0.009]. Duodenal bulb pH was similar in controls and patients with active duodenal ulceration; however, bulb pH was less than 4 for a significantly greater period of time in healed duodenal ulceration compared with active ulcer patients, particularly after the meal. In conclusion, duodenal ulcer disease is associated with disturbed gastroduodenal motility, even when the ulcer is quiescent and when intraduodenal acidity is low. In healed duodenal ulceration, disturbed motility may promote ulcer relapse by impairing acid clearance from the bulb. However, in active ulceration other factors such as mucosal bicarbonate secretion may have a more influential role in determining intraduodenal pH.     

Epithelial cell proliferation in duodenal ulcer

Epithelial cell proliferation in the duodenum was investigated in 50 patients by incubating mucosal biopsy samples with tritiated thymidine, followed by autoradiography. Fifteen patients had a normal duodenum, 15 duodenal ulcer undergoing elective surgery, 10 perforated duodenal ulcer, and 5 severe non-ulcer-associated duodenitis. The mean crypt cell labelling index in the duodenal bulb of controls was 8.8 +/- 0.4% (mean +/- SEM), at the edge of perforated ulcers 19.1 +/- 2.0%, at the edge of elective ulcers 18.6 +/- 1.4%, and in biopsy specimens from non-ulcer-associated duodenitis 14.0 +/- 1.2%. The mean labelling index in the distal first part of duodenum of control patients was 9.1 +/- 0.8 similar to the values found in histologically normal specimens distal to ulcer or duodenitis. The results indicate active epithelial cell proliferation in both duodenal ulcer and duodenitis. There was no evidence of impairment of epithelial cell proliferation in duodenal ulcer patients.     

Gastroduodenal peptic ulcers, duodenal adhesions, and upper gastrointestinal motility disturbances in patients who have undergone cholecystectomy

The frequency of duodenal and gastric ulcer disease, the thickness of the pyloric muscle, and adhesions of the duodenum were evaluated in a routine, consecutive, prospective autopsy series of 100 patients, and the length of the pyloric canal, adhesions of the duodenum, and motility disturbances in the upper gastrointestinal series were studied in a separate radiologic material of 69 symptomatic patients with cholecystectomy in their history. Both series were compared with matched unoperated controls. The frequency of active gastric ulcers and ulcer scars was observed to be increased and that of active duodenal ulcers and ulcer scars decreased among the cholecystectomized patients in the autopsy series (p = 0.01 in both cases). This difference was not as pronounced when only active ulcers were included, but for active duodenal ulcers the difference was still significant (p = 0.04). One-fourth of the cholecystectomized patients but none of the controls had severe adhesions of the duodenum. In the autopsy series the thickness of the pyloric muscle and in the radiologic series the length of the radiologic pyloric canal were thickened/lengthened in an average of 26%/11% in patients who had undergone cholecystectomy (p less than 0.001 and p less than 0.10, respectively). The lengthening of the pyloric canal was in significant positive correlation with the motility disturbance/adhesion score of the upper gastrointestinal series.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer

BACKGROUND: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer. METHODS: Duodenal and gastric biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer, gastric ulcer or chronic gastritis. The extent of gastric metaplasia was evaluated histologically and endoscopically using the methylene blue test. In this study, we performed competitive polymerase chain reaction, a highly sensitive and quantitative method for determining the amount of H. pylori gastric and duodenal mucosa. The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in the three patient groups were compared. The correlation between the amount of H. pylori in the duodenum and gastric antrum and extent of gastric metaplasia were also determined. RESULTS: The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in patients with duodenal ulcer were much higher than in patients with gastric ulcer or chronic gastritis. A positive correlation was found between the amount of H. pylori in the duodenum and the extent of gastric bulb and that in the antrum. CONCLUSIONS: The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.     

Enzyme activities in the duodenal mucosa in duodenal ulcer patients

The mucosal enzyme activities of 11 marker enzymes from the brush border, basolateral membrane, and lysosomes of 45 patients with an active duodenal ulcer (DU) were determined by analysis of homogenized biopsy specimens obtained from the duodenal bulb and descending duodenum at endoscopy. They were compared with activities measured in 22 controls. In the duodenal bulb lactase (p less than 0.005), neutral-alpha-glucosidase (p less than 0.0005), and monoamine oxidase (p less than 0.0005) were significantly decreased in DU patients. In the descending duodenum all the brush border enzymes except sucrase were significantly decreased when compared with controls. DU patients with inflammation in the biopsy specimens from the duodenal bulb had decreased levels of lactase (p less than 0.05), sucrase (p less than 0.05), neutral-alpha-glucosidase (p less than 0.05), leucyl-beta-naphthylamidase (p less than 0.05), and acid phosphatases (p less than 0.05) when compared with DU patients with normal histology in this region. In the descending duodenum the activities of leucyl-beta-naphthylamidase (p less than 0.05) were decreased in patients with inflammation compared with those without such histologic changes. DU patients who had taken antacids before the investigation had decreased activities of lactase (p less than 0.05) in the descending duodenum when compared with those who had not taken antacids. Activities of lactase (p less than 0.005), sucrase (p less than 0.005), neutral-alpha-glucosidase (p less than 0.05), and acid beta-glucuronidase (p less than 0.0005) in the descending duodenum were significantly lower in smokers than in non-smokers with active DU.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Altered Concentrations of Gastrin-Releasing Polypeptide and Somatostatin in Fundic and Duodenal Bulb Mucosa of Patients with Duodenal Ulcer Disease

The concentrations of gastrin-releasing polypeptide, somatostatin (SS), and gastrin in extracts of endoscopically obtained biopsies from the fundus, antrum, and duodenum of patients with uncomplicated bile stones (controls) or duodenal ulcer disease were measured with specific radioimmunoassays. The validity of the tissue sampling was confirmed by characteristic and significant differences between gastrin concentrations at the different biopsy sites. Gastrin-releasing polypeptide levels were at their highest in the fundic and duodenal bulb compared to the antrum in controls (p less than 0.01), whereas no differences in gastrin-releasing polypeptide content of the different parts of the stomach were found in duodenal ulcer patients. Compared to controls gastrin-releasing polypeptide in duodenal ulcer patients was reduced in fundic and duodenal bulb mucosa (p less than 0.01). SS levels were highest (p less than 0.05) in the first part of duodenum in controls. Compared to controls duodenal ulcer patients had lower SS concentrations present in fundic (p less than 0.01) and highest SS concentrations present in duodenal bulb mucosa (p less than 0.01). There was no correlation between acid secretion and mucosal gastrin-releasing polypeptide or SS concentrations in any part of the stomach and duodenum.     

Duodenal bulb acidity in patients with duodenal ulcer

Intraluminal pH was measured simultaneously in the human stomach and proximal duodenum with six small glass electrodes tied together at 1.5-cm intervals. Twenty-four healthy control subjects and 44 patients with duodenal ulcer disease were studied under fasting conditions and for 3 h after a standard liquid meal. Mean and median hydrogen ion activity, percentage of time with pH below 2 and 3, and the frequency of pH fluctuations were calculated from digital pH data sampled at a frequency of once per second from each electrode. None of these measurements of acidity differed significantly between the two groups or between subgroups of normosecretor controls and hypersecretor ulcer patients. At the time of pH study 15 of the patients had endoscopically verified active ulcer disease and 13 patients were without disease activity. Gastric as well as duodenal bulb acidity was the same in these two subgroups. We conclude that even though duodenal ulcer patients deliver more acid into the duodenum, this does not cause increased luminal acid aggression.     

Epithelial Cell Proliferation in Duodenal Ulcer

Epithelial cell proliferation in the duodenum was investigated in 50 patients by incubating mucosal biopsy samples with tritiated thymidine, followed by autoradiography. Fifteen patients had a normal duodenum, 15 duodenal ulcer undergoing elective surgery, 10 perforated duodenal ulcer, and 5 severe non-ulcer-associated duodenitis. The mean crypt cell labelling index in the duodenal bulb of controls was 8.8 ± 0.4% (mean ± SEM), at the edge of perforated ulcers 19.1 ± 2.0%, at the edge of elective ulcers 18.6 ± 1.4%, and in biopsy specimens from non-ulcer-associated duodenitis 14.0 ± 1.2%. The mean labelling index in the distal first part of duodenum of control patients was 9.1 ± 0.8 similar to the values found in histologically normal specimens distal to ulcer or duodenitis. The results indicate active epithelial cell proliferation in both duodenal ulcer and duodenitis. There was no evidence of impairment of epithelial cell proliferation in duodenal ulcer patients.     

Role of mucosal blood flow in duodenal ulcer formation induced by dulcerozine

To clarify the role of mucosal blood flow in the pathogenesis of ulcer formation, the authors investigated dulcerozine-induced duodenal ulcers in rats. Administration of dulcerozine, 500 mg/kg by intragastric route or 250 mg/kg given intraperitoneally, induced acute ulcers in the duodenum, but not the stomach, in all rats. Using the pyloric ligation method, it was determined that although dulcerozine significantly increased gastric acid secretion, no duodenal ulcers were observed in these animals. The administration of 1 ml of 0.1 N HC1 every hour for 6 hours did not induce duodenal ulceration. The mucus glycoprotein content of the corpus, antrum and proximal duodenum did not differ following dulcerozine administration. Duodenal mucosal blood flow, which was measured by an electrolytically generated hydrogen gas clearance technique, decreased significantly following dulcerozine administration even in pylorus-ligated rats. In contrast, there was an increase in the gastric mucosal blood flow following administration of the drug. Therefore, not only an increase in gastric acid secretion but also a decrease in duodenal mucosal blood flow are suggested to be responsible for dulcerozine-induced duodenal ulceration.     

Role of mucosal blood flow in duodenal ulcer formation induced by dulcerozine

To clarify the role of mucosal blood flow in the pathogenesis of ulcer formation, the authors investigated dulcerozine-induced duodenal ulcers in rats. Administration of dulcerozine, 500 mg/kg by intragastric route or 250 mg/kg given intraperitoneally, induced acute ulcers in the duodenum, but not the stomach, in all rats. Using the pyloric ligation method, it was determined that although dulcerozine significantly increased gastric acid secretion, no duodenal ulcers were observed in these animals. The administration of 1 ml of 0.1 N HCl every hour for 6 hours did not induce duodenal ulceration. The mucus glycoprotein content of the corpus, antrum and proximal duodenum did not differ following dulcerozine administration. Duodenal mucosal blood flow, which was measured by an electrolytically generated hydrogen gas clearance technique, decreased significantly following dulcerozine administration even in pylorus-ligated rats. In contrast, there was an increase in the gastric mucosal blood flow following administration of the drug. Therefore, not only an increase in gastric acid secretion but also a decrease in duodenal mucosal blood flow are suggested to be responsible for dulcerozine-induced duodenal ulceration.     

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.     

Lysolecithin: A factor in the pathogenesis of gastric ulceration?

Lysolecithin is formed when pancreatic juice and bile mix in the duodenum. Lysolecithin concentrations have been measured in intermittent samples of night gastric juice from patients with gastric ulcers and duodenal ulcers and in normal controls. In gastric ulcer patients, the mean of the peak concentrations (444 mug/ml) and mean of concentrations in all samples (199 mug/ml) were significantly higher than in controls (34 mug/ml and 18 mug/ml respectively). Duodenal ulcer patients had normal or moderately raised values. The levels in gastric ulcer patients were as high as those which have been found experimentally to cause severe damage to the gastric mucosal barrier, and it is concluded that lysolecithin may be as important, or more important, than bile salts in the destruction of the gastric mucosal barrier and therefore in the aetiology of gastric ulcer.     

Circadian pattern of intragastric acidity in duodenal ulcer patients: a study of variations in relation to ulcer activity.

The relation between intragastric acidity and duodenal ulcer activity was studied prospectively in 21 patients with endoscopically proved duodenal ulcers. The 24 hour intragastric acidity was measured on four separate occasions by continuous recording using combined glass electrodes: (a) in the presence of an ulcer crater without treatment; (b) during active ulceration being treated with ranitidine; (c) during early healing after a six week course of ranitidine; (d) during late healing six months after acute ulceration. Intragastric acidity was also monitored in 20 healthy subjects. At all stages of ulcer activity and during all predefined time periods, duodenal ulcer patients had significantly higher gastric acidity than healthy control subjects. Duodenal ulcer patients showed a similar circadian pattern of intragastric acidity during exacerbation of ulcer disease and in remission during the early and late ulcer healing periods. These results argue against a direct relation between the activity of duodenal ulcer disease and gastric acidity. It is concluded that the chronic recurrent course of duodenal ulcer disease does not result from a fluctuation in intragastric acidity.     

Prevalence of non-Helicobacter pylori duodenal ulcer in Karachi, Pakistan

AIM:To determine the prevalence of non-Helicobacter pylori (H pylori)-related duodenal ulcer in patients with acid-peptic diseases. METHODS: Medical records of patients who attended the Gastroenterology Department at Aga Khan University Hospital from 1999 to 2001 and had endoscopic diagnosis of duodenal ulcers were reviewed. Duodenal ulcer associated with H pylori was diagnosed on the basis of endoscopy, rapid urease test and histopathology whereas histories of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) related duodenal ulcers. Non-H pylori, non-NSAID duodenal ulcers were those without H pylori infection and history of NSAID intake. Co-morbid conditions associated were noted. RESULTS: Of 2 260 patients, 10% (217/2 260) had duodenal ulcer. Duodenal ulcer related to H pylori infection accounted for 53% (116/217), NSAID-related 10% (22/217), non-H pylori non-NSAID 29% (62/217), and 8% (17/217) had both H pylori infection and histories of NSAID intake. Fifteen percent (18/116)_patients had past histories of peptic ulcer disease in H pylori infection, while 8% (5/62) in non-H pylori non-NSAID ulcer. Co-morbid conditions in H pylori infection were seen in 23% (27/116) and 34% (21/62) in non-H pylori non-NSAID ulcer. CONCLUSION: Incidence of H pylori infection related with duodenai ulcer is common. In the presence of co-morbids, non-H pylori and non-NSAID duodenal ulcer is likely to be present.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients

Background. Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either, whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients.Aims. To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status.Patients and methods. A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination.Results. There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum.Conclusion. Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Duodenal Acid Clearance in Humans: Observations Made with Intraluminal Impedance Recording

Duodenal acid clearance appears to be involved not only in the pathogenesis of duodenal ulcer disease but also in functional dyspepsia. Duodenal contractile activity can help to maintain neutral pH in the duodenum by mixing acid with bicarbonate or by aborally transporting the acid load. Intraluminal impedance recording, allowing the detection of nonacid liquid boluses, can be carried out concomitantly with antroduodenal manometry and pH recording and may thus provide useful information about the mechanisms involved in duodenal clearance of endogenous acid and volume boluses. Eight H. pylori-negative healthy volunteers were studied with two catheters positioned across the pylorus, allowing the recording of five impedance signals (one antral, one pyloric, and three duodenal) simultaneously with six pressure signals (two antral, one pyloric, and three duodenal) as well as distal antral and proximal duodenal pH. During phase II of the migrating motor complex, which is known to be associated with the highest duodenal acid exposure, each duodenal acidification event (defined as a pH drop > 2 pH units) was characterized by its maximal amplitude, duration, temporal relationship with antroduodenal manometric events, and relation to impedance variations. Acid was considered to have been cleared from the duodenum when the preacidification pH was restored (± 0.2 unit). A total of 164 duodenal pH drops were recorded during the 323 min of phase II recordings. Eleven percent of the duodenal acidification events were short-lived (< 10 sec). All of these events were temporally associated with a propagated antroduodenal contraction and a short-lived drop in impedance, suggesting rapid aboral passage of the acid bolus. The long-lived duodenal acidification events lasted a mean of 32 sec (range, 25–66 sec). In 90% of these events an antroduodenal propagated contraction was recorded at the time of onset. Repetitive duodenal contractions followed the onset of the long-lived acidification events in 34% of the cases. These remained present until complete clearance of the acid. In 81% of the long-lived acidification events, recovery of the associated impedance drop occurred simultaneously with the pH recovery, suggesting a complete clearance of the bolus. Less frequently (19%), the duodenal pH recovered while the impedance remained low, suggesting that the bolus was not cleared but neutralized. Interdigestive duodenal acidification events usually last about 30 sec. They evoke duodenal contractions in only one-third of cases. Combined pH and impedance recording makes it possible to distinguish between neutralization of acid boluses and their complete total clearance.     

Gastric metaplasia of regenerating duodenal mucosa and deformity of duodenal bulb: A correlative study

The correlation between the presence and degree of gastric metaplasia of regenerating duodenal mucosa and the deformity of duodenal bulb was studied. Based on the endoscopically morphological patterns of bulb, the duodenal ulcers were divided into three types: type I, with a normal-shaped bulb; type II, with a mildly deformed bulb; and type III, with a markedly deformed bulb. A total of 159 patients with active duodenal ulcers were scheduled to be treated with H₂-receptor antagonists. Of these patients, 124 proved to have a healed duodenal ulcer 4 weeks after initial treatment upon follow-up endoscopic examinations. Two biopsies were taken from the centre of the ulcer scar when the ulcer was found to be healed for light microscopic study. Histologically, the degree of gastric metaplasia was divided into three grades: grades 0, 1 and 2. The results show that a healed duodenal ulcer with a normal-shaped bulb is not frequently accompanied by gastric metaplasia. However, a healed ulcer with a markedly deformed bulb has a high incidence and degree of gastric metaplasia, which may be easily colonized by Helicobacter pylori and thus develop an environment of easy recurrence. Therefore, a cycle of healing and recurrence may exist in patients with a duodenal ulcer and a markedly deformed bulb. Eradication of H. pylori may be the best way to break this cycle.