Excessive Duodenogastric Reflux Research Articles

Features of duodenogastric refl ux in gastric ulcer

At the moment the approach to the treatment of gastric ulcer (GU) does not depend on the location of the ulcer in one or another part of the stomach. We compared gastric secretion, duodenogastric refl ux characteristics and Helicobacter pylori infection in patients with “high” and “low” gastric ulcers. 96 patients with recurrent GU were examined; 71.9% of men and 28.1% of women. In 58 patients, a “high” localization of the ulcer was detected, and in 38 patients, a “low” (pyloroantral) ulcer was diagnosed. All patients underwent esophagogastroduodenoscopy and daily intragastric pH-metry prior to the appointment of antisecretory therapy. The data were compared with the results of healthy volunteers. The frequency of detection of Helicobacter pylori infection was comparable with diff erent localization of gastric ulcer. We were able to show that with “high” ulcers, intragastric acidity in terms of fundal and antral pH and its circadian dynamics were comparable to healthy people. With “high” ulcers, the frequency of duodenogastric refl ux was close to normal, but their total duration was higher due to an increase in the proportion of prolonged and high refl ux. With “low” gastric ulcers, we noted a very high and monotonous acidity in the body and antrum of the stomach, combined with a decrease in the frequency and duration of duodenogastric refl ux. Consequently, both “high” and “low” stomach ulcers suggest the appointment of antisecretory drugs. At the same time, the detection of “high” stomach ulcers associated with excessive duodenogastric refl ux can be considered as a basis for prescribing bismuth tricalium dicitrate, including as part of the Helicobacter pylori eradication therapy, or ursodeoxycholic acid.

Duodenogastric reflux induced by endoscopic submucosal dissection

Endoscopic submucosal dissection (ESD) may cause excessive duodenogastric reflux (DGR) in a similar manner to distal gastrectomy, particularly after antral resections. We aimed to examine the occurrence of DGR after ESD. Patients with gastric neoplasm for whom ESD was indicated were categorized according to lesion site: the antral group (lower [L] stomach, n = 46) and the nonantral group (upper or middle [U or M] stomach, n = 49). Endoscopy was performed before ESD, the day after ESD, and 3 months after ESD, and the fasting bile acid concentration (BAC) in the gastric juice was analyzed. BAC values showed significant interaction between time point and group, although this association differed in the antral and nonantral groups. BACs on the day after ESD were higher in the antral group than in the nonantral group, but not the pre-ESD and 3 months post-ESD levels. In the antral group only, fasting BACs increased significantly the day after ESD and decreased to baseline levels 3 months post-ESD. There was also a correlation between BAC and lesion location in the antral subgroups, with significantly higher BACs found the day after ESD in patients with lesser curvature lesions. ESD of lesions in the antral lesser curvature may lead to a transient early increase in DGR. However, ESD does not result in long-term DGR, a factor that is known to increase the risk of carcinogenesis following gastrectomy.

Duodenogastric Reflux Induced By Endoscopic Submucosal Dissection: Contribution of the Resection Area

Background and Aims: As with distal gastrectomy, endoscopic submucosal dissection (ESD) may potentially cause excessive duodenogastric reflux (DGR) as a short- or long-term outcome, particularly after procedures on the antral area, which is thought to play an important role in controlling DGR. Patients and Methods: For patients with gastric neoplasm that ESD was indicated, endoscopy was performed at 3 intervals: pre-ESD; the day after ESD; and 3 months post-ESD, and fasting bile acid (BA) concentration in the gastric juice was analysed. To establish the reliability of the measurement method, simple regrssion analysis between repeated measurements on separate days on eighty-two subjects without active peptic ulcer or gastric cancer was performed. The regression equation indicated: y = 0.6654× + 62.965 (R2= 0.3416, r=0.584, P<0.0001). Results: To establish any time-specific effects, the BA levels of each group were then compared with base-line using the repeated-measure one-way ANOVA. In forty-six patients who underwent ESD for gastric neoplasms located in the L portion according to the UML classification (antral group), fasting BA concentration in gastric juice collected the day after ESD was significantly elevated compared to that collected pre-ESD(1132.8 ± 346.2 vs. 292.8 ± 117.3 μmol/l; ∗ P < 0.004), but not in 49 patients who underwent ESD for lesions located other than the L portion (non-antral group). To establish any group-specific effects, statistical comparisons at each time point between two groups were made by the unpared t-test. The comparison revealed higher BA levels in the antral group than those in the non-antral group the day after ESD(1132.8 ± 346.2 vs. 334.4 ± 96.0 μmol/l;†, P < 0.025), but not base-line and the 3 months later. Furthermore, in the antral group, ESD for lesser curvature lesions showed significantly higher BA concentrations compared to that for the other subgroup which located other than the lesser curvature site. Conclusions: ESD, especially for an antral lesion, leads to a transient increase in the occurrence of DGR immediately after the procedure. However, in the long-term, ESD has not to be concerned about DGR-induced complication, unlike distal gastrectomy. Pathophysiologic effects onto the lesser curvature site in the antrum where the vagus nerve dominantly localized in is rich may most strongly be associated with development of DGR.

Prevalence of pathological duodenogastric reflux and the relationship between duodenogastric and duodenogastrooesophageal reflux in chronic gastrooesophageal reflux disease

The role of duodenogastric reflux in gastrooesophageal reflux disease is still controversial. (i) To determine the prevalence of pathological duodenogastric reflux (DGR) in gastrooesophageal reflux disease patients and (ii) to define the relationship between DGR and duodenogastrooesophageal reflux. We evaluated 92 patients referred for investigation of recurrent reflux symptoms after proton pump inhibitors (PPI) therapy. All the patients filled out symptom questionnaires and underwent endoscopy, oesophageal manometry and combined oesophagogastric pH and bilirubin monitoring. Endoscopy divided the 92 patients into four groups (group I: 25 nonoesophagitis patients, group II: 26 patients with grade A-B oesophagitis, group III: 21 patients with grade C-D oesophagitis and group IV: 20 patients with Barrett's oesophagus. Twenty-four of the 92 patients (26%) showed pathological DGR. Abnormal oesophageal bilirubin exposure was observed in 62 of the 92 patients (67.4%). Of the 62 patients with abnormal oesophageal bilimetry, 15 (24.2%) patients simultaneously showed pathological DGR. The gastric bilirubin exposure in patients with abnormal oesophageal, Bilitec tests did not differ from that in patients with normal oesophageal bilimetry (P>0.05). A weak correlation between oesophageal and gastric bilirubin exposure, both expressed as a percentage of time, was found (r=0.28; P<0.01). Pathological DGR is present in a little more than a quarter of patients with recurrent reflux and dyspeptic symptoms after PPI therapy. Excessive DGR is not a prerequisite for pathological oesophageal exposure to duodenal contents. Gastric bilirubin monitoring may be useful to choose the best surgical treatment for patients with reflux and dyspeptic symptoms refractory to PPI.

Duodenogastric reflux following biliary reconstruction after excision of choledochal cyst

Duodenogastric reflux (DGR) was assessed in patients surgically treated for choledochal cyst, with emphasis on two different biliary reconstruction methods: Roux-en-Y hepaticojejunostomy (HJ) and hepaticoduodenostomy (HD). Gastric bile monitoring with the Bilitec device revealed excessive DGR in patients in the HD group. Endoscopic findings demonstrated mild to moderate gastric mucosal erosion in patients after HD. In contrast, neither DGR nor gastritis was found in patients after HJ. This preliminary study suggests that HJ, rather than HD, should be recommended as a method of biliary reconstruction for pediatric patients with choledochal cyst. Careful observation of DGR should be continued in patients who have undergone HD.

Effects of duodenogastric reflux on gastrin cells, somatostatin cells and serotonin cells in human antral gastric mucosa

Duodenogastric reflux (DGR) has been found to give rise to a hypochlorhydria secondary to alkaline reflux. We investigated whether there is a link between DGR and the gastrin, somatostatin, and serotonin cell numbers and the granular content of gastrin, somatostatin, and serotonin in endocrine cells in human antral mucosa. We investigated 38 selected Helicobacter pylori-negative patients with visual primary excessive DGR in upper endoscopy and symptoms of epigastric pain and bile vomiting. Ten control patients were included in this study. None of the patients had peptic ulcer or had received any medication. Antrum (10 biopsies from five different zones: the lesser and major curvature, the anterior and posterior wall, and the pylorus) and corpus (two biopsies from major curvature about 10 cm below the cardia) biopsy specimens were collected for routine histology, as well as for light and electron immunohistochemistry. In patients without atrophy or intestinal metaplasia and in patients with mild atrophy or mild intestinal metaplasia, the number of gastrin and somatostatin cells was not different from that in controls. In moderate atrophy or moderate intestinal metaplasia, however, the number of gastrin and somatostatin cells decreased. Serotonin cell number was significantly higher in all patients with DGR as compared with controls. The mean somatostatin granular content was increased (3.6±0.2 vs. 3.2±0.1). In addition, lysosomes with engulfed somatostatin granules were found. The mean serotonin granular content was decreased (2.3±0.3 vs. 2.9±0.3), while the mean gastrin granular content remained unchanged (2.5±0.3 vs. 2.4±0.2). Ultrastructurally, the granules in serotonin-positive cells corresponded to the gastric variant or to the intestinal variant of serotonin cells. The endocrine cells were found to have few granules positive for serotonin. It is concluded that DGR inhibits somatostatin granular release, but stimulates both serotonin granular release and serotonin cell growth.

Is duodeno-gastro-esophageal reflux just a bystander of acid reflux?

Duodeno-gastro-esophageal reflux (DGER) as measured with bilirubin monitoring is observed in many patients with reflux disease especially in Barrett's esophagus. As acid suppression is an effective therapy of reflux disease, DGER is frequently just considered as a bystander of acid reflux. To define the importance of DGER, reflux of duodenal contents was evaluated by bilirubin monitoring in the stomach. 100 patients with reflux disease were evaluated (62 m, 38 f, 50 (12) years). 26 patients had Barrett's esophagus, 57 had esophagitis and 17 non- erosive reflux disease (pH pos.). All patients were evaluated with simultaneous 24-hour bilirubin monitoring in the esophagus and stomach. Results were compared to 35 measurements of healthy volunteers in the esophagus and 41 measurements in the stomach. Normal values: DGER - Exposure time esophagus > 11.8 % using an absorbance value > 0.14, duodenogastric reflux (DGR) - Exposure time stomach >24.8 % using an absorbance value > 0.25. 56 % of the patients had DGER, 41 % had DGR. 29 of the 41 patients with DGR had DGER (71 %), while 27 of the 56 patients with DGER had physiologic duodenogastric reflux (48 %). About 30 % of the patients with reflux disease show DGER combined with excessive DGR. Therefore, DGER is not just a bystander of acid reflux. The excessive DGR in some patients adds additional potentially dangerous substances to the esophageal reflux.

Gastric bilirubin monitoring to assess duodenogastric reflux.

Duodenogastric reflux (DGR) was assessed with 24-hour gastric bilirubin monitoring in 345 patients (219 men; 49 +/- 13 years) with foregut symptoms and 41 healthy subjects (24 men, 28 +/- 5 years). Bilirubin exposure was measured as percent time above absorbance level 0.25 and excessive DGR was defined above the 95th percentile of normal values (>24.8%). DGR was highest following Billroth II gastric resection (60 +/- 24%, N = 15). Patients after cholecystectomy (28 +/- 25%, N = 25), patients with gastroesophageal reflux disease (24 +/- 24%, N = 199), and patients with nonulcer dyspepsia (23 +/- 21%, N = 61) had a significantly higher exposure to DGR than healthy subjects (7 +/- 8%, P < 0.0001). In conclusion, gastric bilirubin monitoring is useful for the assessment of DGR specifically in symptomatic patients following gastric resection. Increased amounts of DGR may further be of clinical importance in patients with reflux disease or nonulcer dyspepsia and following cholecystectomy.

Gastric symptoms and duodenogastric reflux in patients referred for gastroesophageal reflux symptoms and endoscopic esophagitis

Background: The role of excessive duodenogastric reflux (DRG) in the genesis of gastric symptoms in patients primarily referred for both gastroesophageal reflux (GER) symptoms and esophagitis is poorly understood. Methods: The study is based on the clinical, endoscopic, histologic, and 24-hour gastric data from the Bilitec optoelectronic device (Prodotec, Florence, Italy, licensed by Synectics Medical, Stockholm, Sweden) from 49 patients having both typical GER symptoms and gastric symptoms suggestive of excessive DGR (ie, epigastric pain, nausea, or bilious vomiting) in the absence of previous esophageal or gastric surgery (group I). Helicobacter pylori organisms were searched for on antral biopsy specimens with use of the Giemsa method. The percentages of total, upright, and supine time during which absorbance exceeded various thresholds through all the working range of the Bilitec device were calculated. Bilitec data from group 1 were compared with those from 16 patients with endoscopic esophagitis and GER symptoms only (group 2) and 25 healthy subjects (group 3). Results: The prevalence of an abnormal Bilitec test result in group 1 increased from 27% (13/49) at the 0.25 absorbance threshold to 36% (18/49) at thresholds ranging from 0.40 to 0.60 and to 41% (20/49) when multiple thresholds ranging from 0.25 to 0.60 were considered. In group 2 one patient had an abnormal Bilitec test result at the 0.25 to 0.30 threshold, whereas the other 15 patients had a normal test result. H pylori antral infection was present in 14 group 1 patients. None of these had an abnormal Bilitec test result, whereas the test was positive in 40% of the H pylori–negative patients without endoscopic gastritis and in 70% of H pylori–negative patients with endoscopic gastritis ( P = .001). Conclusions: Twenty-four-hour intragastric bile monitoring provides the clinician with unequivocal evidence of excessive DGR in 41% of patients with an intact stomach having endoscopic esophagitis, GER symptoms, and gastric symptoms suggestive of DGR. The most dependable data are obtained when absorbance thresholds higher than 0.40 are considered. H pylori antral infection and excessive DGR at 24-hour intragastric bile monitoring are mutually exclusive. (Surgery 1999;125:480-6.)

Pathologic duodenogastric reflux associated with persistence of symptoms after cholecystectomy

The aim of this study was to determine whether increased duodenogastric reflux contributes to postcholecystectomy symptoms. Gastric pH monitoring, hepatobiliary scintigraphy, gastric emptying scans, and gastric acid analysis were performed in asymptomatic (n = 10) and in symptomatic (n = 27) patients after cholecystectomy. Normal subjects (n = 20), patients with dyspepsia related to gastric acid hypersecretion (n = 20), patients with reflux gastritis after gastric surgery (n = 10), and patients with confirmed primary pathologic duodenogastric reflux (n = 10) were studied as controls. Symptomatic patients also underwent upper gastrointestinal endoscopy. Symptomatic patients had significantly increased interprandial gastric exposure to pH < 3 compared with asymptomatic subjects, which correlated well with a high incidence of hepatobiliary scans positive for abnormal duodenogastric reflux and chronic gastritis on endoscopy. Gastric alkaline exposure in symptomatic patients was similar to that seen in patients with primary pathologic duodenogastric reflux and patients with duodenogastric reflux related to gastric surgery. Gastric acid secretion and gastric emptying were not altered. Five patients tested before and after laparoscopic cholecystectomy showed that nocturnal gastric alkalization was enhanced after operation. This study suggests that excessive duodenogastric reflux may be responsible for persistence of symptoms after cholecystectomy.

Double-blind placebo controlled cross-over trial of cisapride in postgastrectomy patients with duodenogastric reflux (DGR)

• Double-Blind Placebo Controlled Cross-Over Trial of Cisapride in Postgastrectomy Patients with Duodenogastric Reflux (DGR). M. Vaezi*, R. Sears*, J. Richter #. *U Ala, B'ham;#Cleveland Clin. Excessive DGR is responsible for upper GI symptoms in about 15% of partial gastrectomy patients. Medical treatment has been disappointing, necessi tat ing surgical interventions in many patients. Using ambulatory esophageal bilirubin monitoring (Bilitec 2000), we evaluated the efficacy of cisapride in improving DGR and pat ient-symptoms. METHODS: Ten chronically symptomatic partial gastrectomy VA patients (5 BI, 5 BII) (8M, x age 57) with DGR by Bilitec, without acid reflux, randomized to either placebo or cisapride (20 mg qid) in double-blinded crossover study. Using Bilitec and standard 2200 calorie, liquid diet, DGR evaluated at baseline and after 1 month on each therapy. Daily diary of severity/frequency of upper GI symptoms recorded and mean monthly scores determined. At end of each treatment month , overal l global a s se s smen t made of s y m p t o m improvements. RESULTS: x&+SE. Wilcoxon, Fisher's tests; * p 0.14 Baseline Placebo Cisapride Total 26.2-+3.6 17.5+_2.1 11.2-+3.7 Upright 26.4+4.1 12.8-+3.5 7.1-+2.9 Supine 21.0+3.6 25.7+5.6 11.9-+3.8 Compared to placebo, cisapride significantly decreased DGR by 45% in upright and 54% in supine positions. There was no order effect. Overall symptoms improved in 70% of patients on cisapride compared to 10%'on placebo tp 7 and bili abs. > 0.14. RESULTS: x-+SE;ANOVA;*p 7 7.2-+1.8 6.1-+1.8 6 .0-+1.7 5.7-+1.6 4.6-+1.5 bili>.14 0.7-+0.2 11.1-+5.0 20.1-+8.4 25.9-+5.9* 48.0-+4.8*# B_~dmM) 0.03-+0.0 0.09-+0.03* 0.16-+0.05 0.24-+0.07_.* 0.50+-0,10# % Time pH 0.14 and gastric BA only discriminated complicated Barrett's from other patient groups. Linear regression found significant correlation (R=0.7, p 0.14 (R=0.3, p>.05), while correlation remained strong for % time pH 7 did not differentiate patients. CONCLUSIONS: 1) pH < 4 is a better predictor of GERD severity. 2) Bile reflux shows parallel increase over GERD spectrum, but only discriminates complicated Barrett's patients from other GERD patient groups. 3) Our study supports the 1 ° role of acid in GERD, but suggests a possible synergistic role for bile acids in complicated Barrett's patients.

Duodenogastric reflux and foregut carcinogenesis

Epidemiologic cohort studies have established that after distal gastric resection, there is a higher risk of gastric carcinoma. It is likely that a main factor of this higher risk is the excessive duodenogastric reflux induced by surgery, because the incidence of stump carcinomas is higher in Billroth II than in Billroth I, and most of the stump carcinomas are located near the stoma. In addition, several groups of investigators have suggested that duodenogastric reflux per se induces stump carcinomas in rats. There is another human duodenogastric reflux, the primary duodenogastric reflux, through the pylorus. Experiments in animals have demonstrated that this type of duodenal reflux also induces gastric carcinomas in the antrum of the stomach that has not undergone surgery. Recent clinical attention has focused on the role of duodenogastric reflux in the pathogenesis of Barrett's esophagus and subsequent esophageal adenocarcinomas. Experimentally, reflux of duodenal contents into the esophagus can cause not only Barrett's esophagus and subsequent adenocarcinomas, but also squamous cell carcinomas. These findings suggest that duodenogastric reflux may be implicated in gastric and esophageal, that is, foregut carcinogenesis.

Abnormal plasma gut hormones in pathologic duodenogastric reflux and their response to surgery

Fasting and postprandial plasma levels of the gut hormones gastrin, cholecystokinin (CCK), secretin, glucose-dependent insulinotropic polypeptide, motilin, neurotensin, peptide YY (PYY), enteroglucagon, glucagon, insulin, and pancreatic polypeptide were measured in 11 patients with alkaline gastritis associated with excessive duodenogastric reflux not related to previous gastric surgery (primary DGR), 12 primary DGR patients after pancreatico-biliary diversion ("duodenal switch" procedure), and in 10 age-matched healthy controls. Gastric emptying of a semisolid oatmeal was also measured in patients with primary DGR and in patients after bile diversion. Fasting plasma levels of the distal gut hormone neurotensin and the pancreatic islet hormone insulin were significantly greater in patients with primary DGR compared with controls. Neurotensin levels were normal in patients studied after bile diversion. Postprandial plasma levels, incremental integrated and total integrated responses for CCK, secretin, insulin, neurotensin, PYY, and enteroglucagon, were significantly greater in patients with primary DGR compared with controls. The majority of these responses normalized after bile diversion; however, the postprandial response for insulin and enteroglucagon remained elevated. Patients with primary DGR had a rapid early postprandial phase of gastric emptying of solids, which showed a significant correlation with plasma neurotensin levels. Bile diversion produced a significant delay in this lag-phase of gastric emptying. These abnormalities in gut regulatory hormones appear to be adaptive changes to rapid early postprandial gastric emptying, probably related to antropyloric dysmotility, which has been implicated in the pathogenesis of this condition. Measurement of these gastrointestinal hormones may become useful in the diagnosis of primary DGR.

Functional foregut abnormalities in Barrett's esophagus

The factors predisposing to the development of Barrett's esophagus in patients with gastroesophageal reflux disease are unclear. We compared symptoms, esophageal acid and alkaline exposure (pH < 2, < 3, < 4, and > 7), lower esophageal sphincter resistance, esophageal clearance function, the gastric secretory state, gastric emptying, and duodenogastric reflux in 15 patients with Barrett's esophagus with 24 patients with esophagitis and with 22 normal subjects. Compared with patients with esophagitis, patients with Barrett's esophagus had less heartburn and regurgitation but had an increased frequency and duration of reflux episodes and percent time pH less than 2, less than 3, less than 4, and pH greater than 7 on ambulatory 24-hour esophageal pH monitoring. This was associated with a decreased lower esophageal sphincter resistance, a decreased contraction amplitude in the distal area of the esophagus, an increased frequency of nonperistaltic contractions and contractions less than 30 mm Hg on 24-hour ambulatory esophageal motility monitoring, increased basal and stimulated gastric acid secretion, and a higher prevalence of excessive duodenogastric reflux. These data show that despite less symptoms patients with Barrett's esophagus have a markedly increased esophageal acid and alkaline exposure compared with patients with esophagitis. This appears to be because of persistent reflux of highly concentrated gastric acid and duodenal contents across a mechanically defective lower esophageal sphincter in combination with inefficient esophageal clearance function.

Complications of gastroesophageal reflux disease. Role of the lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and duodenogastric reflux.

The factors contributing to the development of esophageal mucosal injury in gastroesophageal reflux disease (GERD) are unclear. The lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and the presence of excessive duodenogastric reflux (DGR) was evaluated in 205 consecutive patients with GERD and various degrees of mucosal injury (no mucosal injury, n = 92; esophagitis, n = 66; stricture, n = 19; Barrett's esophagus, n = 28). Manometry and 24-hour esophageal pH monitoring showed that the prevalence and severity of esophageal mucosal injury was higher in patients with a mechanically defective lower esophageal sphincter (p less than 0.01) or increased esophageal acid/alkaline exposure (p less than 0.01) as compared with those with a normal sphincter or only increased esophageal acid exposure. Complications of GERD were particularly frequent and severe in patients who had a combination of a defective sphincter and increased esophageal acid/alkaline exposure (p less than 0.01). Combined esophageal and gastric pH monitoring showed that esophageal alkaline exposure was increased only in GERD patients with DGR (p less than 0.05) and that DGR was more frequent in GERD patients with a stricture or Barrett's esophagus. A mechanically defective lower esophageal sphincter and reflux of acid gastric juice contaminated with duodenal contents therefore appear to be the most important determinants for the development of mucosal injury in GERD. This explains why some patients fail medical therapy and supports the surgical reconstruction of the defective sphincter as the most effective therapy.

Clinical Use of 24-Hour Gastric pH Monitoring vs O-diisopropyl Iminodiacetic Acid (DISIDA) Scanning in the Diagnosis of Pathologic Duodenogastric Reflux

The efficacy of o-diisopropyl iminodiacetic acid (DISIDA) scanning was compared with that of computerized analysis of 24-hour gastric pH monitoring to diagnose excessive duodenogastric reflux in 22 normal volunteers and 106 consecutive patients with foregut symptoms. DISIDA scanning had a false-positive rate of 18% in the normal volunteers. Gastric pH monitoring showed an increasing prevalence of duodenogastric reflux in patients with increasing clinical evidence of this condition, which was not seen with DISIDA scanning. Both DISIDA scanning and gastric pH monitoring identified duodenogastric reflux in most patients who had had previous pyloroplasty or antrectomy. Only gastric pH monitoring, however, showed a significantly increased prevalence of duodenogastric reflux in symptomatic patients after previous cholecystectomy compared with those who had not undergone previous surgery. These data suggest that 24-hour gastric pH monitoring is superior to DISIDA scanning in identifying duodenogastric reflux as a cause of foregut symptoms.

Interrelationships among gastric mucosal morphology, secretion, and motility in peptic ulcer disease.

Pathophysiologic abnormalities associated with ulcer disease include gastritis (particularly of the antral mucosa), excessive duodenogastric reflux, and altered motor activity of the stomach. It is not known whether these abnormalities are interrelated and whether they occur during periods of ulcer inactivity. We have tested the hypothesis that the morphological abnormalities of the gastric mucosa in inactive ulcer disease are proportional to an alteration of the gastric luminal milieu itself due to abnormal secretory and motor function. Thus, multiple endoscopic biopsies and 24-hr physiologic measurements were performed in 12 patients with well-documented ulcers in the past (seven type I gastric ulcer patients, five duodenal ulcer patients), now clinically and endoscopically in remission. Seven healthy individuals underwent similar studies and served as controls. Histologic quantification of inflammation and metaplasia (expressed as a gastritis index) was found to be significantly different among groups (P less than 0.01). Gastric ulcer patients exhibited a higher gastritis index than controls, while duodenal ulcer patients were intermediate. A significant inverse relationship was found between gastritis index and postprandial motility index (R2 = 0.59, P less than 0.01) and a nonsignificant trend between gastritis index and fasting motility index. There was no difference among groups or detectable associations between gastritis index and intragastric pH or bile acid concentration. We conclude that gastric mucosal disease, expressed as gastritis index, persists during inactive ulcer disease. There is an association with antral hypomotility, which is more strongly manifested postprandially. It is not associated with gastric pH or bile acid concentration. Gastric mucosal inflammation and antral hypomotility predispose to ulceration rather than simply accompanying it.

Duodenogastric reflux in the dog, a clinicopathological study

In an experimental group of dogs which included seven clinically healthy dogs and 34 dogs with symptoms of (upper) gastrointestinal disease, nine dogs had endoscopic signs of duodenogastric reflux and 13 dogs had a positive duodenogastric reflux test. Endoscopic examination and the reflux test were in agreement in seven dogs (dogs with duodenogastric reflux) but not in eight dogs (dogs with potential duodenogastric reflux). Examination of dogs with duodenogastric reflux showed bile stained gastric material; thick red rugal folds; petechia in the antral mucosa in three dogs; five dogs with histological signs of gastritis; four dogs with signs of enteritis; four with gastric acid hyposecretion and four with a delayed gastric emptying. Two dogs with potential duodenogastric reflux had endoscopic reflux gastritis; three dogs had histological gastritis and seven enteritis. The present study indicates that excessive duodenogastric reflux is likely to play a role in the pathogenesis of canine gastritis.