OBJECTIVE: Visualization of enterogastric reflux (EGR) may be present during hepatobiliary imaging. Reflux of bile may damage the gastric mucosa, altering its function, and cause such symptoms as epigastric pain, heartburn, nausea, intermittent vomiting and abdominal fullness. These symptoms also are associated with gallbladder disease. The aim of this study was to quantitate the EGR index (EGRI) and to determine if a difference exists in normal and abnormal responses using standard cholecystokinin (CCK)-augmented hepatobiliary imaging. METHODS: This study used 129 patients. LAO dynamic data on a 128 x 128 matrix at a rate of 1 frame/min were obtained. After the gallbladder ejection fraction (GBEF) was determined, the EGRI (%) was calculated by relating the counts in the gastric ROI to the counts in the hepatobiliary ROI at a specified time. The results were compared with the patient's final clinical diagnosis. RESULTS: Normal responders (GBEF > or = 35%) had a higher EGRI than abnormal responders with a P = 0.001 EGR observed in 75 patients (58.1%). Significant reflux (EGRI > or = 14.2% at 15 min) was observed in 29 additional patients (22.5%). Patients with EGRI > or = 24.5% showed a strong association with the pathophysiologic syndrome of gastritis, alkaline reflux, gastric ulcer and gastro esophageal reflux disease. There was no EGR observed in the remaining 25 patients (19.4%). CONCLUSION: This simple addition to the CCK-augmented hepatobiliary imaging may both detect and quantitate abnormal EGR as the cause of the patient's symptoms in the presence of a normal GBEF result, and/or those patients with risk factors for gastritis. (+info)
Cell proliferation in type C gastritis affecting the intact stomach.
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AIMS: Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. It has been shown previously that type C gastritis is associated with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach. METHODS: Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives between 1994 and 1997. A control group of nine normal antral biopsies was also selected and all underwent MIB-1 immunostaining. The gastric glands were divided into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gland base) and the numbers of positively staining nuclei for 500 epithelial cell nuclei were counted in each zone to determine the percentage labelling index (LI%). RESULTS: Cell proliferation was significantly higher in all three zones of the gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8-99.2), controls 4.7 (range, 2.0-11.3); zone 2, median LI% in type C gastritis 94.7 (range, 28.8-98.7), controls 40.2 (range, 23.1-70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3-96.0), controls 2.6 (range, 0.9-8.7). CONCLUSIONS: Bile reflux is thought to act as a promoter of gastric carcinogenesis in the postsurgical stomach. The same may be true in the intact stomach. (+info)
Bile reflux gastritis and Barrett's oesophagus: further evidence of a role for duodenogastro-oesophageal reflux?
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BACKGROUND: There is increasing evidence that reflux of bile plays a part in the pathogenesis of Barrett's oesophagus. Bile injury to the gastric mucosa results in a "chemical" gastritis in which oedema and intestinal metaplasia are prominent. AIM: To determine if patients with Barrett's oesophagus have more bile related changes in antral mucosa than patients with uncomplicated gastro-oesophageal reflux disease (GORD) or non-ulcer dyspepsia (NUD). PATIENTS AND METHODS: Patients were identified by a retrospective search of pathology records and those with a clinically confirmed diagnosis of either Barrett's oesophagus or reflux oesophagitis who had oesophageal and gastric biopsies taken at the same endoscopy and had no evidence of Helicobacter pylori infection entered the study. Control biopsies were taken from H pylori negative NUD patients. Antral biopsies were examined "blind" to clinical group and graded for a series of histological features from which the "reflux gastritis score" (RGS) and "bile reflux index" (BRI) could be calculated. The reproducibility of these histological scores was tested by a second pathologist. RESULTS: There were 100 patients with Barrett's, 61 with GORD, and 50 with NUD. The RGSs did not differ between groups. BRI values in the Barrett's group were significantly higher than those in GORD subjects (p=0.014) which in turn were higher than those in NUD patients (p=0.037). Similarly, the frequency of high BRI values (>14) was significantly greater in the Barrett's group (29/100; 29%) than in the GORD (9/61; 14.8%) or NUD (4/50; 8%) group. However, agreement on BRI values was "poor", indicating limited applicability of this approach. CONCLUSION: Patients with Barrett's oesophagus have more evidence of bile related gastritis than subjects with uncomplicated GORD or NUD. The presence of bile in the refluxate could be a factor in both the development of "specialised" intestinal metaplasia and malignancy in the oesophagus. (+info)
Influence of pantoprazole on oesophageal motility, and bile and acid reflux in patients with oesophagitis.
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BACKGROUND: Reflux of duodeno-gastric juice into the oesophagus appears to be involved in the pathogenesis of both reflux oesophagitis and oesophageal adenocarcinoma. Although proton pump inhibitors have been shown to decrease acid reflux and heal oesophagitis, their effect on biliary reflux and motility is less clear. AIM: To investigate whether pantoprazole also reduces bile reflux and whether this is paralleled by a change in oesophageal motility. METHODS: Combined 24-h measurements of intraoesophageal bilirubin concentration, pH and pressure were performed in 18 symptomatic patients with endoscopically proven reflux oesophagitis before and on day 28 of treatment with pantoprazole, 40 mg/day, under standardized conditions. A reflux symptom score was determined initially and every 2 weeks thereafter. After 56 days on medication, a control endoscopy was performed. RESULTS: The symptom score and the acid and bile reflux improved significantly, whereas the motility parameters did not change during the study period. Helicobacter pylori-positive patients had a significantly higher bile reflux time (32.1 +/- 4.3%) than H. pylori-negative patients (16.3 +/- 3.1%) (P=0.009). The endoscopic healing rate was 89%. The cough symptoms disappeared in three of four patients. CONCLUSIONS: The proton pump inhibitor pantoprazole decreases both acid and bile reflux. The decrease of bile reflux cannot be explained by increased oesophageal clearance as oesophageal motility did not improve with therapy. Interestingly, H. pylori infection of the stomach was associated with higher levels of oesophageal bile reflux. (+info)
Bile reflux gastritis and intestinal metaplasia at the cardia.
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BACKGROUND AND AIMS: Intestinal metaplasia (IM) at the cardia is likely to be a precursor of cardia cancer. Previous work has shown that it is associated with chronic inflammation attributable to either gastro-oesophageal reflux disease (GORD) or Helicobacter pylori infection. An alternative aetiological factor is bile reflux. Duodenogastric reflux brings about histological changes in the gastric mucosa that can be graded and used to calculate a bile reflux index (BRI). We used the BRI to assess whether reflux of bile plays a part in the development of cardia IM. METHODS: Histological changes in simultaneous gastric antrum and cardia biopsies from 267 dyspeptic patients were independently graded by two pathologists. The association between cardia IM and age, sex, clinical group, H pylori status, increased BRI (>14), and inflammation at the cardia were evaluated using logistic regression. RESULTS: A total of 226 patients had adequate cardia and antral biopsies; 149 had GORD and 77 had non-ulcer dyspepsia. Cardia IM was present in 66 (29%) patients, of whom 28 (42%) had complete IM. Increasing age, male sex, chronic inflammation, and a high BRI emerged as significant independent associations with cardia IM. Clinical group and H pylori status were not independent risk factors. CONCLUSIONS: Histological evidence of bile reflux into the stomach is associated with cardia IM. This could have an important bearing on carcinogenesis at this site. (+info)
Efficacy and one year follow up of argon plasma coagulation therapy for ablation of Barrett's oesophagus: factors determining persistence and recurrence of Barrett's epithelium.
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INTRODUCTION: Barrett's epithelium (BE) has malignant potential. Neither acid suppression nor antireflux surgery produce consistent or complete regression of the metaplastic epithelium. Endoscopic thermoablation with argon plasma coagulation (APC) offers a different approach but factors influencing its outcome have not been systematically examined. AIM: To assess the efficacy of APC and factors influencing initial and one year outcome. METHODS: Fifty patients, mean age 61.4 years, mean BE length 5.9 cm (range 3-19), underwent APC therapy at four weekly intervals while receiving proton pump inhibitor (PPI) therapy. BE margins were marked by India ink tattooing and extent was documented by grid drawings, photography, and 2 cm interval quadrantic jumbo biopsies. Twenty four hour ambulatory oesophageal pH studies were done while on PPIs before and after APC therapy, and Bilitec bilirubin monitoring after APC completion. RESULTS: A total of 68% of patients achieved >90% BE ablation after a median of four APC sessions. Persistent BE (>10% original BE area) was associated with longer initial BE length despite more APC sessions. Persistent acid and bile reflux on PPIs, although commoner in this group, were not significantly different from those successfully ablated. Fifteen of 34 patients (44%) with successful macroscopic clearance had buried glands, present in 8.3% of a total of 338 biopsies. At the one year follow up, only 32% of those with initial successful ablation showed no recurrence. BE recurred or increased in most with mean segment length increases of 1.1 cm and 1.6 cm, respectively, in patients with previous full ablation and those with persistent BE. The presence of buried glands did not predict BE recurrence. Patients who reduced their PPI dose had significantly greater BE recurrence. CONCLUSIONS: APC is most effective for shorter segment BE ablation but "buried" glands do occur. Recurrence of BE is common at one year, especially in those with initial persistent and/or long segment BE and those who reduce their PPI dose. (+info)
The effect of famotidine on gastroesophageal and duodeno-gastro-esophageal refluxes in critically ill patients.
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AIM: To investigate the effect of famotidine on gastroesophageal reflux (GER) and duodeno-gastro-esophageal reflux (DGER) and to explore it's possible mechanisms. To identify the relevant factors of the reflux. METHODS: Nineteen critically ill patients were consecutively enrolled in the study. Dynamic 24 hours monitoring of GER and DGER before and after administration of famotidine was performed. The parameters of gastric residual volume, multiple organ disorder syndrome (MODS) score, acute physiology and chronic health evaluation II (APACHE II) score and PEEP were recorded. Paired t test; Wilcoxon signed ranks test and Univariate analysis with Spearman's rank correlation were applied to analyse the data. RESULTS: Statistical significance of longest acid reflux, reflux time of pH<4 and fraction time of acid reflux was observed in ten critically ill patients before and after administration. P value is 0.037, 0.005, 0.005 respectively. Significance change of all bile reflux parameters was observed before and after administration. P value is 0.007,0.024, 0.005, 0.007, 0.005. GER has positive correlation with APACHE II score and gastric residual volume with correlation coefficient of 0.720, 0.932 respectively. CONCLUSION: GER and DGER are much improved after the administration of famotidine. GER is correlated with APACHE II score and gastric residual volume. (+info)
Reflux and Barrett's oesophagitis after gastric surgery--long-term follow-up and implications for the roles of gastric acid and bile in oesophagitis.
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BACKGROUND: The role of gastric acid is difficult to separate from that of bile in oesophageal reflux, and the complications of this can take many years to develop. Gastric surgery patients provide a good model for both significant bile reflux and marked gastric acid inhibition. AIM: To study the oesophageal abnormalities in gastric surgery patients undergoing long-term follow-up, compared with patients with intact stomachs. METHODS: Two hundred and forty adult patients were endoscoped regardless of their age, sex or type of surgical procedure. Oesophageal damage was graded on a scale of 0-5, and biopsies were taken to exclude neoplasia, to diagnose Barrett's oesophagus and to identify Helicobacter pylori. RESULTS: Of the 240 patients studied, 140 had undergone gastric surgery 27 years (19-31 years) [median (interquartile range)] prior to endoscopy, and these patients had milder oesophageal scores and fewer cases of Barrett's oesophagitis. Of the 119 patients with post-surgical bile reflux gastritis, 31 (26%) had oesophagitis, two (1.7%) had Barrett's oesophagitis and oesophageal scores of 0 (0-1) were found. These results compared with corresponding values of 37 (37%; P = 0.11), 11 (11%; P = 0.007) and 0 (0-2) (P = 0.046), respectively, in 100 patients with intact stomachs. In addition, of the 83 patients with vagotomy, 19 had oesophagitis (23%; P = 0.05), none had Barrett's oesophagitis and lower oesophageal scores (P = 0.02) were found. CONCLUSIONS: The prevalence and severity of reflux and Barrett's oesophagitis are not increased in patients with a long history of gastric surgery, particularly after vagotomy, and despite being at risk of bile reflux. (+info)