Corpus gastritis in patients with endoscopic diagnosis of reflux oesophagitis and Barrett's oesophagus

BACKGROUND: A high level of gastric acid secretion is considered to be a risk factor for reflux oesophagitis or Barrett's oesophagus. Corpus gastritis may have a protective effect on the oesophagus, because of decreased gastric acid output. AIM: To determine if corpus gastritis is associated with reflux oesophagitis or Barrett's oesophagus. METHODS: Three antral and two corpus biopsies were taken from consecutive patients in whom Helicobacter pylori testing was requested during endoscopy at a single centre between January 1995 and May 1997. Antral and corpus gastritis was studied by histology; H. pylori was studied by histology, culture and CLO test. A regression model was used to test for correlation between reflux oesophagitis, Barrett's oesophagus and risk factors. RESULTS: During the study period, 676 patients had biopsies taken during upper gastrointestinal endoscopy. Endoscopic signs of reflux oesophagitis and Barrett's oesophagus were observed in 125 and 23 patients, respectively. Corpus gastritis was found in 59% of patients without reflux oesophagitis or Barrett's oesophagus, 45% of patients with reflux oesophagitis and 30% of patients with Barrett's oesophagus. Two hundred and fifty-seven patients underwent follow-up endoscopy after H. pylori therapy. During a mean follow-up of 3 months, the incidence of reflux oesophagitis was not statistically different for patients with healing of corpus gastritis (10/98; 10%) and patients with persistent gastritis (8/97; 8%). CONCLUSIONS: Corpus gastritis was less common in patients with an endoscopic diagnosis of reflux oesophagitis or Barrett's oesophagus.     

The prescribing of acid suppressants prior to the endoscopic diagnosis of Barrett's oesophagus and oesophagitis

BACKGROUND: There has been a dramatic rise in incidences of Barrett's oesophagus and oesophageal adenocarcinoma. It has been suggested that the introduction and use of acid suppression therapy may be a factor in the rising incidences of Barrett's oesophagus and oesophageal adenocarcinoma. METHODS: This was a record linkage study, using a prescribing database and an endoscopy database. Patients who had undergone their first endoscopy during the period 1992-1995 and received the diagnosis of Barrett's oesophagus or oesophagitis were identified. The prescribing of acid suppressants was compared for the 3 years prior to endoscopy, between those with Barrett's oesophagus and those with oesophagitis. RESULTS: There was no significant difference between the Barrett's patients and the oesophagitis patients in the proportion that had been exposed to acid suppression therapy (53.4% vs. 51.7%, P=0.704). The mean number of days of prescribing among those who had been exposed to acid suppression therapy was higher in the Barrett's group (340.5 vs. 237.0 days, P=0.001). CONCLUSIONS: Patients with Barrett's oesophagus have received more acid suppressant therapy prior to diagnosis. The reasons for this are not clear. However, 46.6% of Barrett's patients have not been exposed to acid suppressant therapy.     

Barrett's oesophagus: optimal strategies for prevention and treatment

Barrett's oesophagus is a change in the lining of the distal oesophagus recognised at endoscopy and documented to have intestinal metaplasia by biopsy. It is thought that it is an acquired condition resulting from chronic gastro-oesophageal reflux disease (GORD). Barrett's oesophagus has the potential to progress to adenocarcinoma of the oesophagus. Evidence to support the association between Barrett's oesophagus and GORD appears to be strong but circumstantial. The intermediate steps that lead from GORD to Barrett's oesophagus are speculative and the timeline for the development of this condition remains obscure. It has yet to be demonstrated that erosive oesophagitis is a necessary intermediate step for the development of Barrett's oesophagus. In spite of effective therapy, documentation that medical or surgical therapy prevents Barrett's oesophagus is lacking. The goal of screening for Barrett's oesophagus is ultimately to improve the survival of patients with adenocarcinoma of the oesophagus. This goal has not been achieved and the evidence-based criteria for screening remain to be defined. Medical and surgical therapy of Barrett's oesophagus is effective in controlling reflux, although not proven to prevent neoplastic progression of the at risk mucosa. Endoscopic techniques of mucosal injury have been applied as alternatives to oesophagectomy in efforts to prevent progression to cancer. Surveillance endoscopy and biopsy is the currently accepted method aimed at early intervention and improved survival for oesophageal adenocarcinoma. A working surveillance protocol to accomplish this is proposed based on dysplasia grade. If no dysplasia is found and confirmed with subsequent endoscopy and biopsy, a 3-year interval is recommended. If only low grade dysplasia is confirmed, then annual endoscopy until no dysplasia is recognised is recommended. On the basis of defined risk factors, high grade dysplasia can lead to intense surveillance every 3 months or an intervention. Future developments in understanding the biology of Barrett's oesophagus and in therapeutic interventions will provide an opportunity for more effective screening, surveillance and prevention of neoplastic progression.     

Maximal acid reflux control for Barrett's oesophagus: feasible and effective

The treatment of patients with Barrett's oesophagus is controversial. Debate exists regarding the use and value of high dose acid suppression as the standard of practice. Despite prolonged use of high dose proton pump inhibitors (40 mg omeprazole, 60 mg lansoprazole), most studies have shown no convincing evidence of significant regression of Barrett's length. These studies, however, have used fixed doses of proton pump inhibitors and did not regularly document control of oesophageal acid exposure. AIM: To determine whether regression of Barrett's epithelium can be achieved with documented maximal acid suppression. METHODS: We have prospectively followed nine patients with Barrett's oesophagus (eight male; mean age 60 years) for more than 1 year. They were all treated using medical therapy with pH monitoring documenting oesophageal acid exposure over 24 h < 1.6% of the time, and with two or more esophagogastroduodenoscopies performed by the same endoscopist. RESULTS: Acid control was individually tailored and achieved with proton pump inhibitor b.d. (omeprazole 20 mg or lansoprazole 30 mg) and ranitidine at bedtime (HS) (Ran) if necessary. All nine patients (100%) showed some evidence of regression. All nine patients (100%) showed a decrease in Barrett's length (mean 2 cm, range 1-3 cm). Six out of nine (66.67%) patients showed evidence of squamous islands on the last oesophagogastroduodenoscopy. The mean total distal oesophageal acid exposure was 0.38% (range: 0-1.5%). The mean follow-up of patients was 54 months (range: 13-118 months). CONCLUSIONS: Consistent and individually tailored maximal acid suppression documented by pH-metry is achievable and may result in decreased length and development of squamous islands in patients with Barrett's epithelium. This approach should be further evaluated as potentially the preferred medical treatment for these patients.     

The modified glucose clearance test: a novel non-invasive method for differentiating non-erosive reflux disease and erosive oesophagitis

Background Impaired salivary secretion has been reported to cause abnormal acid clearance from the oesophagus in gastro‐oesophageal reflux disease (GERD). However, few studies have explained the differences between non‐erosive reflux disease (NERD) and erosive oesophagitis (EO) with respect to salivary secretion. Aim To elucidate these differences, we measured salivary secretion by using the modified glucose clearance test (mGCT). Methods All subjects completed endoscopic examinations, the frequency scale for the symptoms of GERD questionnaire and the mGCT comprising a resting GCT (measured as RGC time) and a chewing‐stimulated GCT (SGC time). Results Resting glucose clearance time was 18.5 min in control group and significantly longer in NERD and EO groups (28.5 and 39.0 min respectively). SGC time was 6.1 min in control group and 7.2 min in NERD group and significantly longer in EO group (10.2 min) than in the control and NERD groups. Conclusions In the EO group, both resting and stimulated salivary secretions were less than in control group. However, in the NERD group, resting salivary secretion was decreased, but stimulated salivary secretion was similar to that of the control group. Therefore, these results may help in explaining the differences in the pathogenesis of NERD and EO.     

Pantoprazole 20 mg is effective for relief of symptoms and healing of lesions in mild reflux oesophagitis

Aim:

To investigate the efficacy of a low dose of pantoprazole, a gastric proton pump inhibitor, for the relief of symptoms and healing of lesions in mild gastro-oesophageal reflux disease (GERD), and to compare it with the efficacy of ranitidine.

Methods:

Patients with endoscopically established GERD (Stage I, Savary–Miller classification) were enrolled into a randomized, double-blind, parallel-group and multicentre study (intention-to-treat n = 209, age range 19–82 years). They were treated once daily with oral pantoprazole 20 mg or ranitidine 300 mg, for up to 8 weeks. End-point parameters included relief of symptoms (heartburn, acid regurgitation, pain on swallowing) and the healing of GERD lesions. Relief from symptoms was assessed after 2 and 4 weeks, and endoscopically confirmed healing of lesions after 4 and 8 weeks.

Results:

The proportion of patients reporting complete relief from symptoms after 2 weeks was greater in the pantoprazole than in the ranitidine group (69 vs. 48%, P < 0.01), with further improvements seen in the pantoprazole group after 4 weeks (80 vs. 65%, P < 0.05, Cochran–Mantel/Haenszel test). Healing of lesions was confirmed in 70/87 (80%) patients after 4 weeks (pantoprazole group), as compared with 55/86 (64%) patients (ranitidine group) (P < 0.05, per protocol population); after 8 weeks the respective results were 78/87 (90%) and 63/86 (73%) patients (P < 0.01). Both study medications were well tolerated.

Conclusion:

Low-dose pantoprazole (20 mg) is clinically superior to ranitidine (300 mg) in providing fast relief from symptoms and healing of lesions in patients with mild GERD.

     

Clinical trial: dexlansoprazole MR, a proton pump inhibitor with dual delayed-release technology, effectively controls symptoms and prevents relapse in patients with healed erosive oesophagitis

Background  Dexlansoprazole MR heals all grades of erosive oesophagitis (EO).
Aim  To assess efficacy and safety of dexlansoprazole MR in maintaining healed EO and heartburn relief.
Methods  In this randomized, double-blind trial, 445 patients with healed EO received dexlansoprazole MR 30 mg or 60 mg or placebo once daily for 6 months. This trial assessed maintenance of endoscopic healing (primary endpoint) and continued symptom relief based on daily diaries (secondary endpoints).
Results  Dexlansoprazole MR 30 mg and 60 mg were superior to placebo for maintaining healed EO ( P  <   0.0025; Hochberg's). By life-table analysis, maintenance rates were 75%, 83% and 27% for dexlansoprazole MR 30 mg, 60 mg and placebo respectively. Crude maintenance rates were 66% for both dexlansoprazole MR doses and 14% for placebo. Dexlansoprazole MR controlled heartburn (medians of 91–96% for 24-h heartburn-free days, 96–99% for heartburn-free nights). The only more common adverse event occurring at a significantly higher rate in dexlansoprazole MR groups than placebo when analysed per patient-months of exposure was upper respiratory tract infection.
Conclusions  Dexlansoprazole MR effectively maintained EO healing and symptom relief; most patients were heartburn-free for >90% of days. Both doses were well tolerated.