Lack of proton pump inhibitor trial prior to commencing therapy for eosinophilic esophagitis is common in the community.

Eosinophilic esophagitis is characterized by eosinophil inflammation restricted to the esophagus and the resulting symptoms of esophageal dysfunction. Critical to the diagnosis of eosinophilic esophagitis is a trial of proton pump inhibitor therapy to exclude alternative causes of esophageal eosinophilia such as proton pump inhibitor-responsive esophageal eosinophilia. While consensus guidelines recommend a proton pump inhibitor trial prior to diagnosis, little is known about its implementation in clinical practice. The primary aim of this study is to assess the frequency of proton pump inhibitor trial prior to the diagnosis of eosinophilic esophagitis in community practice. The secondary aim is to assess the frequency of other treatments for eosinophilic esophagitis, including topical steroids and/or dietary therapy, in patients who did not undergo a proton pump inhibitor trial prior to diagnosis or who had an alternative diagnosis to eosinophilic esophagitis upon completed workup. We conducted a single-center, case series of patients referred to the Hospital of the University of Pennsylvania for eosinophilic esophagitis management between 2010 and 2015. This case series consisted of 125 patients who were referred from community practitioners with a presumptive diagnosis of eosinophilic esophagitis. Upon review, 90 out of 125 (72%) patients had not had a proton pump inhibitor trial or esophageal pH testing prior to the diagnosis of eosinophilic esophagitis being made. Of these patients, 77.8% (70/90) had already received either topical steroid or dietary therapy for presumed eosinophilic esophagitis. Of the 125 patients initially diagnosed with eosinophilic esophagitis, 32 (25.6%) were found to have an alternative diagnosis, and 79.2% of this subset of patients (25/32) had previously received topical steroid or dietary therapy. This study demonstrates that a substantial number of patients with presumed eosinophilic esophagitis have not had a proton pump inhibitor trial prior to diagnosis in community practice. This led to the misclassification of patients and potentially to the use of less optimal medical therapies in a substantial number of these patients.

Clinical presentation and disease course of patients with esophagogastric junction outflow obstruction.

Esophagogastric junction outflow obstruction, characterized by preserved peristalsis in conjunction with an elevated integrated relaxation pressure, can result from specific anatomic variants or may represent achalasia in evolution. There is limited information on the clinical significance of this diagnosis. The aim of this study is to describe the clinical characteristics and outcomes in our cohort of patients with esophagogastric junction outflow obstruction.Consecutive adult patients who had undergone high-resolution esophageal manometry between February 2013 and November 2015 with a diagnosis of esophagogastric junction outflow obstruction were identified. Electronic medical records were reviewed to determine: (1) secondary causes of esophagogastric junction outflow obstruction; (2) treatment; and (3) natural history. Improvement in symptoms noted during follow-up evaluation was considered to be a favorable outcome. Worsening of symptoms or no change in symptoms was considered to be an unfavorable outcome.Of 874 manometries performed during this time period, 83 met the criteria for esophagogastric junction outflow obstruction. Of these patients, 11 had secondary causes: paraesophageal hernia (4), Nissen fundoplication (2), esophageal stricture (3), prior laparoscopic band placement (1), and diverticulum (1). All of these secondary causes were identified by barium esophagram. The remaining 72 patients were categorized as idiopathic esophagogastric junction outflow obstruction. Two patients developed type II achalasia on follow-up. An additional two patients had no symptoms as testing was performed for preoperative evaluation prior to bariatric surgery, leaving 68 patients for symptom follow-up analysis. Of these, 19 had a favorable outcome, 18 had an unfavorable outcome, and 31 were lost to follow-up. Of those with a favorable outcome, 6 patients underwent treatment: medication (3), botulinum toxin injection followed by laparoscopic Heller myotomy (1), botulinum toxin injection and medication (1), and bougie dilation (1). Of the 18 patients with an unfavorable outcome, 6 patients underwent treatment: botulinum toxin injection (5) and medication (1). Computed tomography scan or endoscopic ultrasound was performed in 40% of patients with available follow-up and none of these studies revealed secondary causes. The overall median follow-up time was 5 months.Esophagogastric outflow obstruction is a manometric finding of unclear significance. Secondary causes should first be excluded with structural studies. The evolution of esophagogastric junction outflow obstruction to achalasia is rare. Symptoms in patients with esophagogastric junction outflow obstruction do not always require treatment and treatment response is variable. The challenge in managing these patients lies in distinguishing which patients will need intervention. Further studies are needed for consideration of subgrouping this disease or modifying the categorization into clinically relevant entities.

Alginate therapy is effective treatment for GERD symptoms: a systematic review and meta-analysis.

In patients with gastroesophageal reflux disease (GERD) and erosive esophagitis, treatment with proton pump inhibitors (PPIs) is highly effective. However, in some patients, especially those with nonerosive reflux disease or atypical GERD symptoms, acid-suppressive therapy with PPIs is not as successful. Alginates are medications that work through an alternative mechanism by displacing the postprandial gastric acid pocket. This study performed a systematic review and meta-analysis to examine the benefit of alginate-containing compounds in the treatment of patients with symptoms of GERD. PubMed/MEDLINE, Embase, and the Cochrane library electronic databases were searched through October 2015 for randomized controlled trials comparing alginate-containing compounds to placebo, antacids, histamine-2 receptor antagonists (H2RAs), or PPIs for the treatment of GERD symptoms. Additional studies were identified through a bibliography review. Non-English studies and those with pediatric patients were excluded. Meta-analyses were performed using random-effect models to calculate odds ratios (OR). Heterogeneity between studies was estimated using the I2 statistic. Analyses were stratified by type of comparator. The search strategy yielded 665 studies and 15 (2.3%) met inclusion criteria. Fourteen were included in the meta-analysis (N = 2095 subjects). Alginate-based therapies increased the odds of resolution of GERD symptoms when compared to placebo or antacids (OR: 4.42; 95% CI 2.45-7.97) with a moderate degree of heterogeneity between studies (I2 = 71%, P = .001). Compared to PPIs or H2RAs, alginates appear less effective but the pooled estimate was not statistically significant (OR: 0.58; 95% CI 0.27-1.22). Alginates are more effective than placebo or antacids for treating GERD symptoms.

Alginate therapy is effective treatment for gastroesophageal reflux disease symptoms: a systematic review and meta-analysis.

In patients with gastroesophageal reflux disease (GERD) and erosive esophagitis, treatment with proton pump inhibitors (PPIs) is highly effective. However, in some patients, especially those with non-erosive reflux disease or atypical GERD symptoms, acid suppressive therapy with PPIs is not as successful. Alginates are medications that work through an alternative mechanism by displacing the post-prandial gastric acid pocket. We performed a systematic review and meta-analysis to examine the benefit of alginate-containing compounds in the treatment of patients with symptoms of GERD.PubMed/MEDLINE, Embase and the Cochrane library electronic databases were searched through October 2015 for randomized controlled trials comparing alginate-containing compounds to placebo, antacids, histamine-2 receptor antagonists (H2RAs) or PPIs for the treatment of GERD symptoms. Additional studies were identified through bibliography review. Non-English studies and those with pediatric patients were excluded. Meta-analyses were performed using random-effects models to calculate odds ratios (OR). Heterogeneity between studies was estimated using the I2 statistic. Analyses were stratified by type of comparator. The search strategy yielded 665 studies and 15 (2.3%) met inclusion criteria. Fourteen were included in the meta-analysis (N = 2095 subjects). Alginate-based therapies increased the odds of resolution of GERD symptoms when compared to placebo or antacids (OR: 4.42; 95% CI 2.45-7.97) with a moderate degree of heterogeneity between studies (I2 = 71%, P = .001). Compared to PPIs or H2RAs, alginates appear less effective but the pooled estimate was not statistically significant (OR: 0.58; 95% CI 0.27-1.22). Alginates are more effective than placebo or antacids for treating GERD symptoms.

Proton pump inhibitors: are they overutilised in clinical practice and do they pose significant risk?

Proton pump inhibitors are highly effective acid suppressants with decades of use highlighting positive outcomes in millions of patients worldwide, and they offer minimal risk of adverse events. PPIs are considered overutilised when prescribed without an appropriate indication, when patients are left on them 'indefinitely' without appropriate indications and when they are continued after being utilised for most cases of hospital SUP. While several adverse outcomes have been linked to PPI therapy, most data are from retrospective observational studies that may be subject to confounding and bias.

Safety profile of dexlansoprazole MR, a proton pump inhibitor with a novel dual delayed release formulation: global clinical trial experience.

BACKGROUND: Dexlansoprazole MR is a dual delayed release formulation of dexlansoprazole, an enantiomer of lansoprazole. AIM: To assess safety of dexlansoprazole MR in phase 3 clinical trials. METHODS: Data from 4270 patients receiving dexlansoprazole MR 30 mg (n = 455), 60 mg (n = 2311) or 90 mg (n = 1864); lansoprazole 30 mg (n = 1363); or placebo (n = 896) in six randomized controlled trials and a 12-month safety study were pooled. Safety was assessed via adverse events, vital signs, electrocardiograms, clinical laboratory results and gastric biopsies. Adverse events were summarized per 100 patient-months of exposure to account for imbalances in study drug exposure. RESULTS: The number of patients with > or =1 treatment-emergent adverse event per 100 patient-months was higher in placebo (24.49) and lansoprazole (21.06) groups than in any dexlansoprazole MR (15.64-18.75) group. Fewer patients receiving dexlansoprazole MR discontinued therapy because of an adverse event (P < or = 0.05 vs. placebo). Seven patients died of events considered unrelated to study drug. Mean serum gastrin rose in all groups except placebo; increases were not dose-related. No clinically concerning trends were seen in gastric biopsy results. Endocrine cell hyperplasia, dysplasia and neoplasia were not observed. CONCLUSION: Dexlansoprazole MR 30-90 mg has a safety profile comparable to that of lansoprazole.

Review article: dual delayed release formulation of dexlansoprazole MR, a novel approach to overcome the limitations of conventional single release proton pump inhibitor therapy.

BACKGROUND: Proton pump inhibitors (PPIs) provide the most effective pharmacotherapy for treating acid-related disorders. However, PPIs do not completely control acid over 24 h with once-daily dosing. AIMS: To discuss limitations inherent in the pharmacokinetics (PK) and pharmacodynamics of conventional PPI formulations, which provide a single drug release. Also, to consider approaches to extending the duration of acid suppression focusing on dexlansoprazole MR, a PPI with a novel Dual Delayed Release (DDR) formulation. METHOD: We reviewed the available literature regarding marketed and investigational PPIs. RESULTS: Non-standard dosing of currently marketed PPIs has produced incremental advances in acid control. Multiple approaches are being evaluated to enhance acid suppression with PPIs. Dexlansoprazole MR is a DDR formulation of dexlansoprazole, an enantiomer of lansoprazole, with two distinct drug release periods to prolong the plasma dexlansoprazole concentration-time profile and extend duration of acid suppression. Clinical studies show that dexlansoprazole MR produces a dual-peak PK profile that maintains therapeutic plasma drug concentrations longer than lansoprazole, with a single-peak PK profile, and increases the percentage of time that intragastric pH >4. CONCLUSIONS: Novel drug delivery platforms, including the dexlansoprazole MR DDR formulation, may improve acid suppression and offer benefits over conventional single release PPI formulations.

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.

Effect of pantoprazole in older patients with erosive esophagitis.

Several studies suggest that older adults with gastroesophageal reflux disease (GERD) are more likely to develop complications, including erosive esophagitis, but it is unclear whether erosive esophagitis is more difficult to treat in older patients. The purpose of this study was to determine if adults > or = 65 years with erosive esophagitis are more difficult to treat than younger adults. The study was a post hoc analysis of two double-blind, randomized, multicenter trials of patients with erosive esophagitis. Patients received pantoprazole 40 mg once daily, nizatidine 150 mg twice daily or placebo. Patients were evaluated for endoscopic healing at 4 and 8 weeks. Patients recorded typical reflux symptoms using a daily diary to note presence or absence of symptoms. Results showed that 44, 13 and 11 patients > or = 65 years and 210, 69, and 71 patients < 65 received pantoprazole 40 mg daily, nizatidine 150 mg twice daily, or placebo, respectively. Eighty-six percent (86%[76%, 97% CI]) of older and 83% (78%, 88% CI) of younger pantoprazole-treated patients were healed at 8 weeks; 46% (19%, 73% CI) and 35% (24%, 46% CI) of nizatidine-treated and 27% (1%, 54% CI) and 34% (23%, 45% CI) of placebo-treated were healed at 8 weeks. Median time to persistent absence of GERD-related symptoms was similar for older and younger patients treated with pantoprazole. We conclude that older patients with erosive esophagitis do not appear to have more difficult-to-treat disease. Erosive esophagitis is effectively healed and GERD symptoms are controlled in older patients using pantoprazole 40 mg daily.

Evaluation of a locally produced rapid urease test for the diagnosis of Helicobacter pylori infection.

BACKGROUND: The rapid urease test (RUT) is used at Groote Schuur Hospital for diagnosing Helicobacter pylori infection. This is an in-house method, which has not been validated. OBJECTIVE: To validate our practice of reading the RUT immediately after endoscopy (RUT(0)), by comparing this with a reading at 24 hours (RUT(24)) and with histological analysis. DESIGN: Ninety consecutive patients undergoing upper endoscopy over a 6-week period from October 2005 to November 2005, and in whom rapid urease testing was indicated, were included in the study. Patients with recent exposure (within 2 weeks of endoscopy) to proton pump inhibitors (PPIs), histamine receptor antagonists (H2RAs) and antibiotics (confounders) were noted and included in the cohort. Two antral and two body biopsies were taken for histological examination and a third antral biopsy was placed in the RUT bottle. Both haematoxylin and eosin and modified Giemsa staining methods were used to identify H. pylori. The RUT was read immediately (within 5 minutes of upper endoscopy) (RUT(0)), as per our current practice, and each specimen was re-read at 24 hours (RUT(24)). Sensitivity, specificity, positive and negative predictive values and the impact of confounders were calculated. RESULTS: Of the 90 patients undergoing rapid urease testing, 39% were male and 61% were female, with a mean age of 55 years (range 22-79 years). Histological examination revealed H. pylori in 67.8% (N=61) of the biopsy specimens. In the 65 patients without confounders, the sensitivity and specificity of the RUT(0) were 65.9% and 100% respectively, and 90.9% and 100% for RUT(24). After including the 25 patients with confounders, the sensitivity and specificity were 68.8% and 100% for RUT(0), and 90.1% and 100% for RUT(24) respectively. Thirteen RUT(0) specimens (30.9%) that were initially negative became positive at the RUT(24) reading. There were 6 (9.8%) RUT(0)- and RUT(24)-negative but histology-positive specimens. Four of these 6 false-negative RUT(24) results could be accounted for by a low H. pylori density on histological analysis (2 patients were taking PPIs). Confounders did not alter the sensitivity and specificity outcomes or impact on the number of false-negative RUTs. CONCLUSIONS: Our locally prepared RUT is a specific test for the detection of H. pylori infection. The sensitivity is greatly enhanced by reading the test at 24 hours. The use of PPIs, H(2)RAs and antibiotics preceding endoscopy did not impact significantly on the results.

Dose-response evaluation of the antisecretory effect of continuous infusion intravenous lansoprazole regimens over 48 h.

BACKGROUND: Attainment of intragastric pH < 6.0 may require high-dose continuously infused proton pump therapy. AIM: To assess the pharmacokinetic and pharmacodynamic dose-responses of continuous infusion regimens of lansoprazole. METHODS: Healthy adult subjects were assigned to lansoprazole 60-mg intravenous bolus, followed by 6-mg/h continuous infusion; a 90-mg intravenous bolus followed by 6-, 7.5-, or 9-mg/h continuous infusion; or placebo. RESULTS: Mean intragastric pH values for lansoprazole regimens ranged from 4.8 to 5.2 (0-24 h), 5.5 to 6.0 (>24 to 48 h) and 5.2 to 5.6 (0-48 h). Within these three intervals, the percentages of time intragastric pH exceeded 4, 5 and 6 ranged from 65% to 96%, 54% to 88% and 30% to 61% respectively. Pharmacokinetic parameters were dose-independent with steady-state plasma concentrations achieved within 6-12 h postdose and maintained over 48 h. The mean systemic clearance of lansoprazole was lower in CYP2C19 heterozygous metabolizers than in homozygous extensive metabolizers (9.2 vs. 16.5 L/h), with substantial variability resulting in overlapping ranges of clearance values for both subpopulations. All lansoprazole regimens were well-tolerated. CONCLUSIONS: Lansoprazole administered as a 60-mg intravenous bolus followed by 6-mg/h continuous infusion produced intragastric pH effects comparable with those of higher dosage regimens.

Lansoprazole regimens that sustain intragastric pH > 6.0: an evaluation of intermittent oral and continuous intravenous infusion dosages.

BACKGROUND: Orally and intravenously administered proton pump inhibitors have been shown to reduce rebleeding rates, surgery and transfusion requirement. AIM: To compare lansoprazole intravenous and orally disintegrating tablet (Prevacid SoluTab) regimens with a pantoprazole intravenously administered regimen in sustaining intragastric pH >6.0. METHODS: Two similarly designed three-way, randomized crossover studies each enrolled 36 Helicobacter pylori-negative healthy volunteers. Study 1 regimens included intravenously administered bolus followed by 24-h continuous infusion (lansoprazole 90 mg, 6 mg/h; lansoprazole 120 mg, 6 mg/h; pantoprazole 80 mg, 8 mg/h). Study 2 regimens included intravenous bolus followed by lansoprazole orally disintegrating tablet or intravenous continuous infusion for 24 h (lansoprazole 90 mg, lansoprazole orally disintegrating tablet 60 mg every 6 h; lansoprazole 120 mg, 9 mg/h; pantoprazole 80 mg, 8 mg/h). Percentage of time pH >6.0 was assessed with 24-h intragastric pH monitoring. RESULTS: All regimens produced comparable gastric acid suppression. In both studies, regimens superior to pantoprazole included lansoprazole 90 mg, 6-mg/h; lansoprazole 90 mg, lansoprazole orally disintegrating tablet 60 mg q.d.s. and lansoprazole 120 mg, 9 mg/h (P < or = 0.013). The lansoprazole 120-mg, 6-mg/h regimen (P = 0.082) was not superior to pantoprazole in percentage of time intragastric pH >6.0. Mild reaction at the intravenous injection site was the most frequently reported adverse event. CONCLUSIONS: The intravenous bolus and continuously infused lansoprazole or intravenous bolus and intermittent lansoprazole orally disintegrating tablet regimens are as effective as intravenous pantoprazole in sustaining intragastric pH >6.0.

Three-year oral pantoprazole administration is effective for patients with Zollinger-Ellison syndrome and other hypersecretory conditions.

BACKGROUND: Zollinger-Ellison syndrome and idiopathic hypersecretion are gastrointestinal hypersecretory conditions requiring long-term maintenance. AIMS: The safety and efficacy data for short-term (6-month) treatment of Zollinger-Ellison syndrome and idiopathic hypersecretion with oral pantoprazole were previously published. This study extends the initial observations to 3 years. METHODS: The primary efficacy end point for this report was the control of gastric acid secretion in the last hour before the next dose of oral pantoprazole (acid output of <10 mmol/h; <5 mmol/h in subjects with prior acid-reducing surgery). Dose titration was permitted to a maximum of 240 mg per 24 h. RESULTS: Twenty-four subjects completed the study. The acid output of 28 of 34 subjects was controlled at initial enrolment. The mean acid output rates were <10 mmol/h throughout the 36 months of treatment for 90-100% of the patients. The majority of the patients were controlled with b.d. doses of 40 or 80 mg pantoprazole at 36 months (acid output was controlled in 24 of 24 subjects). Pantoprazole was generally well tolerated with minimal adverse events reported. CONCLUSIONS: Maintenance oral pantoprazole therapy up to 3 years at dosages of 40-120 mg b.d. was effective and well tolerated in patients with Zollinger-Ellison syndrome and other hypersecretory conditions.

Comparison of the effects of intravenously and orally administered esomeprazole on acid output in patients with symptoms of gastro-oesophageal reflux disease.

BACKGROUND: Intravenous esomeprazole may be beneficial for patients who cannot take oral medications. AIM: To compare intravenous esomeprazole with oral esomeprazole for effects on maximal acid output during pentagastrin stimulation in patients with gastro-oesophageal reflux disease symptoms. METHODS: In four separate open-label, randomized, two-way crossover studies, adult patients were administered esomeprazole 20 or 40 mg once daily either orally or intravenously (by 15-min infusion or 3-min injection) for 10 days and switched to the other formulation with no washout period. Basal acid output and maximal acid output were measured on days 11, 13 and 21. RESULTS: In the four studies (total of 183 patients), least-squares mean maximal acid output ranged from 3.0 to 4.1 mmol/h after intravenous esomeprazole 40 or 20 mg and from 2.2 to 3.3 mmol/h after oral esomeprazole 20 or 40 mg. Differences between formulations were small and not statistically significant but did not meet the prospectively defined criterion for non-inferiority of the intravenous formulation. Median basal acid output values ranged from 0.04 to 0.27 mmol/h after intravenous administration and from 0.05 to 0.25 mmol/h after oral esomeprazole. CONCLUSIONS: Intravenous esomeprazole is an acceptable alternative to the oral formulation for treatment of up to 10 days of duration.

Postprandial oesophageal integrated acidity is a reliable predictor of gastro-oesophageal reflux disease.

BACKGROUND: Measurement of oesophageal acid exposure parameters postprandially has been shown to distinguish gastro-oesophageal reflux disease patients from normal individuals. AIMS: To calculate the accuracy of postprandial oesophageal integrated acidity in diagnosing gastro-oesophageal reflux disease. METHODS: Ambulatory 24-h pH studies of 626 patients were analysed retrospectively. Gastro-oesophageal reflux disease, defined as pH < 4 for > 4.2% of time, was identified in 305 subjects. Postprandial oesophageal integrated acidity was measured for 2 and 3 h after the largest meal peak as determined from gastric pH. Postprandial symptom-associated probability was calculated. RESULTS: Gastro-oesophageal reflux disease subjects had a greater postprandial oesophageal integrated acidity than non-gastro-oesophageal reflux disease subjects [median (IQR): 0.57 (0.08-2.66) vs. 0.03 (0.01-0.15) mmol*h/L]. Median postprandial oesophageal integrated acidity did not differ with gender or age in gastro-oesophageal reflux disease and non-gastro-oesophageal reflux disease subjects (P > 0.05 for all). A 3-h postprandial oesophageal integrated acidity value of 0.121 mmol*h/L had a 71.1% sensitivity and 71.7% specificity in diagnosing gastro-oesophageal reflux disease. Gastro-oesophageal reflux disease subjects with symptoms had a higher postprandial oesophageal integrated acidity than those without (P = 0.043), whereas non-gastro-oesophageal reflux disease subjects with and without symptoms did not differ (P = 0.74). The correlation between symptom-associated probability and postprandial oesophageal integrated acidity was poor (gastro-oesophageal reflux disease: r = 0.15; non-gastro-oesophageal reflux disease: r = 0.25). CONCLUSION: Postprandial oesophageal integrated acidity provides a robust estimation of oesophageal acid exposure and may predict symptoms in gastro-oesophageal reflux disease patients.

Pantoprazole provides rapid and sustained symptomatic relief in patients treated for erosive oesophagitis.

BACKGROUND: Effective symptom control is a primary concern of most heartburn suffers. AIM: To compare the safety and efficacy of pantoprazole, placebo and the H2 antagonist nizatidine in relieving symptoms in patients with erosive oesophagitis. METHODS: Data from two randomized, double-blind studies were pooled. Patients received pantoprazole 10, 20 or 40 mg, or placebo daily (study 1, n = 603), or pantoprazole 20 or 40 mg daily or 150-mg nizatidine b.d. (study 2, n = 243) for either 4 or 8 weeks. Endoscopy was performed at baseline, week 4 and week 8. Persistent absence of symptoms was defined as the first day that no symptoms were reported by the patient on that day or any subsequent study day. RESULTS: A significantly higher percentage (P < 0.05) of pantoprazole patients reported elimination of all symptoms by week 8. Daytime heartburn, night-time heartburn and regurgitation were significantly better controlled with pantoprazole (with a dose-response at most time-points). Absence of symptoms was a powerful predictor of healing; presence of symptoms correlated poorly. CONCLUSION: Pantoprazole is more effective than placebo or nizatidine for controlling heartburn and acid regurgitation in patients with erosive oesophagitis. Relief of GERD symptoms is highly predictive of healing of erosive oesophagitis at 4 and 8 weeks.

Intravenous and oral lansoprazole are equivalent in suppressing stimulated acid output in patient volunteers with erosive oesophagitis.

BACKGROUND: Some patients requiring acid suppression may be unable to take oral medications. AIM: To compare the gastric acid inhibition effects of lansoprazole 30 mg administered either intravenous or orally in erosive oesophagitis patients. METHODS: The study included 87 Helicobacter pylori-negative patients with erosive oesophagitis. Each patient received 7 days of lansoprazole 30 mg orally prior to being randomized in a 3:1 fashion to intravenously lansoprazole 30 mg or intravenously placebo for 7 days. Basal acid output and pentagastrin-stimulated acid output were measured on days 8, 9 and 15. RESULTS: Median pentagastrin-stimulated acid output was 7.2 mmol/h after 7 days of oral lansoprazole. The median pentagastrin-stimulated acid output increased to 7.6 mmol/h after 7 days of intravenous lansoprazole compared with 26.9 mmol/h after intravenous placebo (P < 0.001). CONCLUSIONS: Lansoprazole 30 mg administered intravenous was equivalent to the 30 mg oral capsule in gastric acid suppression. Intravenous proton pump inhibitor therapy represents an important treatment option for those with acid-related diseases who are unable to take oral medications.

Pantoprazole maintenance therapy prevents relapse of erosive oesophagitis.

OBJECTIVES: To compare the safety and efficacy of pantoprazole with ranitidine for the maintenance of endoscopically documented healed (grade 0 or 1) erosive oesophagitis. METHODS: Patients (371) were randomly assigned to receive pantoprazole 10, 20 or 40 mg or ranitidine 150 mg. Endoscopies were performed after 1, 3, 6 and 12 months or when symptoms suggesting relapse (grade = 2) developed. Gastric biopsies were obtained at baseline and on at least one postbaseline visit. Symptom-free days and Gelusil use were assessed. RESULTS: Pantoprazole was significantly (P < 0.001) more effective in maintaining erosive oesophagitis healing. After 12 months, 33%, 40%, 68% and 82% of patients remained healed for the ranitidine and pantoprazole 10, 20 and 40 mg groups, respectively. Daytime and night-time heartburn were eliminated in > 90% of days for the pantoprazole 40 mg group. Gelusil use was significantly lower with pantoprazole 20 and 40 mg than with ranitidine (P < 0.02) during the first 9 months. CONCLUSIONS: Twelve months of maintenance therapy with pantoprazole (10-40 mg once daily) was superior to ranitidine (150 mg twice daily) in maintaining erosive oesophagitis healing. Pantoprazole 40 mg provided the most consistent efficacy and was well tolerated.

Radiographically diagnosed antral gastritis: findings in patients with and without Helicobacter pylori infection.

The purpose of this study was to characterize the radiographic findings of antral gastritis and to determine whether there are differences in the appearance of antral gastritis in patients with and without Helicobacter pylori infection. A search of radiology, endoscopy and pathology files revealed 90 patients with antral gastritis on double contrast upper gastrointestinal tract studies who had endoscopy with testing for H. pylori. The barium studies were evaluated to further characterize the findings of antral gastritis without knowledge of the H. pylori status of the patients or of the endoscopy or pathology findings. The radiographic findings of antral gastritis included thickened folds in 67 patients (74%), polypoid antral gastritis (a subset of patients with thickened folds) in 6 (9%), antral erosions in 21 (23%), enlarged areae gastricae in 14 (16%), crenulation of the lesser curvature in 4 (4%), mucosal nodularity in 2 (2%), a hypertrophied antral-pyloric fold in 2 (2%) and antral striae in 1 (1%). 43 patients (48%) with antral gastritis were H. pylori positive and 47 patients (52%) were H. pylori negative. Thickened folds were detected in 39 H. pylori-positive patients (91%) with antral gastritis vs 28 H. pylori-negative patients (60%) (p<0.001); polypoid gastritis in 6 H. pylori-positive patients (14%) vs 0 H. pylori-negative patients (p<0.05); enlarged areae gastricae in 14 H. pylori-positive patients (33%) vs 0 H. pylori-negative patients (p<0.0001); and antral erosions in 2 H. pylori-positive patients (5%) vs 19 H. pylori-negative patients (40%) (p<0.0001). Our experience suggests that antral gastritis caused by H. pylori infection is associated with characteristic features on double contrast studies (including thickened folds, polypoid gastritis and enlarged areae gastricae) and that this condition is rarely associated with antral erosions. Thus, radiologists can often suggest whether the patient's gastritis is caused by H. pylori on the basis of radiographic findings.