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Helicobacter ISSN 1523-5378
Journal compilation 2007 Blackwell Publishing Ltd, Helicobacter 12 (Suppl. 1): xx–xx Helicobacter pylori and Non-malignant Diseases
Theodore Rokkas,* Ilkay Simsek† and Spiros Ladas‡
*Gastroenterology Department, Henry Dunant Hospital, Athens, Greece, †Gastroenterology Department, Dokuz Eylul University Hospital, Izmir, Turkey, ‡Division of Gastroenterology and Endoscopy, Attikon University General Hospital, Athens, Greece Keywords
Abstract
GERD, NSAIDs, peptic ulcer disease, non-ulcer In recent years, the focus of Helicobacter pylori clinical research has been mainly on gastric malignancy. However, the role of H. pylori in non-malignant diseases,such as peptic ulcer, gastroesophageal reflux disease (GERD) and non-ulcer Reprint request to: Professor Spiros Ladas, MD, dyspepsia, as well as non-steroidal anti-inflammatory drug consumption, is still Division of Gastroenterology and Endoscopy, Attikon University General Hospital, 1 Rimini of great interest. A 1- to 2-week course of H. pylori eradication therapy is an effective treatment for H. pylori-positive peptic ulcer disease and a positive CagA status is a predictor for successful eradication of H. pylori. Antral prostaglandin-E2-basal levels appear to be critical for the development of aspirin-inducedgastric damage in subjects without H. pylori infection. In clinical practice,among patients treated with proton-pump inhibitors, H. pylori status has noeffect on the speed or degree of GERD symptom relief. For the management ofdyspepsia in primary care, antisecretory therapy confers a small insignificantbenefit compared to strategies based on H. pylori testing while these latterstrategies may be cost-effective. H. pylori eradication therapy has a small butstatistically significant effect on H. pylori-positive non-ulcer dyspepsia. Aneconomic model suggests that this modest benefit may still be cost-effective butmore research is needed.
were an increase in the proportion of peptic ulcers healed Peptic Ulcer Disease
initially and an increase in the proportion of patients free Over the last year a number of papers concerning various from relapse following successful healing. Eradication aspects of the association of Helicobacter pylori with peptic therapy was compared to placebo or pharmacologic ulcer disease (PUD) have been published. The majority therapies in H. pylori-positive patients. Secondary aims examined the effectiveness of various H. pylori treatments included symptom relief and adverse events. Sixty-three and will be reviewed in the Treatment section.
trials were eligible and 56 trials were finally included. For Murakami et al. [1] examined the possible relationship duodenal ulcer healing, eradication therapy was superior between peptic ulcer recurrence and the presence or to ulcer-healing drugs (34 trials, 3910 patients, relative risk absence of maintenance therapy with an H -receptor [RR] of ulcer persistence = 0.66; 95% confidence interval antagonist administered until evaluation of H. pylori [CI] 0.58–0.76) and no treatment (two trials, 207 patients, eradication. The results of this study suggested that main- RR 0.37; 95% CI 0.26–0.53). For gastric ulcer healing, no tenance therapy with an H -receptor antagonist post- significant difference was detected between eradication eradication therapy is likely to greatly reduce the ulcer therapy and ulcer-healing drugs (14 trials, 1572 patients, recurrence rate without affecting the evaluation of RR 1.25; 95% CI 0.88–1.76). In preventing duodenal ulcer recurrence, no significant differences were detected between Eradication of H. pylori reduces the relapse rate of PUD.
eradication therapy and maintenance therapy with Ford et al. examined the magnitude of this effect in their ulcer-healing drugs (four trials, 319 patients, RR of ulcer systematic review and meta-analysis [2], which was an recurrence = 0.73; 95% CI 0.42–1.25), but eradication update of a previous systematic review [Cochrane Data- therapy was superior to no treatment (27 trials, 2509 base Sits Rev. 2004;(4):CD003840]. The primary outcomes patients, RR 0.20; 95% CI 0.15–0.26). In preventing Journal compilation 2007 Blackwell Publishing Ltd, Helicobacter 12 (Suppl. 1): 20–22
H. pylori and Non-malignant Diseases gastric ulcer recurrence, eradication therapy was superior rabeprazole doses were the same in H. pylori-positive to no treatment (11 trials, 1104 patients, RR 0.29; 95% CI patients, whereas in H. pylori-negative subjects, 20 mg 0.20–0.42). The authors concluded that a 1- to 2-week b.i.d. was superior for prevention of nocturnal acid course of H. pylori eradication therapy is an effective treat- ment for H. pylori-positive PUD. The role of the cagA status The effect of H. pylori eradication on the development of H. pylori strains as a predictive factor for the outcome of of GERD is controversial. Vakil et al. [7] determined the eradication therapy is controversial. Suzuki et al. in their incidence of symptoms of reflux disease and erosive systematic review and meta-analysis [3] confirmed the esophagitis and also their relationship to changes in histo- importance of the presence of cagA as a predictor for suc- logic gastritis in patients with non-ulcer dyspepsia (NUD) cessful eradication of H. pylori.
over 12 months. Gastric biopsies were scored using themodified Sydney classification. The results showed thatantrum-predominant gastritis is the most common pattern Non-Steroidal Anti-inflammatory Drug
of gastritis seen in NUD in Western populations. Heartburn Consumption
and regurgitation improve after eradication therapy or Last year relatively few studies examined the association placebo in patients with NUD and the development of of H. pylori with non-steroidal anti-inflammatory drugs (NSAIDs). The mechanisms by which H. pylori and low- The impact of long-term acid suppression on the gastric dose aspirin induce gastric damage are not completely mucosa remains controversial. Lundell et al. [8] reported elucidated. Thus, Venerito et al. [4] evaluated the effects of on further observations concerning an established cohort low-dose aspirin on gastric damage, mucosal prostaglandin- of patients with GERD, after a 7-year follow up. Among E2 levels, and cyclooxygenase-enzyme expression in the original cohort randomized for either omeprazole relation to H. pylori status. They concluded that in healthy treatment or anti-reflux surgery, 117 and 98 patients subjects, low-dose aspirin given for 1 week does not affect remained in the medical and surgical arms, respectively.
cyclooxygenase expression or mucosal prostaglandin-E2 Gastric biopsies were taken at baseline and throughout the levels. Antral prostaglandin-E2 basal levels appear to be study. Results showed that long-term omeprazole therapy critical for development of aspirin-induced gastric damage does not alter the exocrine oxyntic mucosal morphology in subjects without H. pylori infection.
in H. pylori-negative patients, but mucosal endocrine cellsappear to be under proliferative stimulation: changes inmucosal inflammation and atrophy were observed in Gastroesophageal Reflux Disease
As with the association of H. pylori infection and NSAIDs,last year few studies were devoted to the association of Dyspepsia and Non-ulcer Dyspepsia
H. pylori and gastroesophageal reflux disease (GERD).
Several studies suggested that proton-pump inhibitors Hu et al. [9] compared empirical prokinetics, the H. pylori suppress gastric acid more effectively in H. pylori-infected test-and-treat strategy and empirical endoscopy in a 1-year than in non-infected patients, but no evaluation of the study on primary-care patients presenting with dyspepsia.
short-term clinical response was performed. De Boer et al.
They found the three strategies equally effective. Empirical [5] studied whether H. pylori infection influences the prokinetic treatment was the least expensive but peptic response rate or speed of symptom control in patients with ulcers were sometimes missed, whereas the H. pylori test- GERD treated with rabeprazole. They did not find an effect and-treat strategy was indeed the most cost-effective on either of these parameters according to H. pylori status.
option. An economic evaluation of empirical antisecretory Infected patients and non-infected patients can therefore therapy versus H. pylori test-and-treat strategy in the be treated with a similar dose or rabeprazole. When management of dyspepsia patients presenting in primary treating heartburn with rabeprazole, physicians do not care was performed by Jarbol et al. [10]. Thus, a need to consider the patients’ H. pylori status and most randomized trial in 106 general practices in the County patients (> 80%) have adequate symptom relief after just of Funen, Denmark, was designed in order to obtain a few days of treatment. Rabeprazole (10 mg b.i.d.) is often clinical outcome measures and resource utilization data administered as an eradication therapy for H. pylori and prospectively. Seven hundred and twenty-two dyspeptic has also been proposed as a therapy for refractory GERD.
patients presenting with more than 2 weeks of epigastric However, there has not been a comprehensive assessment pain or discomfort were randomized in one of three initial of its acid-suppressive effects. Shimatani et al. [6] compared management strategies: 1, empirical antisecretory therapy, the acid-suppressive effects of rabeprazole (10 mg b.i.d.
2, testing for H. pylori, or 3, empirical antisecretory therapy, or 20 mg b.i.d.). They found that the effects of the two followed by H. pylori testing if symptoms improved.
Journal compilation 2007 Blackwell Publishing Ltd, Helicobacter 12 (Suppl. 1): 20–22
H. pylori and Non-malignant Diseases Cost-effectiveness and incremental cost-effectiveness References
ratios of the strategies were determined. They concluded 1 Murakami K, Sato R, Okimoto T, Watanabe K, Nasu M, that empirical antisecretory therapy confers a small but Kodama M, Fujioka T. Maintenance therapy with H -receptor not significant benefit and costs more than test-and-treat antagonist until assessment of Helicobacter pylori eradication can strategies for H. pylori, therefore it is probably not a cost- reduce recurrence of peptic ulcer after successful eradication of the effective strategy for the management of dyspepsia in organism: prospective randomized controlled trial. J Gastroenterol Hepatol 2006;21:1048–53.
primary care. Undoubtedly, H. pylori is the main cause of 2 Ford AC, Delaney BC, Forman D, Moayyedi P. Eradication therapy PUD but its role in NUD is less clear. Moayyedi et al.
for peptic ulcer disease in Helicobacter pylori positive patients. examined this question in their recent systematic Cochrane Database Syst Rev 2006;2:CD003840.
review and meta-analysis [11] which was an update of 3 Suzuki T, Matsuo K, Sawaki A, et al. Systematic review and a previous systematic review [Cochrane Database Syst meta-analysis: importance of CagA status for successful eradication of Helicobacter pylori infection. Aliment Pharmacol Ther Rev. 2005;(1):CD002096]. They determined the effect of H. pylori eradication on dyspepsia symptoms in patients 4 Venerito M, Treiber G, Wex T, Kuester D, Roessner A, Di Mario F, with NUD. They included all parallel group randomized Malfertheiner P. Effects of low-dose aspirin on gastric erosions, controlled trials (RCTs) comparing drugs to eradicate cyclooxygenase expression and mucosal prostaglandin-E2 do not H. pylori with placebo or other drugs known not to depend on Helicobacter pylori infection. Aliment Pharmacol Ther 2006;23:1225–33.
eradicate H. pylori for patients with NUD and 21 RCTs met 5 de Boer W, de Wit N, Geldof H, Hazelhoff B, Bergmans P, the inclusion criteria. Eighteen trials compared antisecretory Smout A, Tytgat G. Does Helicobacter pylori infection influence dual or triple therapy with placebo antibiotics with or response rate or speed of symptom control in patients with without antisecretory therapy, and evaluated dyspepsia gastroesophageal reflux disease treated with rabeprazole? at 3–12 months. Seventeen of these trials gave results as Scand J Gastroenterol 2006;41:1147–54.
6 Shimatani T, Moriwaki M, Xu J, Tazuma S, Inoue M. Acid- dichotomous outcomes evaluating 3566 patients and there suppressive effects of rabeprazole: comparing 10 mg and 20 mg was no significant heterogeneity between the studies.
twice daily in Japanese Helicobacter pylori-negative and -positive There was a 10% relative risk reduction in the H. pylori CYP2C19 extensive metabolisers. Dig Liver Dis 2006;38:802–8.
eradication group (95% CI 6–14) compared to the placebo.
7 Vakil N, Talley NJ, Stolte M, Sundin M, Junghard O, The number needed to treat in order to cure one dyspeptic Bolling-Sternevald E. Patterns of gastritis and the effect of eradicating Helicobacter pylori on gastro-oesophageal reflux disease patient was 14 (95% CI 10–25). Three further trials in Western patients with non-ulcer dyspepsia. Aliment Pharmacol compared bismuth-based H. pylori eradication with an alternative pharmacologic agent. These trials were smaller 8 Lundell L, Havu N, Miettinen P, et al. Changes of gastric mucosal and had a shorter follow up but suggested that H. pylori architecture during long-term omeprazole therapy: results of a eradication was more effective than either H -receptor randomized clinical trial. Aliment Pharmacol Ther 2006;23:639– 47.
9 Hu WH, Lam SK, Lam CL, et al. Comparison between empirical antagonists or sucralfate in treating NUD. H. pylori prokinetics, Helicobacter test-and-treat and empirical endoscopy in eradication therapy has a small but statistically significant primary-care patients presenting with dyspepsia: a one-year study. effect in H. pylori-positive NUD patients. An economic World J Gastroenterol 2006;12:5010–6.
model suggests that this modest benefit is cost-effective 10 Jarbol DE, Bech M, Kragstrup J, Havelund T, Schaffalitzky de Muckadell OB. Economic evaluation of empirical antisecretory therapy versus Helicobacter pylori test for management of dyspepsia: a randomized trial in primary care. Int J Technol Assess Health Care 2006;22:362–71.
Conflicts of interest
11 Moayyedi P, Soo S, Deeks J, et al. Eradication of Helicobacter pylori for non-ulcer dyspepsia. Cochrane Database Syst Rev The authors have declared no conflicts of interest.
Journal compilation 2007 Blackwell Publishing Ltd, Helicobacter 12 (Suppl. 1): 20–22

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