Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Ptevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease:systemic review
- MOHAMMED S ABSAR (6 April 2003)
-
Increased prevalence of Helicobacter pylori in patients with GORD in Greek cohorts
- Jannis Kountouras, Christos Zavos, Dimitrios Chatzopoulos (9 April 2003)
-
Prevalence of H. pylori infection in gastro-oesophageal reflux disease is lower compared with whom?
- Grigoris I Leontiadis, Virender K Sharma, Colin W Howden and Savvas Kadis (25 April 2003)
|
|
|||
|
MOHAMMED S ABSAR, specialist registrar in surgery trafford general hospital,Manchester
Send response to journal:
|
Dear editor Ptevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease:systemic review This was an interesting reading and clearly brings forward the point that Gastro intestinal reflux disease(GORD) has got a definite aetiopathology and presence of H pylori infection makes the situation worse rather than being a cause for it.The review however does not mention whether the studies considered were randomised or not for if we are considering H pylori infection in symptomatic patients who had endoscopy for upper gasro intestinal symptoms then the incidence and prevalence of H pylori infection would be higher depending on unit protocols. The review however confirms finding from previous single studies which show use of H pylori eradication therapy benefits those with H pylori infection associated with symptoms of GORD.A very nice and informative review. Mr M S Absar Specialist registrar in surgery Trafford general hospital home address- 37 cavendish way roton OL2 5DQ Ph-0161 2902832 Email-drshamimabsar@hotmail.com Competing interests: None declared |
|||
|
|
|||
|
Jannis Kountouras, Associate Professor of Medicine Aristotle University of Thessaloniki, 8 Phanariou St, Byzantio, 551 33, Thessaloniki, GREECE, Christos Zavos, Dimitrios Chatzopoulos
Send response to journal:
|
Dear Editor – We read with great interest the paper by Raghunath et al (1). We have conducted 3 different randomised studies concerning H. pylori infection (Hp-I) and GORD. First, we investigated 69 patients with GORD and irritable bowel syndrome (2). The inclusion and exclusion criteria matched those of Raghunath et al. Apart of the oesophagus, biopsy specimens were obtained from stomach for histological examination (Crezyl fast violet and/or Giemsa staining), which represents the actual gold standard for diagnosis of Hp-I. Presence of Hp was found in 56 out of 69 (81.2%) patients. This prevalence was higher compared with some previously published figures for Greek cohort and other ethnic populations (3). Second, we studied a different cohort of 30 patients in order to estimate the effect of Hp eradication therapy in the course of GORD (4). Hp-I was confirmed in 24 out of 30 (80%) patients by histology and CLOtest. Evaluation of Hp triple eradication therapy (rabeprazole, amoxicillin, clarithromycin) was made according to the upper gastrointestinal endoscopical, clinical (LA classification and LIKERT scale, respectively), and histological findings. Eight weeks post eradication treatment, endoscopical, clinical and histological resolution of persistent oesophagitis was noticed. Third, we investigated the histological presence of oesophagitis and the Hp prevalence in 31 patients with non-endoscopical reflux disease (NERD) (5). In 25 out of 31 (80.6%) patients there was histological presence of oesophagitis, and in 13 out of 25 (52%) patients Hp-I was detected.
Our data show that Hp prevalence is higher among patients with GORD than in general Greek population, and that Hp eradication leads to remission of endoscopical, clinical, and histological findings, thereby suggesting a contribution of Hp-I to the pathogenesis of GORD. Besides, Hp-I in patients with NERD does not seem to differ from that in general population. Mechanisms by which Hp may be involved in the pathophysiology of GORD include: Hp-induced release of several mediators (such as prostaglandins), nitric oxide and cytokines that may adversely affect the lower oesophageal sphincter, and direct adverse effects on the oesophageal mucosa by Hp products (phospholipase, cytotoxin and ammonia derivatives), or Hp-accompanied gastrin release that, in turn, stimulates gastric acid production (increased acidity along with a higher volume of gastric juice may exacerbate reflux disease). However, more and larger cohort studies in different geographical areas are needed to elucidate the relationship between Hp-I and GORD. Jannis Kountouras MD, PhD, Christos Zavos MD, and Dimitrios Chatzopoulos MD Correspondence to: Jannis Kountouras, Gastroenterologist, Associate Professor of Medicine, Aristotle University of Thessaloniki, 8 Phanariou St, Byzantio, 551 33, Thessaloniki, Macedonia, Greece. E-mail: jannis@med.auth.gr References: 1. Raghunath A, Hungin APS, Wooff D, Childs S. Prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease: systematic review. BMJ 2003;326:737. 2. Kountouras J, Chatzopoulos D, Zavos C, Boura P, Venizelos J, Kalis A. Efficacy of trimebutine therapy in patients with gastroesophageal reflux disease and irritable bowel syndrome. Hepatogastroenterology 2002;49:193-7. 3. The EUROGAST Study Group. Epidemiology of, and risk factors for, Helicobacter pylori infection among 3194 asymptomatic subjects in 17 populations. Gut 1993; 34: 1672-6. 4. Kountouras J, Chatzopoulos D, Boura P, Kouklakis G, Zavos C, Venizelos I, et al. GERD, H. pylori infection (HP-I) and rabeprazol (RAB). Annals of Gastroenterology 2001;14:340. (Abstract) 5. Kountouras J, Kouklakis G, Karatzoglou P, Chatzopoulos D, Zavos C, Touloumis L, et al. [Histological presence of oesophagitis in patients with NERD]. Annals of Gastroenterology 2002;15(Suppl):84. (Abstract in Greek) Competing interests: None declared |
|||
|
|
|||
|
Grigoris I Leontiadis, Senior Clinical Fellow in Gastroenterology Department of Gastroenterology, Queen Elizabeth Hospital, Gateshead, Tyne & Wear NE9 6SX, Virender K Sharma, Colin W Howden and Savvas Kadis
Send response to journal:
|
To the Editor Dear Sir, The systematic review by Raghunath et al (1) was a well-intentioned attempt to clarify the prevalence of Helicobacter pylori (Hp) infection in patients with gastro-oesophageal reflux disease (GORD). However, the conclusion that the prevalence of Hp infection was significantly lower in patients with than without GORD may be potentially misleading. The rigorous methodological approach of Raghunath et al was undermined by the diversity of the control groups of the included studies. The pooled control group was heterogeneous and consisted of asymptomatic subjects as well as patients with either functional dyspepsia or a wide range of presenting problems such as anaemia, diarrhea, nausea/vomiting and chest pain. What would be the clinical relevance of such a comparison? It would probably have made more sense to compare the prevalence of Hp infection in patients with GORD with its prevalence in age- and sex- matched asymptomatic controls in the general population. Four of the studies identified by Raghunath et al seemed to have used asymptomatic subjects as controls (2-5), although a more detailed review of the individual methods sections reduced this number to three (3-5). We proceeded to combine the results of these three studies with the aid of RevMan software. There was statistically significant heterogeneity (P<0.001), which thereby necessitated the use of the random effects model; the pooled odds ratio was 0.57 (95% confidence interval 0.24 to 1.39). This indicates that the prevalence of Hp infection in patients with GORD does not differ significantly from the prevalence in asymptomatic controls. However, apart from the statistical heterogeneity, there was considerable clinical heterogeneity. Therefore, this conclusion should be regarded with the same caution as the conclusion of Raghunath et al. There is a danger that meta-analyses of observational studies produce very precise but spurious results; the statistical combination of data should therefore not be a prominent component of these systematic reviews. The thorough consideration of possible sources of heterogeneity among observational studies (something that Raghunath et al have done in the full version of their paper on bmj.com) will provide more insights than the mechanistic calculation of an overall measure of effect (6). Raghunath et al have inadvertently mixed studies from high and low Hp prevalence countries. In countries with high Hp prevalence and a high ratio of corpus-predominant to antral-predominant gastritis (e.g. Japan), most Hp-positive patients will have hypochlorhydria and may therefore be “protected” against GORD. However, in areas of low Hp prevalence with a high ratio of antral-predominant to corpus-predominant gastritis (e.g. Germany), most Hp-positive patients will have elevated acid secretion; if they also have a defective lower oesophageal sphincter function, they may be more likely to have symptoms of GORD. It is not Hp that is negatively associated with GORD, but acid secretion. Hp is one potential cause of reduced acid secretion, but only if it causes a corpus-predominant gastritis or pangastritis – as it is likely to do in developing countries (that seem to have a low GORD prevalence) but unlikely to do in western countries (where there is, of course, a much higher prevalence of GORD). Finally, we agree with the suggestion of Raghunath et al that further case-control studies are required to clarify the epidemiological relationship between Hp and GORD. However, the main problem with case- control studies is not their lack of precision but the fact that some studies produce confounded or biased findings (6). Therefore, the emphasis should be on the design rather than the size of these studies. In particular, the control group has to be carefully defined and the confounding factors for Hp infection (such as age and socio-economic status) have to be taken into consideration. Grigoris I Leontiadis
Virender K Sharma
Colin W Howden
Savvas Kadis
References: 1. Raghunath A, Hungin APS, Wooff D, Childs S. Prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease: systematic review. BMJ 2003; 326: 737-9. 2. Koike T, Ohara S, Sekine H, Iijima K, Kato K, Shimosegawa T, et al. Helicobacter pylori infection prevents erosive reflux oesophagitis by decreasing gastric acid secretion. Gut 2001; 49: 330-334. 3. Hackelsberger A, Schultze V, Gunther T, von Arnim U, Manes G, Malfertheiner P. The prevalence of Helicobacter pylori gastritis in patients with reflux oesophagitis: a case-control study. Eur J Gastroenterol Hepatol 1998; 10: 465-468. 4. Haruma K, Hamada H, Mihara M, Kamada T, Yoshihara M, Sumii K, et al. Negative association between Helicobacter pylori infection and reflux esophagitis in older patients: case-control study in Japan. Helicobacter 2000; 5: 24-29. 5. Manes G, Mosca S, Laccetti M, Lioniello M, Balzano A. Helicobacter pylori infection, pattern of gastritis, and symptoms in erosive and nonerosive gastroesophageal reflux disease. Scand J Gastroenterol 1999; 34: 658-662. 6. Egger M, Davey Smith G, Schneider M. Systematic reviews of observational studies. In: Egger M, Davey Smith G, Altman D, eds. Systematic reviews in health care: Meta-analysis in context. London: BMJ Publishing Group 2001: 211-227. Competing interests: None declared |
|||