|Year : 2011 | Volume
| Issue : 3 | Page : 142-145
The relationship between helicobacter pylori infection and gastro-esophageal reflux disease
Batool M Mahdi
Department of Microbiology, Al-Kindi College of Medicine Baghdad University, AL-Nahda Square, Baghdad, Iraq
|Date of Web Publication||9-Nov-2011|
Batool M Mahdi
Department of Microbiology, Al-Kindi College of Medicine Baghdad University, AL-Nahda Square, Baghdad
Source of Support: None, Conflict of Interest: None
Background : Gastro-esophageal reflux disease is a common condition, affecting 25%-40% of the population. Increasing attention has been paid to the relationship between Helicobacter pylori infection and reflux esophagitis. Aim: The aim of this study was to investigate the association between CagA+ H. pylori and endoscopically proven gastro-esophageal reflux disease. Patients and Methods: The study group included 60 hospital patients with gastro-esophageal reflux disease between 2007 and 2009 as compared with 30 healthy patients from a control group that was age and sex matched. Helicobacter pylori CagA+ was identified by an immunological test (Immunochromatography test) (ACON, USA). Results : Helicobacter pylori CagA+ was present in 42/60 (70%) of the patients with gastro-esophageal reflux disease and in 11/30 (36.6%) patients in the control group (p=0.002). The Odds ratio = 0.8004 with 95% Confidence Interval = from 0.3188 to 2.0094. The relative risk=1.35 that indicates an association between Helicobacter pylori and disease. Conclusions: The presence of Helicobacter pylori is significantly increased in patients with gastro-esophageal reflux disease as compared with the control group.
Keywords: Gastro-esophageal reflux disease, Helicobacter pylori, CagA+
|How to cite this article:|
Mahdi BM. The relationship between helicobacter pylori infection and gastro-esophageal reflux disease. North Am J Med Sci 2011;3:142-5
|How to cite this URL:|
Mahdi BM. The relationship between helicobacter pylori infection and gastro-esophageal reflux disease. North Am J Med Sci [serial online] 2011 [cited 2020 Jan 25];3:142-5. Available from: http://www.najms.org/text.asp?2011/3/3/142/86207
| Introduction|| |
Gastro-esophageal reflux disease (GORD) results from abnormal esophageal acid exposure. Therefore, acid secretion is a necessary requirement for disease development. In the presence of atrophic pan gastritis, acid production is decreased and the esophagus is less likely to be exposed to acid reflux  . The effects of Helicobacter pylori (H. pylori) infection on the pathogenesis of GORD have been studied in many reports. Infection with H. pylori produces an increase in basal and stimulated gastric acid output through the secretion of gastrin, somatostatin, and inflammatory mediators  , which is a possible cause of GORD  . Colonization of gastric mucosa by H. pylori may result in hypochlorhydria in patients with diffuse gastritis and gastric atrophy  and who seem to be at less risk of developing GORD  . Therefore, association between H. pylori infection and development of either hypochlorhydria or hyperacid secretion depends on the inflammatory response of the gastric mucosa. Thus, the effect of H. pylori infection on the development of GORD is contradictory and is an intricate relationship  . Another study found that H. pylori eradication did not aggravate the course of GORD  .
The reciprocal influence of H. pylori and GORD occurs concomitantly  and their relationship has been apparent as nearly none to a protective role of H. pylori against GORD development. Therefore, both conditions coexist in a considerable number of patients and the association varies according to the background prevalence of the infection in the populations studied. Thus, the role of H. pylori in the development of GORD has not been established  .
The main aim of this study was to investigate the relationship between CagA+ H. pylori and endoscopically proven gastro-esophageal reflux disease .
| Patients and Methods|| |
The study group included 60 patients who had been endoscopically diagnosed with gastro-esophageal reflux disease. These patients had a history of heartburn and dyspepsia at least three times a week for a period of more than three months and had been referred for gastrointestinal endoscopy at Al-Kindi Hospital, Baghdad, between 2007 and 2009.
The exclusion criteria included patients with a history of upper gastrointestinal (GI) surgery, malignancy, esophageal varices, and antibiotics or bismuth consumption during the last six months It also included patients using H2 blockers, proton pump inhibitors (PPIs), alcohol, or non-steroidal anti-inflammatory drugs (NSAIDs) during the last four weeks. The control group was comprised of 30 healthy volunteers without any symptom of upper GI diseases.
The GORD group and control groups were sex and age matched. Written informed consent was obtained for all upper endoscopy and biopsy procedures. The study was approved by the Ethics Committee of the Al-Kindi Teaching Hospital and University of Health and Al-Kindi College of Medicine-Baghdad University.
Blood samples (5 mL) were drawn into plain vacutainers from the antecubital veins of patients. The blood was allowed to clot for 30 minutes and centrifuged at 2000g for 15 minutes for clear separation of serum. Separated serums were stored at −20°C until analyzed. CagA antibodies Immunoglobulin G (IgG) for H. pylori were determined using an immunological test (immunochromatography test) (ACON, USA). Endoscopy was performed on the GORD patients and histopathological study was conducted on biopsy specimens that had been obtained from the gastric mucosa to confirm the diagnosis and presence of H. pylori in atrophic gastritis patients.
Data were analyzed using descriptive statistics (frequencies for tables, mean and standard deviation) and inferential statistics (Chi- square test). Odds ratio (OD), (95% confidence interval (CI) and relative risk (RR) were calculated to evaluate the association between H. pylori and GORD. All of these were performed using MiniTab statistical software program 13.20. A P-value of ≤ 0.05 was considered significant.
| Results|| |
The results of this study revealed that male patients constituted 66.6% of the studied group and this was not significantly different from the control group as shown in [Table 1]. There was no significant difference in mean age allocation and smoking between the GORD patients and control group [Table 2] and [Table 3]. The youngest age of the patients in the GORD group was 19 years and the oldest age was 84 years. In the control group, the youngest age was 20 years and the oldest age was 76 years.
|Table 3: Relationship of smoking between GORD patients and control group|
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There is a significant increase in H. pylori infection (p=0.002) in GORD patients when compared with the control group. The Odds ratio (OD)= 0.8004 with 95% CI= from 0.3188 to 2.0094. The relative risk = 1.35, which indicates an association between H. pylori and GORD as shown in [Table 4].
| Discussion|| |
The aim of this study was to investigate the relationship between cagA+ H. pylori and endoscopically proven GORD. We found no significant difference in age, sex and smoking between the two groups. There was a significant (P=0.002) increase in CagA+ H. pylori in GORD disease (70%). Another study found that the prevalence of H pylori infection in patients with gastro-esophageal reflux disease was 38.2% (range 20.0%-82.0%)  . Spechler showed that H. pylori did not affect the pathogenesis of GORD  . In 2001, Warburton-Timms et al  demonstrated that CagA+ H. pylori were found in 81% of patients with a normal esophagus, in 70% with mild esophagitis, in 69% with moderate esophagitis, and in 46% with severe esophagitis. This heterogeneity between the studies may be due to the geographical location of the studies due to the difference in the prevalence of H. pylori in the Far East, North America and Western Europe. For example, a study from South America showed a higher prevalence of GORD with H. pylori that is in agreement with our study  . Other studies reported higher percentages of GORD with H. pylori by Gisbert et al. in 2001  (57%) and in 1996 by Liston et al.  (76%) that was in accordance with our results. This gives the impression that H. pylori in patients with gastro-esophageal reflux disease is lower in countries where the prevalence of H. pylori in the general population is high. The cause may be related to many factors, such as study design, selection of cases and controls, severity of disease activity, dietary, genetic factors and method of testing for H. pylori.
The relationship between H. pylori and GORD was assessed by Odds ratio that describes the strength of association between the two  . In our study, Odds ratio was 0.8004 with 95% CI= from 0.3188 to 2.0094 and relative risk= 1.35, which indicates an association between H. pylori and GORD. Other studies illustrated the range of Odds ratio from 0.16  to 1.58  , while others demonstrated similar results to this study , . This heterogeneity among results may be due to the location of the studies.
As mentioned previously, H. pylori in patients with gastro-esophageal reflux disease from the Far East differs from Western Europe and North America. In 2010, Roman and Pandolfino  mentioned that environmental factors had an effect. The severity of H. pylori gastritis (Hp gastritis) had an effect on GORD development. H. pylori with predominant antral gastritis is responsible for increased gastric acid secretion and thus promotes GORD. Conversely, H. pylori with diffuse gastritis induces gastric atrophy. In this particular case, H. pylori eradication may restore acid secretion and lead to a more scathing refluxate in patients with predisposing conditions for GORD.
| Conclusion|| |
In this study, the presence of Helicobacter pylori was significantly increased in patients with gastro-esophageal reflux disease.
| Acknowledgement|| |
The author thanks all who helped in this study. There was no conflict of interest in this article.
| References|| |
|1.||Koike T, Ohara S, Sekine H, et al. Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis. Am J Gastroenterol 1999; 94:3468-3472. |
|2.||Smith JTL, Pounder RE, Nwokolo CU, et al. Inappropriate hypergastrinemia in asymptomatic healthy subjects infected with Helicobacter pylori infection. Gut 1990; 31:522-525. |
|3.||Boyd EJS. The prevalence of esophagitis in patients with duodenal ulceration. Am J Gastroenterol 1996; 91:1539-1543. |
|4.||El Omar EM, Oien K, El-Nujumi A, et al. Helicobacter pylori infection and chronic acid hyposecretion. Gastroenterology 1997; 113:15-24. |
|5.||Ohara S, Sikne H, Iijima K, et al.. Gastric mucosal atrophy and prevalence of Helicobacter pylori in reflux esophagitis of the elderly. Jpn J Gastroenterol 1996; 93:235-239. |
|6.||McNamara D, O'Morain C. Gastro-esophageal reflux disease and Helicobacter pylori: an intricate relation. Gut 1999; 45:113-117. |
|7.||Malfertheiner P. Helicobacter pylori eradication does not exacerbate gastro-esophageal reflux disease. Gut 2004; 53:312-313. |
|8.||Blaser MJ. Hypothesis: the changing relationship of Helicobacter pylori and humans: implications for health and disease. J Infect Dis 1999; 179:1523-1530. |
|9.||Luman W. Helicobacter pylori: causation and treatment. JR Coll Physicians Edinburgh 2005; 35: 45-49. |
|10.||Raghunath A, Pali A, Hungin S, et al . Prevalence of Helicobacter pylori in patients with gastro-esophageal reflux disease: systematic review. BMJ 2003; 326:737-739. |
|11.||Spechler SJ. Does Helicobacter pylori infection contribute to gastro-esophageal reflux disease?. Yale J Biol Med 1998; 71:143-148. |
|12.||Warburton-Timms VJ, Charlett A, Valori RM, et al. The significance of CagA+ Helicobacter pylori in reflux esophagitis. Gut 2001; 49:341-346. |
|13.||Csendes A, Smok G, Cerda G, et al. Prevalence of Helicobacter pylori infection in 190 control subjects and in 236 patients with gastro-esophageal reflux, erosive esophagitis or Barrett's esophagus. Dis Esophagus 1997; 10:38-42. |
|14.||Gisbert JP, de Pedro A, Losa C, et al. Helicobacter pylori and gastro-esophageal reflux disease: lack of influence of infection on twenty-four-hour esophageal pH monitoring and endoscopic findings. J Clin Gastroenterol 2001; 32:210-214. |
|15.||Liston R, Pitt MA, Banerjee AK. Reflux esophagitis and Helicobacter pylori infection in elderly patients. Postgrad Med J 1996; 72: 221-223. |
|16.||Bland JM and Altman DG. Statistics Notes: The odds ratio. BMJ 2000; 320:1468. |
|17.||Koike T, Ohara S, Sekine H, et al. Helicobacter pylori infection inhibits reflux esophagitis by inducing atrophic gastritis. Am J Gastroenterol 1999; 94:3468-3472. |
|18.||Hackelsberger A, Schultze V, Gunther T, et al. The prevalence of Helicobacter pylori gastritis in patients with reflux esophagitis: a case-control study. Eur J Gastroenterol Hepatol 1998; 10: 465-468. |
|19.||Manes G, Mosca S, Laccetti M, et al. Helicobacter pylori infection, pattern of gastritis, and symptoms in erosive and nonerosive gastro-esophageal reflux disease. Scand J Gastroenterol 1999; 34:658-662. |
|20.||Roman S, Pandolfino JE. Environmental - lifestyle related factors. Best Pract Res Clin Gastroenterol 2010; 24:847-859. |
[Table 1], [Table 2], [Table 3], [Table 4]