|Year : 2016 | Volume
| Issue : 1 | Page : 22-25
Association of Helicobacter pylori infection with gastroesophageal reflux disease
Aswathy Chandramohan, AV Ramadevi, KT Shenoy, Sheela Vasudevan
Department of Pathology, Sree Gokulam Medical College and Research Foundation, Trivandrum, Kerala, India
|Date of Web Publication||2-Jun-2016|
Sree Gokulam Medical College and Research Foundation, Trivandrum - 695 606, Kerala
Source of Support: None, Conflict of Interest: None
Introduction: The study was conducted to determine the association of Helicobactor pylori with endoscopic and histological parameters of gastroesophageal reflux disease (GERD). Materials and Methods: A cross-sectional study was undertaken. A total of 79 patients were evaluated prospectively in the endoscopic unit of a gastroenterology department for symptoms compatible with GERD. In all cases, routine endoscopy and Los Angeles grading of GERD were performed. In each subject, biopsies were taken from 3 cm above the squamocolumnar junction and from the antrum and assessed histologically. Results: Majority of the patients presented with complaints of heartburn (84.8%) and regurgitation (75.9%). Nonerosive reflux disease was present in only five patients. Endoscopically, the remaining 74 cases were graded as follows: 25 had GERD A, 10 had GERD B, 35 had features of Barrett's esophagus, and 4 had miscellaneous findings. H. pylori positivity was present in 33.3% of patients with GERD A and 4.8% of those with GERD B. Majority of the histological parameters such as elongation of lamina propria papillae, intraepithelial inflammatory infiltrate, ballooning degeneration, lack of surface maturation, and dilatation and congestion of lamina propria capillaries did not show statistically significant association with H. pylori. The overall H. pylori prevalence was found to be 26.58% (21/79). Conclusion: On endoscopy, with the increased GERD severity, H. pylori incidence decreased. H. pylori was found to have no significant association with majority of the histological parameters.
Keywords: Endoscopy, gastroesophageal reflux disease, Helicobacter pylori, histology, special stain
|How to cite this article:|
Chandramohan A, Ramadevi A V, Shenoy K T, Vasudevan S. Association of Helicobacter pylori infection with gastroesophageal reflux disease. Arch Med Health Sci 2016;4:22-5
|How to cite this URL:|
Chandramohan A, Ramadevi A V, Shenoy K T, Vasudevan S. Association of Helicobacter pylori infection with gastroesophageal reflux disease. Arch Med Health Sci [serial online] 2016 [cited 2020 Aug 6];4:22-5. Available from: http://www.amhsjournal.org/text.asp?2016/4/1/22/183368
| Introduction|| |
Helicobacter pylori , previously named Campylobacter pyloridis , is a Gram-negative, microaerophilic bacterium colonizing the stomach. It was identified in 1982 by Marshall and Warren. Gastroesophageal reflux disease (GERD) is a common condition with a variety of clinical manifestations and potentially serious complications. The role of H. pylori infection in GERD has received attention only recently. However, the evidence for an association between H. pylori and GERD is still uncertain. As the prevalence of H. pylori decreases, an increase in GERD, Barrett's esophagus, and adenocarcinoma of the distal esophagus and proximal stomach have been noticed. This suggests that H. pylori infection protects against these esophageal diseases.,
Four biopsy specimens (two from the antrum and two from the body) have a high probability of establishing the correct diagnosis of H. pylori status. Histological demonstration of H. pylori has a sensitivity and specificity >90%. Histological demonstration of H. pylori is done by hematoxylin and eosin stain or special stains such as Giemsa, Warthin Starry, or Half Grams. Diagnosis of GERD is based on a combination of clinical symptoms, endoscopic findings, and histological changes. In patients with normal or near normal endoscopic finding (nonerosive reflux disease), the major diagnostic burden lies with the histology. The main histological features of GERD assessed include basal cell hyperplasia, elongation of lamina propria papillae, increased intraepithelial inflammation including eosinophils, neutrophils and lymphocytes, and dilatation of intercellular spaces.
| Materials and Methods|| |
The present study was carried out in the Departments of Pathology and Department of Gastroenterology of Sree Gokulam Medical College. A total of 79 patients were evaluated prospectively in the endoscopic unit of gastroenterology department for symptoms compatible with GERD in a cross-sectional study lasting from December 2011 to October 2013.
Cases were selected based on a validated questionnaire which included demographic features, risk factors, and clinical features. Noncooperative patients, patients with a history of gastric surgeries, patients with esophageal varices, and sick patients were excluded from the study. Patients gave their informed consent to be a part of the study.
A routine endoscopy was performed by the same gastroenterologist on all patients. GERD was graded in accordance with the Los Angeles classification. Endoscopic pictures and reports were collected to know the macroscopic features. In each subject, two biopsies were taken: One from 3 cm above the squamocolumnar junction and other from the antrum.
The biopsy specimens were fixed in 10% formalin and embedded in paraffin wax. They were cut and stained using H and E. Specimens from antrum were evaluated only for the presence or absence of H. pylori organism. These specimens were stained with Giemsa, Half Grams, and Warthin Starry stains in addition to H and E for a demonstration of H. pylori. The histological evaluation of the specimens was done by the same pathologists. Histopathological features of GERD were studied in the biopsy taken from 3 cm above the squamocolumnar junction. Association of presence or absence of H. pylori organism with GERD was noted.
Data entered in Microsoft Excel were filtered and coded. Data were analyzed using SPSS version 16 Simple proportions and Chi-square values with the level of significance were evaluated and interpreted.
| Results|| |
The mean age of the patients was 46.1 ± 12.2 years. Among the 79 patients included in the study group, 72.2% were males. About 29.1% of the subjects were smokers and 40.5% were alcoholics. Majority of the patients presented with complaints of heartburn (84.8%) and regurgitation (75.9%).
Nonerosive reflux disease, with normal endoscopic findings and typical symptoms of GERD, was present in only five patients. Endoscopic findings of GERD were graded according to Los Angeles classification as A, B, C, and D. Twenty-five patients had GERD A and ten patients had GERD B. None of the patients had Grade C or D. Thirty-five subjects had findings of Barrett's esophagus and four of them presented miscellaneous findings [Table 1].
|Table 1: Association between Helicobacter pylori and endoscopic features of Helicobacter pylori|
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The association between the presence or absence of H. pylori organism and histological parameters of GERD such as elongation of lamina propria papillae (P value 0.6), intraepithelial inflammatory infiltrate (P value 0.056), ballooning degeneration (P value 0.7), lack of surface maturation (P value 1), and dilatation and congestion of lamina propria capillaries (P value 0.44) was found to be statistically not significant. However, basal cell hyperplasia (P value 0.03) and dilatation of intercellular spaces (P value 0.025) were found to have a significant association with H. pylori [Figure 1]. Thus, majority of the histological parameters were found to have a negative association with H pylori .
|Figure 1: Distribution of patients according to biopsy findings and the existence of Helicobacter pylori|
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| Discussion|| |
The aim of our study was to find the association of presence or absence of H. pylori organism on endoscopic and histological features of GERD. The overall prevalence H. pylori was found to be 26.58% (21/79). H. pylori positivity was present in 33.3% of patients with endoscopic finding of Los Angeles Grade A and 4.8% of those with Grade B. Thus, as the severity of GERD increases, H. pylori positivity decreases. Majority of the histological parameters also were found to have a statistically negative association with H. pylori .
The presence of H. pylori was evaluated in all antral biopsies using H and E, Half Grams, Giemsa, and Warthin Starry stains. The organism could be identified much better in special stains than in H and E. Silver stain (Warthin Starry) brought out the organism clearly and easily [Figure 2].
|Figure 2: Helicobacter pylori in (a) H and E stain, (b) Giemsa stain, (c) Half Grams stain, and (d) Warthin Starry stain|
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A major limitation of our study was that we could take only one biopsy from antrum to avoid inconvenience to the patient. However, even from the single biopsy we were able to clearly demonstrate H. pylori with the help of all our special stains.
The prevalence of H. pylori infection is lower in GERD patients compared to general population. The absence of H. pylori is associated with more severe GERD. The results indicate a protective role of H. pylori against GERD. The finding of a close association between H. pylori positivity and less serious endoscopic findings in the present study is consistent with many other studies.,,,,,, Corley et al ., Shirota et al ., and Chung et al . also found that H. pylori infection is inversely associated with GERD.,, However, Yarandi et al . found that GERD patients were more likely to harbor H. pylori than non-GERD patients. Wu et al . found that eradicating H. pylori increases esophageal acid exposure and in some cases worsened reflux symptoms. Several other studies have found that H. pylori eradication had no impact on GERD.,,
The role of H. pylori infection in GERD has received attention only recently. Little is known about the relationship between H. pylori infection and the histological variables in GERD. The fact that there appears to be no correlation between the H. pylori positivity and many of the histological changes probably implies that these are provoked by mechanisms other than H. pylori infection.,
| Conclusion|| |
On endoscopy, as the severity of GERD increases, H. pylori positivity decreases. H. pylori was found to have no significant association with majority of the histological parameters. Thus, H. pylori infection was found to have a negative association with endoscopic and histological parameters of GERD.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Wang AY, Peura DA. The prevalence and incidence of Helicobacter pylori
-associated peptic ulcer disease and upper gastrointestinal bleeding throughout the world. Gastrointest Endosc Clin N
Raghunath A, Hungin AP, Wooff D, Childs S. Prevalence of Helicobacter pylori
in patients with gastro-oesophageal reflux disease: Systematic review. BMJ 2003;326:737.
Chait MM. Gastroesophageal reflux disease: Important considerations for the older patients. World J Gastrointest Endosc 2010;2:388-96.
Pera M, Cameron AJ, Trastek VF, Carpenter HA, Zinsmeister AR. Increasing incidence of adenocarcinoma of the esophagus and esophagogastric junction. Gastroenterology 1993;104:510-3.
Armstrong D, Bennett JR, Blum AL, Dent J, De Dombal FT, Galmiche JP, et al.
The endoscopic assessment of esophagitis: A progress report on observer agreement. Gastroenterology 1996;111:85-92.
Garrido Serrano A, Lepe Jiménez JA, Guerrero Igea FJ, Perianes Hernández C. Helicobacter pylori
and gastroesophageal reflux disease. Rev Esp Enferm Dig 2003;95:788-90, 785-7.
Gatopoulou A, Mimidis K, Giatromanolaki A, Polichronidis A, Lirantzopoulos N, Sivridis E, et al.
Impact of Helicobacter pylori
infection on histological changes in non-erosive reflux disease. World J Gastroenterol 2004;10:1180-2.
Wu JC, Sung JJ, Chan FK, Ching JY, Ng AC, Go MY, et al. Helicobacter pylori
infection is associated with milder gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2000;14:427-32.
Manes G, Pieramico O, Uomo G, Mosca S, de Nucci C, Balzano A. Relationship of sliding hiatus hernia to gastroesophageal reflux disease: A possible role for Helicobacter pylori
infection? Dig Dis Sci 2003;48:303-7.
Vicari JJ, Peek RM, Falk GW, Goldblum JR, Easley KA, Schnell J, et al.
The seroprevalence of cagA-positive Helicobacter pylori
strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998;115:50-7.
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
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;34:658-62.
Jonaitis LV, Kiudelis G, Kupcinskas L. Characteristics of patients with erosive and nonerosive GERD in high-Helicobacter-pylori
prevalence region. Dis Esophagus 2004;17:223-7.
Corley DA, Kubo A, Levin TR, Block G, Habel L, Rumore G, et al. Helicobacter pylori
and gastroesophageal reflux disease: A case-control study. Helicobacter
Shirota T, Kusano M, Kawamura O, Horikoshi T, Mori M, Sekiguchi T. Helicobacter pylori
infection correlates with severity of reflux esophagitis: With manometry findings. J Gastroenterol 1999;34:553-9.
Chung SJ, Lim SH, Choi J, Kim D, Kim YS, Park MJ, et al. Helicobacter pylori
serology inversely correlated with the risk and severity of reflux esophagitis in Helicobacter pylori
endemic area: A matched case-control study of 5,616 health check-up Koreans. J Neurogastroenterol Motil 2011;17: 267-73.
Yarandi SS, Nasseri-Moghaddam S, Mostajabi P, Malekzadeh R. Overlapping gastroesophageal reflux disease and irritable bowel syndrome: Increased dysfunctional symptoms. World J Gastroenterol 2010;16:1232-8.
Wu JC, Chan FK, Wong SK, Lee YT, Leung WK, Sung JJ. Effect of Helicobacter pylori
eradication on oesophageal acid exposure in patients with reflux oesophagitis. Aliment Pharmacol Ther 2002;16:545-52.
Verma S, Jackson W, Floum S, Giaffer MH. Gastroesophageal reflux before and after Helicobacter pylori
eradication. A prospective study using ambulatory 24-h esophageal pH monitoring. Dis Esophagus 2003;16:273-8.
Tefera S, Hatlebakk JG, Berstad A. The effect of Helicobacter pylori
eradication on gastro-oesophageal reflux. Aliment Pharmacol Ther 1999;13:915-20.
Manifold DK, Anggiansah A, Rowe I, Sanderson JD, Chinyama CN, Owen WJ. Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori
gastritis. Eur J Gastroenterol Hepatol 2001;13:535-9.
Quigley EM. New developments in the pathophysiology of gastro-oesophageal reflux disease (GERD): Implications for patient management. Aliment Pharmacol Ther 2003;17 Suppl 2:43-51.
Pace F, Porro GB. Gastroesophageal reflux and Helicobacter pylori
: A review. World J Gastroenterol 2000;6:311-4.
[Figure 1], [Figure 2]