• Tahir Bashir
  • Muhammad Arif Nadeem
  • Sajid Nisar
  • Fawad Ahmad Randhawa
  • Abida Pervaiz


Background: Helicobacter pylori (H. pylori) is one of the common causes of dyspepsia. The present study was conducted to find the frequency of H. pylori in the distal oesophageal mucosa of patients with dyspepsia. Methods: This descriptive cross sectional study was conducted in Services Hospital Lahore. History and physical examination was recorded and after informed consent oesophagoduodenoscopy of all the patients with the symptoms of dyspepsia was done. Findings were noted and gastric antral and distal oesophageal biopsies taken simultaneously. Both specimen were preserved in 10% formalin and sent for histopathological examination for the presence of H. pylori. Results: Out of the 116 patients, 16 patients were between ages 16–30, 82 patients were between ages 31–45 years and 18 were over 45 years of age. Thus percentage of subjects between 31–45 years was maximum i.e., 70.68%. Seventy-six (65.5%) of the patientswere male and 40 (34.5%) were females.The H pylori was found in 40 (34.5%) patients in gastric antral biopsy and it was isolated in only 14 (12.1%) patients in distal esophageal biopsies.Conclusion: H. pylori positivity was low in the distal oesophageal mucosa of patients with dyspepsia despite its presence in gastric mucosa. A close relationship could not be established between H. pylori in the distal oesophagus and gastric antral mucosa in dyspeptic patients. Based on these findings, it seems that there is no significant evidence for an important pathogenic role for H. pylori infection in the development of pathologic dyspepsia and chronic gastroesophageal reflux disease.Keywords: Helicobacter pylori, dyspepsia, reflux, gastroesophageal


Shrestha S, Paudel P, Pradhan GB, Shrestha L, Bhattachan CL. Prevalence study of H. pylori infection in dyspeptic patients coming to Nepal Medical College Teaching Hospital, Jorpati, Kathmandu. Nepal Med Coll J 2012;14:229–33.

Frenck RW Jr, Clemens J. Helicobacter in the developing world. Microbes Infect 2003;5:705–13.

Domınguez-Bello MG, Beker B, Guelrud M, Vivas J, Peraza S, Perez ME, et al. Short report: socioeconomic and seasonal variations of Helicobacter pylori infection in patients in Venezuela. Am J Trop Med Hyg 2002;66:49–51.

Blaser MJ, Atherton JC. Helicobacter pylori persistence: biology and disease. J Clin Invest 2004;113:321–33.

Rugge M, Di Mario F, Cassaro M, Baffa R, Farinati F, Rubio J Jr, et al. Pathology of the Gastric Antrum and Body Associated with Helicobacter Pylori Infection in Non-Ulcerous Patients: Is the Bacterium a Promotor of Intestinal Metaplasia? Histopathology 1993;22:9–15.

Xia HH, Kalantar JS, Talley NJ, Wyatt JM, Adams S, Chueng K, et al. Antral-type mucosa in the gastric incisura, body, and fundus (antralization): a link between helicobacter pylori infection and intestinal metaplasia. Am J Gastroenterol 2000;95:114–21.

Herbella FA, Patti MG. Gastroesophageal reflux disease: from pathophysiology to treatment. World J Gastroenterol 2010; 16:3745–9.

Pei Z, Bini EJ, Yang L, Zhou M, Francois F, Blaser MJ. Bacterial biota in the human distal esophagus. Proc Natl Acad Sci U S A 2004;101:4250–5.

Cellini L, Grande R, Artese L, Marzio L. Detection of Helicobacter pylori in saliva and esophagus. New Microbiol 2010;33:351–7.

Weiss J, Tsang TK, Meng X, Zhang H, Kilner E, Wang E, et al. Detection of Helicobacter pylori gastritis by PCR: correlation with inflammation scores and immunohistochemical and CLO test findings. Am J Clin Pathol 2008;129:89–96.

Ackermark P, Kuipers EJ, Wolf C, Breumelhof R, Seldenrijk CA, Timmer R, et al. Colonization with cagA-positive Helicobacter pylori strains in intestinal metaplasia of the esophagus and the esophagogastric junction. Am J Gastroenterol 2003;98:1419–24.

Wu AH, Crabtree JE, Bernstein L, Hawtin P, Cockburn M, Tseng CC, et al. Role of Helicobacter pylori CagA+ strains and risk of adenocarcinoma of the stomach and esophagus. Int J Cancer 2003;103:815–21.

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.

Pei Z, Yang L, Peek RM, Jr Levine SM, Pride DT, Blaser, MJ. Bacterial biota in reflux esophagitis and barrett’s esophagus. World J Gastroenterol 2005;11:7277–83.

Csendes A, Smok G, Cerda G, Burdiles P, Mazza D, Csendes P. Prevalence of Helicobacter pylori infection in 190 control subjects and in 236 patients with gastroesophageal reflux, erosive esophagitis or Barrett's esophagus. Dis Esophagus.1997;10:38–42.

Henihan RD, Stuart RC, Nolan N, Gorey TF, Hennessy TP, O'Morain CA. Barrett's esophagus and the presence of Helicobacter pylori. Am J Gastroenterol. 1998;93:542–6.

Oberg S, Peters JH, Nigro JJ, Theisen J, Hagen JA, DeMeester SR, et al. Helicobacter pylori is not associated with the manifestations of gastroesophageal reflux disease. Arch Surg. 1999;134:722–6.

Yerra LN, Bhasin DK, Panigrahi D, Vaiphei K, Sharma BC, Ray P. Prevalence of Helicobacter pylori infection in patients with reflux oesophagitis. .Trop Gastroenterol. 1999;20:175–7.

Jang J, Lee S, Jung Y, Song K, Fukumoto M, Gould VE, et al. Malgun (clear) cell change in Helicobacter pylori gastritis reflects epithelial genomic damage and repair. Am J Pathol 2003;162:1203–11.

Wright TA, Myskow M, Kingsnorth AN. Helicobacter pylori colonization of Barrett’s esophagus and its progression to cancer. Dis Esophagus 1997;10:196–200.

Amini M, Karbasi A, Khedmat H, Jeihounian M. Helicobacter pylori eradication and histopathological esophagitis in dyspeptic patients. Trop Gastroenterol 2010;31:175–9.

Contreras M, Salazar V, García-Amado MA, Reyes N, Aparcero M, Silva, et al. High frequency of Helicobacter pylori in the esophageal mucosa of dyspeptic patients and its possible association with histopathological alterations. Int J Infect Dis 2012;16:e364–70