By Author
  By Title
  By Keywords

April 1992, Volume 42, Issue 4

Original Article


Waquaruddin Ahmed  ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
Huma Qureshi  ( PMRC Research Centre, Jinnah Postgraduatc Medical Centre, Karachi. )
Serajuddaula Syed   ( Department of Pathology, Sindh Medical College, Karachi )
Ejaz Alam  ( PMRC Research Centre Jinnah Postgraduate Medical Centre, Karachi. )
Sarwar J. Zuberi  ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )


To assess the healing and relapse rate of duodenal ulcer (DU) treated with H2 receptor antagonists in helicobacter pylon (HP) positive vs negative cases, we analysed 95 cases of endoscopically proven duodenal ulcer. H. pylon colonization was found in 73 (77%) patients before treatment. No difference was observed in the pre-treatment characteristics between patients with HP positive and HP negative duodenal ulcers. Healing rates with H2 receptor antagonist at 8 weeks were 90% and 91% respectively (NS). No difference in HP colonization was found between patients with and without healed ulcerie, 77% and 78% respectively. Relapse rate within 1 year was 50% in patients with HP positive vs 73% with HP negative cases. We conclude that duodenal ulcer healing and relapse rate is related to acid inhibition rather than HP colonization (JPMA42: 81, 1992).


Since the isolation of HP from the gastric mucosa by Marshall in 1982, it has been considered as an important cause of peptic ulcer disease1. The organism was seen in 87% of patients with gastric or duodenal ulcer and in 90% patients with gastritis2. High intragastric acidity and serum gastrin were found in the infected person, which again supports the infective theory of Du3. With this aetiology, the strategy of the DII therapy is likely to change from acid-inhibition to antimicrobials such as antibiotics and bismuth compound. However, it is still controversial whether HP is a commensal in the gastrointestinal tract or a pathogen for the development ofduodenal ulcer4,5. Moreover, acid inhibitors such as H2 receptor antagonists are still effective for the acceleration ofduodenal ulcer healing without having any potential to inhibit HP colonisation6. This study was done to see the influence of HR on the healing and relapse rate of DII treated with H2 receptor antagonists.


Endoscopically diagnosed cases of duodenal ulcer of at least 3 mm in diameter with an ulcer crater, were included in the study. Cases with systemic disease, major complications of ulcer and operated cases except for simple closure were excluded. All the cases were treated with one of the H2 receptor antagonists (cimetidine 800 mg, famotidine 40mg or ranitidine 300 mg) in noctedose. The treatment was discontinued if the ulcer healed by the 4th week; otherwise continued for further 4 weeks. Patients with unhealed ulcer by8 weeks were assigned to other treatment and excluded from the follow-up study. Healing of the ulcer was defined as complete disap­pearance of the ulcer crater, with scar formation. Patients with healed ulcer were followed endoscopically at 3, 6 and 12 months to see ulcer recurrence. Endoscopies were performed before starting the treatment and at each follow-up session. Local anaes­thesia with 4% xylocaine gargle was given before each procedure. Three mucosal biopsy specimens were ob­tained from the antrum within 5cm from the pylorus. Two specimens were fixed in buffered formalin for histology and one was subjected to CLO test (Delta West limited). The endoscope was cleaned with soap and water, then imersed in 2% glutaraldehyde solution for two minutes after every procedure. The biopsy forceps and biopsy channel were irrigated with soap and water, then sterile water and finally with 70% alcohol at the end of procedure. Specimen fixed in buffered formalin were embedded in paraffin wax, cut into 5 um sections and stained with haematoxylin and eosin. The slides were reviewed for HP by a pathologist in random sequence without any clinical information. Samples with either positive CLO test/histology or both were considered to have HP colonization. Gastritis was waded as mild,. moderate and severe according to the polymor­phonuclear cell and mononuclear cell infiltration7. The statistical analysis was done using chi square test and student \\\'t\\\' test.


Ninety-five cases with endoscopically proven DII were included in the study. Helicobacter pylon was found in 73 (77%) patients. There was no significant difference in age, sex, addictions, NSAID use, blood groups and grades of gastritis between patients with and without HP colonisation (Table I).

Out of 95 patients treated with H2 receptor an­tagonists, ulcer healed in 67 (7 1%) at 4 weeks and in 86 (9 1%) at 8 weeks. Of the 73 cases with HP-positive, 50 (68%) healed at 4 weeks and 66 (90%) at 8 weeks. Similarly of the 22 cases without HP, 17 (77%) healed at 4 weeks and 20 (91%) at 8 weeks, without any significant difference between patients with or without HP-colonization. Sixty-six (77%) out of 86 patients with healed and 7(78%) Out of 9 with unhealed ulcers had HP colonization (N.S.). Seventeen patients were lost to follow-up, 71 patients with healed ulcer received regular endoscopic follow-up and 39 (55%) of these relapsed within one year. Relapse rates of patients with and without HP colonization are shown in Table II.


The relationship between helicobacter pylori and chronic duodenal ulcer disease is currently an area of intense interest. The reported prevalence of antral HP in patients with active duodenal ulceration ranged from 70 - 100%8,9. The reasons for variation are ethnic differences or low sensitivity of diagnostic tests due to focal HP colonization of antral mucosain some patients10. We took three specimens of antral mucosa from different loca­tions for histology and CLO test, the frequency of antral HP colonization in our patients was 77%, which is higher than 70% reported from Taiwan10. It could be due to ethnic difference and younger age group of our patients.  This study showed that the presence of HP in the antrum did not change the healing rate. Although the healing rate was higher (77%) in HP negative as com­pared to the HP positive group (68%) at 4 weeks but the difference was not statistically significant. Healing rates at 8 weeks were also similar in both groups. HP coloniza­tion amongst the patients with healed (77%) and un­healed duodenal ulcer (78%) were similar, thereby suggesting that the healing process takes place despite the presence of bacteria and acid inhibition still plays an important role in the treatment of active duodenal ulcer. It has been reported earlier that the clearance and eradication of HP gives a longer remission period in duodenal ulcer patients treated with colloidal bismuth compounds with or without antibiotics11,12. In the present study we could not find any longer remission in patients who were HP negative vs those who were HP positive. These findings are similar to earlier reports13,14. Although some good prospective studies have shown better healing rates of duodenal ulcer comparable to the results with H2 receptor antagonists and for better remission after tripple regimen therapy (colloidal bis­muth subsitrate for 4 weeks plus metronidazole and amoxycillin for 2 weeks) 11,15. but we will have to weigh out the benefits and potential side effects and tolerability of the patients15. H2 receptor antagonists should probab­ly be the first line of treatment, which can promote ulcer healing without significant difference in ulcer recurrence irrespective of the HP status and HP eradication should be attempted in resistant ulcers, recurrent ulcers and in young persons for whom long term treatment with H2 receptor antagonists or surgery is not desirable.


1. Marshall, B.J. The compylobacter pylori story. Scand. 3. Gastroenterol., 1988:23 (suppl. 146):58-66.
2. Warren,J.R. and Marshall, B.J. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet, 1983; 1:1273-5.
3. Levi, S.. Beardshall, K. and Haddad, G., Playford, k. Ghosh. P. and Calam, 3. Campylobacter pylori and duodenal ulcers. Thegastrin link. Lancet, 1989; 1:1167-8.
4. Wormsley, K.G. Campylobacter pylori and ulcerdisease: a casual connection? Scand. 3. Gastroenterol., 1989; 24 (suppl. 106):53.&
5. Peterson, W.L. Antimicrobial therapy of duodenal ulcer? Hold off for now. Gastroenterology. 1989; 97:508-10.
6. Jones, D.B., Howden, C.W., Burger, D.W., Kerr, GD. and Hunt, R.H. Acid suppression in duodenal ulcer; a mets-analysis to define optimal dosingwith antisecretory drugs. Gut, 1987;28:1 120-7.
7. Kazi, J.L., Jafarey, N.A, Alam, S.M., Zuberi, S.J., Kazi, A.M., Qureshi, H., Ahmed, W.A placebo controlled trial of bismuth salicylate in helicobacter pylori associated gastritis. J. Pak. Med. Assoc.. 1990; 40:154-56.
8. Wyatt. J.I. campylobacter pylori duodenitis and duodenal ulceration in campylobacter pylon and gastroduodenal disease. Edited by B.J. Rathbone and R.V. Heathy. Oxford, Blackwell. 1989; pp. 117-24.
9. Tyylgat, G.N.J. Campylobacter pylori; epidemiological consideration. Scand. J. Gastroenterol., 1989; 24 (suppl. 160):1-2.
10. Lai, K.H., Chang. F.Y., Taay. S.H. and Lu. LC. et at. Medical treatment of duodenal ulcer: Acid inhibition or helicobacter pylori eradication. J. Gastroenterol. Hepatol., 1991; 6:141-4.
11. Borody. Ti.. Cole. P.. Noonan, S.. Morgan, A. et al. Long term campylobacter pylon recurrence posteradication. Gastroenterol., 1988; 95:A43 (AbsL).
12. Coghlan, J.G., Gilligan, D.. Humphries, H. etal. Campylobacter pylori and recurrence of duodenal ulcers: a 12 months follow-up study. Lancet, 1987; 2:1109-11.
13. Deventer, GAy., Elashoff, J.D. and Reedy, TJ. et aL A randomized study of maintenance therapy with ranitidine to prevent the recurrence of duodenal ulcer. N. Engl.J. Med., 1989; 320:1113-19.
14. Bianchi-Porro, G., Lazzaroni, M., Petrillo, M. and DeNicola, C. Relapse rates in duodenal ulcer patients formerly treated with bismuth subcitrate or maintained with cimetidine. Lancet, 1984; 2:698.
15. Glupezyuski, Y., Bourdeaux L, Verhas, M. et al. Short-term double or triple oral drug treatment of helicobacter pylon (Hp) in Central Africa. Gastroenterology, 1990; 98:A48.

Journal of the Pakistan Medical Association has agreed to receive and publish manuscripts in accordance with the principles of the following committees: