Saudi Journal of Gastroenterology
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Year : 1998  |  Volume : 4  |  Issue : 2  |  Page : 65-66
Update on helicobacter pylori diagnosis and treatment

1 Consultant Physician & Gastroenterologist, St. James's University Hospital Leeds, United Kingdom
2 Clinical research fellow, St. James's University Hospital Leeds, United Kingdom

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How to cite this article:
Heatley RV, Moncur P. Update on helicobacter pylori diagnosis and treatment. Saudi J Gastroenterol 1998;4:65-6

How to cite this URL:
Heatley RV, Moncur P. Update on helicobacter pylori diagnosis and treatment. Saudi J Gastroenterol [serial online] 1998 [cited 2022 Jan 17];4:65-6. Available from:

Helicobacter pylori Scientific Name Search s discovered about 15 years ago and since that time has had a great impact on the management of peptic ulcer disease [1],[2] Although there is continued interest in expanding indications for treatment, most diagnostic and therapeutic goals are currently fairly well established.

There are various ways the organism can be detected. Tests can be grouped into those that are invasive, requiring an endoscopy and subsequently relying on histological identification or culture of antral biopsies for microbiological recognition. These are highly specific and sensitive tests, but depend on local expertise and are also thus relatively expensive. A cheaper and more universally available method is to carry out a urease test on antral biopsy material, which depends on the urease enzyme that produces a pH change in an indicator system, thus allowing rapid recognition of the organism. For routine clinical purposes, indirect tests are probably most useful. Serology for circulating antibodies to the organism is useful for demonstrating the presence of infection and has been shown to be of value in aiding decisions on referral of dyspeptic patients for investigation. C-urea breath tests are also dependent on the urease enzyme being present, and are a non-invasive method of demonstrating that H. pylori infection has been eradicated. Its main use is for monitoring success of therapy and is best carried out at least one month after eradication treatment has been completed [3],[4] .

There is now general agreement that attempts at H. pylori eradication should be concentrated on patients with peptic ulcer disease, particularly those with duodenal ulceration [5] . The organism is generally present in all adult patients with duodenal ulcer (DU) disease, certainly in the United Kingdom, and colonises the duodenum because of the pre-existence of duodenal gastric metaplasia. H. pylori eradication has been clearly shown in a number of studies worldwide to reduce the 12­month relapse rate of DU disease from around 80% to 20-30% or, in some studies, even lower [6] .

Unfortunately, mono therapy is generally ineffective in inducing H. pylori eradication. Many of the commonly used dual therapies also appear to lack bactericidal activity against the organism and have produced poor eradication rates. One of the most widely used has been omeprazole and amoxycillin which, disappointingly, only produces eradication in about 50-60% of patients overall. Omeprazole and clarithromycin gives somewhat better results in optimal doses, producing eradication in about 75-80% of patients [4],[7] .

The earliest triple therapies combined bismuth together with metronidazole and tetracycline /amoxycillin. Although initial results were encouraging and despite the considerable number of published studies using this combination, eradication rates as low as 55% have led to a general decline in usage of this combination [8] . Interest now is in triple therapy combinations based upon the acid suppressants omeprazole or ranitidine together with metronidazole/ tinidazole and amoxycillin/ clarithromycin [9],[10] . Although, the results have been variable, some consistent, very high eradication rates have been reported in several large published series with some of these combinations. Quadruple therapy has also been used, consisting of an acid suppressant together with classic bismuth triple therapy. In several comprative studies this has been shown to produce better eradication rates than those achieved with acid-suppressant triple therapies - 93-98% eradication [11] .

We are currently seeing the introduction of the first drug, ranitidine-bismuth citrate, produced specifically to aid H. pylori eradication. This is an entirely new compound combining the tried and tested ranitidine and bismuth, both of which in many years of clinical experience have proven safe and effective. H. pylori eradication has been achieved in between 82­94% of patients treated in comparative studies, using a dual combination with clarithromycin over a 14-day treatment course, figures which have only otherwise been achievable with triple therapy combinations [12] . Ranitidine bismuth citrate used in a triple therapy combination for seven days also gives comparable eradication efficacy to p.p.i.-based triple therapy treatment.

No single compound currently exists which is suitable for and effective at producing eradication in all patients with H. pylori infection. Problems still exist with patient compliance when using complicated multi-drug treatments and the side effects these induce, which are commonly gastrointestinal. Antibacterial resistance, especially to metronidazole, is also a problem. Even if eradication is successful, recrudescence of inadequately treated infection is always a possibility and re-infection itself may also occur although, on current evidence, true re-infection rates in most countries appear fairly low. The recent introduction of the first drug, ranitidine-bismuth citrate, produced specifically for H. pylori eradicatiion is encouraging. This and other developments give the hope that new and more effective regimens will become available in the future. Nevertheless, immunisation against infection with this organism is likely to be the most cost-effective long-term goal [13] .

   References Top

1.Warren JR. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983;1:1273.  Back to cited text no. 1    
2.Marshall B. Unidentified curved bacilli on gastric epithelium in active chronic gasritis. Lancet 1983;1:1273-5.  Back to cited text no. 2    
3.Helicobacter pylori and gastroduodenal disease. Edited by BJ Rathbone, RV Heatley. 2nd edition. Blackwell scientific publications. Oxford 1992, p107.  Back to cited text no. 3    
4.Heatley RV. The H. pylori handbook. Blackwell science, Oxford 1995.  Back to cited text no. 4    
5.Heatley RV. H. pylori infection: how relevant is it clinically? Hospital Update March 1995;119-24.  Back to cited text no. 5    
6.Collins R, Coghland JG, O'Morain C. Helicobacter pylori and ulcer treatment. In: Helicobacter pylori and gastroduodenal disease. Edited by BJ Rathbone, RV Heatley. 2nd edition. Blackwell scientific publictions, Oxford 1992, p224.  Back to cited text no. 6    
7.Penston JG. Helicobacter pylori eradication - understandable caution but no evidence for inaction. Aliment pharmacol therapy 1994;8:369-89.  Back to cited text no. 7    
8.Rauws EAJ, Tytgat GNJ. Helicobacter pylori: Treatment of gastritis. In: Helicobacter pylon and gastroduodenal disease. Edited by BJ Rathbone, RV Heatley. 2nd edition. Blackwell scientific Publication, Oxford 1992.  Back to cited text no. 8    
9.Hentschel E, Brandtatter G, Progosics B, et al. Effect of ranitidine and amoxycillin plus metronidazole on the eradication of Helicobacter pylori and the recurrence of duodenal ulcer. N Engl J Med 1993;328:308-12.  Back to cited text no. 9    
10.Goddard A, Logan R. One-week low-dose triple therapy: new standards for Helicobacter pylori treatment. Eur J Gastroenterol & Hepatol 1995;7:1-3.  Back to cited text no. 10    
11.De Boer WA, Driessen WMM, Jansz AR, Tytgat GNJ. Effect of acid suppression on efficacy of treatment for Helicobacter pylori infection. Lancet 1995; 345:817-20.  Back to cited text no. 11    
12.Heatley RV. Ranitidine bismuth citrate. Prescriber 1995;6:23-7.  Back to cited text no. 12    
13.David G, Blum AL, Corthesy-Theulaz I, Saragra E, Kraenenbuhl JP, Haas R, Michetti P. 11. pylori urease elicits protection against H.felis infection in mice. Gastroenterology 1993; 104 (Suppl A):1035.  Back to cited text no. 13    

Correspondence Address:
Richard V Heatley
Consultant Physician & Gastroenterologist, St. James's University Hospital Leeds
United Kingdom
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Source of Support: None, Conflict of Interest: None

PMID: 19864771

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