Helicobacter pylori is a spiral shaped bacterium found in the mucus layer lining the stomach mucosa. It is the commonest chronic bacterial infection in humans, and is associated with peptic ulcer disease and a number of other conditions.
Helicobacter pylori infects more than half of the population world-wide. Most individuals infected are asymptomatic. The incidence is lower in developed countries and there is an inverse relationship between prevalence and socioeconomic status. It is more prevalent in older adults. Transmission is probably from man to man via faecal-oral or oral-oral routes. It has been demonstrated that iatrogenic spread can occur through contaminated endoscopes.
Tests for Helicobacter pylori are divided into the invasive and non-invasive tests depending on whether endoscopy is required. The serological tests measure specific H. pylori antibodies. A number of such tests are available commercially, the sensitivity and specificity of which vary considerably. Local validation of the tests are desirable. Because the antibodies to H. pylori persist for a long time after H. pylori eradication, the serological tests are not recommended for documentation of success of H. pylori eradication.
Another non-invasive test is the urea breath test. The patient is given either 13C or 14C-labeled urea to drink. The urease produced by H. pylori will metabolize the urea rapidly to ammonia and carbon dioxide which will be absorbed and then exhaled. The amount of labeled carbon in the expired air will be able to determine whether H. pylori is present. It is a very accurate method but is relatively expensive. It is a reliable method to assess the Helicobacter pylori status after treatment.
The invasive tests require upper endoscopy and biopsy of the gastric mucosa. Histological identification of H. pylori has long been considered the gold standard of diagnostic tests. However, it is time consuming and expensive. Histology is generally unnecessary in patients in whom a biopsy urease test is positive. The biopsy urease test is a colorimetric test based on the urease-producing ability of H. pylori. It is quick and accurate. When upper endoscopy is indicated, it is the test of first choice. Culture of biopsy specimens for H. pylori requires an experienced laboratory and is both time-consuming and expensive. It is only indicated when antimicrobial sensitivity testing is required.
Peptic ulcer disease Current scientific evidence points to a strong association between Helicobacter pylori and peptic ulcer disease. Cure of the infection results in a marked reduction in ulcer recurrence. Permanent cure of the peptic ulcer can be achieved. Therefore it is recommended that all gastric and duodenal ulcer patients who are infected with Helicobacter pylori should be given eradication therapy whether the ulcer is active or in remission. This also applies to patients with a history of ulcer bleeding or perforation. In complicated peptic ulcer disease, eradication of H. pylori should be confirmed. If available, the urea breath test is the ideal test to demonstrate H. pylori eradication.
he relationship of non-ulcer dyspepsia to H. Pylori is unclear. Controlled trials do not show significant improvement of symptoms after H. pylori eradication. However, a review of 10 eradication studies found symptom improvement in 73% of the patients that became H. pylori-negative and 45% in patients that remained H. pylori-positive. It is probably advisable to eradicate H. pylori in patients with functional dyspepsia after full investigation, but the strength of evidence is equivocal.
H. pylori plays a role in the pathogenesis of gastric carcinoma. However, eradication therapy for the purpose of preventing gastric carcinoma cannot be recommended at present. A Japanese study showed that patients treated for H. pylori after endoscopic resection of early gastric cancer had no recurrence of cancer while patients not treated had a recurrence rate of 9%. Basing on that evidence, it is recommended that H. pylori eradication should be given to patients following resection of early gastric cancer.
There is strong evidence to implicate H. pylori in the pathogenesis of gastric maltoma. Some studies show partial or complete regression of low-grade maltomas after H. pylori eradication though these studies are small and uncontrolled. It is recommended that H. pylori eradication therapy be given to patients with low-grade maltomas. However, the patients would require careful staging procedures and regular follow-up in specialized centres. Additional treatment modalities may be required.
H. pylori does not have a role in the pathogenesis of gastro-oesophageal reflux disease. Eradication of H. pylori may in fact increase the incidence and severity of gastro-oesophageal reflux disease. On the other hand, long-term PPI treatment of gastro-oesophageal reflux disease may promote the development of atrophic gastritis in patients with H. pylori infection and H. pylori eradication may therefore be beneficial. More studies are needed in this area before firm recommendations could be made.
Routine testing for H. pylori prior to initiating treatment with NSAIDs is impractical because NSAIDs are so commonly used. NSAIDs and H. pylori are independent risk factors, possibly additive, for the development of peptic ulcers. Several studies have shown that H. pylori does not exacerbate NSAID-associated injury. In fact, ulcer healing in NSAID users using anti-secretory agents may be quicker in those who have H. pylori infection. Recent studies have suggested that elimination of H. pylori before NSAID treatment reduces ulcer occurrence. NSAIDs are also known to increase the risk of complication from a pre-existing ulcer, such as those due to H. pylori infection. It is recommended that patients with a past history of peptic ulcer disease should be tested for H. pylori and given H. pylori eradication therapy if positive.
Effective treatment regimens should attain eradication rates of over 90% per protocol and over 80% by intent-to-treat basis. These regimens include 7 days courses of :-
The standard doses of PPI are : omeprazole 20mg, lansoprazole 30mg and pantoprazole 40mg. Metronidazole resistance is a rising problem adversely affecting the outcome of metronidazole containing regimens. If the local metronidazole resistance exceeds 30%, amoxycillin containing regimens are preferred to those containing metronidazole.
The classical triple therapy with colloidal bismuth subcitrate 120mg qid + metronidazole 400mg bd + tetracycline 500mg qid, is effective but requires to be given for 2 weeks.
Dual therapy (PPI or RBC + amoxycillin or clarithromycin) is less effective than the triple therapy regimens.
For treatment failure with PPI triple therapy or RBC triple therapy, an effective regimen which can be tried is the quadruple therapy with the addition of PPI to the classical bismuth triple given in 1 week. Re-infection after successful eradication is uncommon in adults though it may be higher in children.
Lam S K, Talley NJ. Report of the 1997 Asia Pacific Consensus Conference on the management of Helicobacter pylori infection - J. Gastroenterol Hepatol 1998; 13:1-12
The European Helicobacter Pylori Study Group (EHPSG). Current European concepts in the management of Helicobacter pylori infection. The Maastricht Consensus Report. Gut 1997; 41:8-13
Fennerty MB. What are the treatment goals for Helicobacter pylori infection? Gastroenterology 1997; 113:S120-S125
Barkin J. The relation between Helicobacter pylori and nonsteroidal anti-inflammatory drugs. Am J Med 1998; 105(5A):22S-27S
Talley NJ. A Critique of therapeutic trials in Helicobacter pylori-positive functional dyspepsia. Gastroenterology 1994; 106:1174-1183
Talley NJ, Janssens J, et al. Eradication of Helicobacter pylori in functional dyspepsia: randomised double blind placebo controlled trial with 12 months' follow up. BMJ 1999; 318:833-837
Lakeij RJF, Janssen JBMJ et al. Symptom improvement through eradication of Helicobacter pylori in patients with non-ulcer dyspepsia. Aliment Pharmacol Ther 1996; 10:843-850
Lee J, O'Morain C. Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines. Gastroenterology 1997; 113:S99-S106
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