[The role of Helicobacter in ulcerous disease, current treatment].
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"HP testing must be regarded as ONE of the important elements of the proper diagnostic work-up of a DISEASE, managed in close cooperation between GP's and specialists": that's the key message of the national consensus meeting held in CHU Brugmann on February 6th and 7th 1998. HP testing (usually by 2 direct methods: RUT-histology) and eradication treatment (ER), in infected patients, are strongly recommended in: 1. Past or current GDU (absolute indication), regardless of activity, complication(s), NSAID intake; 2. Low-grade MALT Lymphomas (Stage IE1) unequivocally diagnosed, managed and followed-up in specialised centers; 3. Post endoscopic resection of EGC. ER is advisable in HP carriers with a family history of gastric cancer. Chronic atrophic-, lymphocytic-, giant folds gastritis and hyperplastic polyps are acceptable indications for ER as well as scheduled long-term NSAID treatment in individuals with known HP status. Systematic ER in HP+ patients with fully investigated NUD is not indicated but could be considered in individual patients. Extra alimentary disorders and auto immune gastritis are no indication and there was no consensus for a "test and treat" policy in patients under 45 yrs old without alarm symptoms. Systematic screening of asymptomatic individuals is not recommended. A correct monitoring of eradication after treatment is recommended, mainly by UBT. In severe or refractory PUD, symptom recurrence and follow-up of EGC and Maltomas, endoscopic follow-up with HP testing is mandatory. The recommended first line treatment course (except known allergy or intolerance) is PPI full dose bid, Clarithromycin 500 mg bid Amoxycillin 1000 mg bid (7 days minimal 10 days maximal). RBC-based schemes must be locally validated and quadruple therapy is proposed when retreatment is needed. Culture, optional after the first treatment failure, is strongly recommended after a second failure. Overall, ER therapies are safe and neither the decreased efficacy of acid-lowering drugs, nor the possible increased risk of peptic oesophagitis are considered as contra-indications to eradicate. ER is cost-effective and cost-beneficial in PUD and adjusted number of pills delivered would cut costs. No clear economic data are currently available for a potential benefit of ER in GC prevention or NUD management. A national monitoring of HP resistance (Macrolides and Imidazoles) must be organized by specialised centers.
Indications of whom and when to treat Helicobacter pylori infection are reviewed in chronic atrophic gastritis, in particular types of gastritis (lymphocytic, giant fold, auto-immune gastritis), in hyperplastic polyps, before or during treatment with NSAIDs and in association with various extra-digestive diseases. Although there is no convincing evidence that Helicobacter pylori eradication may interrupt or reverse mucosal atrophy and intestinal metaplasia (potentially pre-cancerous lesions), indication for eradication could be considered in young patients if atrophic gastritis is considered as a consequence of chronic superficial gastritis which is reversible after Helicobacter pylori cure. The still evidence limited for a causal relationship between Helicobacter pylori and lymphocytic gastritis, giant folds gastritis and hyperplastic polyps suggests it is acceptable to eradicate Helicobacter pylori in infected patients presenting these special forms of gastritis. Despite the uncertainty on the interactions of Helicobacter pylori and NSAID in the genesis of peptic ulcer disease, it seems acceptable to prescribe eradication treatment in known Helicobacter pylori carriers before a long-term treatment with NSAID. The clinical evidence for an association between Helicobacter pylori and extra-digestive diseases is at the present time too limited to advocate routine eradication in these conditions before large prospective trials are performed.