[Clinical and biological approach to symptomatic biliary lithiasis].
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Biomedical subjects
Publications and source records attributed to E De Koster.
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Gastric carcinoma is the world's overall second most common cancer. Besides obvious environmental factors, recent epidemiological studies and a better knowledge of Helicobacter Pylori biological properties revealed that the microorganism is involved in the first steps of gastric carcinogenesis as proposed by the Correa model (from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma). Significant correlation between the prevalence of H. pylori infection and incidence of gastric carcinoma (mainly the intestinal type) in various geographical areas has been reported. The high prevalence of HP in pre-neoplastic states and in cases of early gastric cancer indicates the infection would precede the development of gastric cancer. HP-related chronic inflammation of gastric mucosa with increased mucosal cell proliferation, deficit in local ascorbic acid concentration, topical ammonia toxicity are putative mechanisms that overexpose a weakened gastric mucosa to environmental carcinogens.
We performed a literature search as well as a review of our own results to evaluate HP serology as a screening method in young dyspeptic patients, prior to endoscopy. This strategy has been proposed by various teams in order to decrease the endoscopy workload. We analysed the results that could be obtained when not performing endoscopy in seronegative patients, in terms of avoided endoscopies and missed lesions. We found that too many lesions would remain undiagnosed, and thus untreated, regarding our reimbursement system, if the strategy was used without a strict selection of patients. The screening might be advisable among highly selected patients, but the percentage of avoided endoscopies would then decrease regarding the total number of endoscopies performed. Our conclusion is that HP serology as a screening method in young dyspeptic patients cannot be advised in Belgium for the time being.
"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.
HP infection of the stomach is not a risk factor for reflux oesophagitis, and may even protect against reflux oesophagitis. HP eradication may lead to an accelerated development of GERD in duodenal ulcer disease patients. It is unknown whether this is also true for HP positive patients who do not suffer from duodenal ulcer disease. HP eradication may decrease the efficacy of acid secretion lowering drugs such as Proton Pump Inhibitors and H2-Receptor Antagonists. It is unclear whether this has any practical consequences, but it cannot be excluded that some patient may need an increased dose of acid secretion lowering drugs after HP eradication for control of symptoms and lesions of GERD. There are conflicting data on the possibility that long-term proton pump inhibitor treatment may accelerate the development of atrophic gastritis in Helicobacter pylori positive patients. The possible acceleration of atrophic gastritis development in HP positive patients using strong acid secretion inhibitors is the strongest argument in favour of eradicating HP in patients receiving long term potent acid inhibition, especially GERD patients. In view of the uncertainty concerning these data, both eradicating and non eradicating HP in patients with GERD can be defended.
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