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Two percent of acute pancreatitis are drug induced. In the present paper, we reported the case of a 39 year-old patient with chronic-hallucinatory schizophrenia who developed symptomatic pancreatitis during the clozapine dose titration performed to reach the therapeutic range. Diagnosis of pancreatitis was suggested by clinical examination and abnormal laboratory values of pancreatic enzymes and confirmed by C-T scan and ultrasonography. The causal incrimination of clozapine in this case seems likely as all other possible causes of pancreatitis were excluded, as AP developed shortly after the introduction of the drug and as the pancreatic enzymes normalized after clozapine was stopped. No rechallenge to confirm the causal relationship was however attempted. So far, only eight cases of acute pancreatitis have been reported in association with clozapine use. Clozapine is an atypical antipsychotic drug which belongs to the chemical class of dibenzodiazepines. The mechanism by which clozapine could produce acute pancreatitis remained unclear. Nevertheless, we advocate a careful biological follow-up (measuring periodically the concentrations of amylase, lipase and triglycerides) during the treatment by clozapine.

"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.

Environmental factors certainly play a role in the appearance of Crohn's disease. Wether or not those factors are infectious agents remains uncertain. Broadly, two classes of infectious hypothesis are currently under investigation. The first one, concerning specific microorganisms (such as mycobacteria and virus) dates back to the first description of the disease in 1913. The second one studies the possible involvement of compounds derived from the intestinal microflora, irrespective to speciation. It appeared more recently and receives more and more attention. These hypothesis are reviewed by the authors with regard to data obtained from epidemiology, clinical and experimental investigations.