Helicobacter pylori eradication is beneficial in the treatment of functional dyspepsia.

AIM: To assess whether the eradication of Helicobacter pylori leads to long-term relief of symptoms in functional dyspepsia. METHODS: Eight hundred patients with functional dyspepsia were randomized to receive double-blind treatment with twice-daily 30 mg lansoprazole, 1000 mg amoxicillin and 500 mg clarithromycin for 7 days (L30AC), twice-daily 15 mg lansoprazole, 1000 mg amoxicillin and 500 mg clarithromycin for 7 days (L15AC), or once-daily 15 mg lansoprazole for 14 days (LP). Dyspepsia and reflux symptoms were monitored for 12 months. RESULTS: In intention-to-treat analysis, the non-ulcer dyspepsia sum score showed a statistically significant benefit in terms of symptom relief in the L30AC group (P = 0.0068) compared with the LP group, but there was no significant difference between the L15AC and LP groups (P = 0.2). When all patients in the two eradication therapy arms were considered together, successful eradication had a significant benefit with regard to the complete absence of symptoms (P < 0.04). H. pylori eradication did not lead to an increase in reflux symptoms. CONCLUSION: This study suggests that H. pylori infection causes dyspeptic symptoms in a subset of patients with functional dyspepsia, and that these patients may obtain long-term symptomatic benefit following H. pylori eradication.

Full length cDNA of rat RT1.DMa and RT1.DMb and expression of RT1.DM genes in dendritic and Langerhans cells.

MHC encoded DM heterodimers and classical MHC class II complexes meet in an endosomal/lysosomal compartment where DM heterodimers support peptide loading of MHC class II. Studies on peptide loading of rat class II and on peptide persistence in cells of the dendritic lineage prompted us to establish full length cDNA clones coding for the subunits alpha and beta of rat DM molecules as well as a mAb directed against the luminal moiety of the beta subunit. Here we describe the establishment of the first full length cDNA clones of rat RT1.DMa and RT1.DMb. The mode of expression of RT1.DM at the transcript level in bone marrow culture-derived dendritic cells, in Langerhans cells and in a number of additional accessory cells is reported. The beta protein was identified in detergent lysates of RT1.DM expressing cells by Western blot analysis using a newly established monoclonal antibody directed against the luminal part of RT1.DMbeta.