| [ Summary ] |
Tolerance during H2RA therapy and rebound acid hypersecretion after cessation of H2RA have been implicated as factors affecting the effectiveness of treatment. The mechanism for tolerance and rebound may be better explained by H2 receptor up-regulation, rather than gastrin-mediated over-stimulation of parietal cells. In contrast to H2RA no tolerance to PPIhas been reported. However, acid rebound has alsobeen observed with PPI. In this case, the onset of the rebound is late, appearing 2 weeks after cessation. The mechanism of acid rebound phenomenon after PPI therapy is clearly distinct from that of H2RA and may be explained by gastrin-induced ECL cell hyperplasia,due to prolonged acid suppression with high-dose PPI. |