M. Curlo

Efficacy of 5-asa in the Treatment of Colonic Diverticular Disease

Objective To assess the therapeutic efficacy of 5-aminosalicylic acid (5-ASA) in patients with colonic diverticular disease performing a systematic review of the literature. Data Sources Cochrane Trial Register (until Issue 4, 2008), Medical Literature Analysis and Retrieval System Online (1966 to October 1, 2008), Excerpta Medica Database (1980 to October 1, 2008), and abstracts from the major US, European, and Asian gastroenterology conferences. Expert opinions sought and reference lists of identified studies and any relevant published reviews checked. Study Selection Randomized controlled trial (RCT) or a controlled clinical trial with a parallel group design using 5-ASA as 1 treatment arm. Results Six RCTs enrolling 818 patients were found: 3 were performed in patients with uncomplicated diverticulitis, and the remaining in patients with symptomatic uncomplicated diverticular disease. The results of these studies showed that patients treated with 5-ASA had significantly better outcomes and that also mesalazine scheduled daily was superior to cyclic administration to prevent relapse of diverticular disease. However, several of these studies have not included an endoscopy at the start of the study and when patients had recurrences. Conclusions From this systematic review, it seems that 5-ASAs may have a role in patients with colonic diverticular disease. However, high-quality well-designed RCTs are necessary to confirm these initial observations.

W1235 Efficacy of 5-ASA in the Treatment of Colonic Diverticular Disease: A Systematic Review

Objective: to assess the therapeutic efficacy of 5-ASA in patients with colonic diverticular disease performing a systematic review of the literature. Data Sources: Cochrane Trial Register (until Issue 4, 2008), MEDLINE (1966 October 1st 2008), EMBASE (1980October 1st 2008) and abstracts from the major US, European and Asian gastroenterology conferences. Expert opinions sought and reference lists of identified studies and any relevant published reviews checked. Study Selection: randomized controlled trial (RCT) or a controlled clinical trial (CCT) with a parallel group design using 5-ASA as one treatment arm. Results: 6 RCTs enrolling 818 patients were found: 3 were performed in patients with uncomplicated diverticulitis, and the remaining in patients with symptomatic uncomplicated diverticular disease. The results of these studies showed that patients treated with 5-ASA had significantly better outcomes and that alsomesalazine scheduled daily was superior to cyclic administration to prevent relapse of diverticular disease. Conclusions: from this systematic review appears that 5-ASAs may have a role in patients with colonic diverticular disease. However high quality well designed RCTs are necessary to confirm these initial observations.

T1979 Pepsinogen II As Marker of Inflammation in H.P Infection and in NSAIDs Damage

NH4Cl prepulse followed by a Na+-free solution. Alkalinization in Na+-free solution represents intracellular acid production and eliminates the possibility of contribution by the Na+/ H+ proteins. Studies were done in the presence or absence of indomethacin (100μM) or acetylsalicylic acid (ASA) (100-500μM). Results: In the presence of indomethacin, a rapid decrease in pHi is seen upon the removal of Na+, followed by an immediate rise in pHi, approaching pH of 7.0. In the absence of indomethacin, no alkalinization was observed until Na+ was added back to the solution. In a separate series of experiments, a similar result was observed with ASA. In the presence of ASA, a rapid alkalinization was observed in the Na+-free solution, representing intracellular acid production. This effect was not seen in the absence of drug. Conclusions: This study suggests that indomethacin and ASA have a direct effect on activation of acid secretion in the parietal cell. This is a novel mechanism in which NSAID use may increase risk of PUD. The direct stimulatory effect on acid secretion provides evidence for a rapid onset of PUD via the decreased barrier function coupled with enhanced acid secretion that occurs in the absence of secretagogues.