E. Morana

A Curcumin-Based 1-Week Triple Therapy for Eradication of Helicobacter pylori Infection: Something to Learn From Failure?

Background:  Curcumin is the principal element of turmeric powder extracted from the root of Curcuma longa. Studies on curcumin have demonstrated some anti‐Helicobacter pylori activity as well as immunomodulating properties. N‐acetylcysteine and lactoferrin with their respective mucolytic and antibacterial activities might also be effective in H. pylori eradication therapy.

P.10 “GASTROPANEL TEST” IN THE CLINICAL OUTCOME OF GERD: PROSPECTIVE SIX MONTHS CLINICAL STUDY

“GASTROPANEL TEST” IN THE CLINICAL OUTCOME OF GERD: PROSPECTIVE SIX MONTHS CLINICAL STUDY L. Guida∗ ,1, P. Perazzo1 , S. Bertolini 1 , E. Morana1, D. Vaira2, C. Scarpignato1 , V. Savarino3 , L. Gatta1, L. Cavallaro4 , G. Cavestro1, M. Rugge3, A. Franze5, F. Di Mario1 1Universita di Parma, Parma; 2Universita di Bologna, Bologna; 3Universita di Padova, Padova; 4Ospedale di Belluno, Belluno; 5Ospedale Maggiore di Parma, Parma

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.