Abstract
Gastro-esophageal reflux disease (GERD) is a multifactorial condition whose main pathogenetic factor is represented by Transient Lower Esophageal Sphincter Relaxations (TLESRs). Many hypotheses have been proposed to identify the mechanisms underlying the onset of TLESRs. One evidence suggested that colonic fermentation of indigestible carbohydrates (fructooligosaccharides, FOS) increases the rate of TLESRs and the number of acid reflux episodes. Alpha-galactosidase is an enzyme allowing better digestion of food rich in FOS that is commonly used to control symptoms of patients affected by Irritable Bowel Sindrome. Aim of our study was therefore to test the possible effect of the assumption of alphagalactosidase on esophageal pH profile in GERD patients. Patients and methods: 9 patients with low-grade esophagitis and typical GI symptoms underwent a basal 24-hour esophageal pH-metric recording. Once confirmed the GERD diagnosis, patients were instructed to assume 1 tablet of alpha-galactosidase 300 GalU (n=5) or placebo (n=4) before meals for the following four weeks. At the end of treatment a second 24-h esophageal pH-metry was performed. Heartburn and regurgitation were also scored (score: intensity x duration) at baseline and after 4 weeks. Results: Patients receiving alpha-galactosidase showed a reduced number of acid reflux episodes/24 hours as compared to baseline (60±25 vs 118±40, p<0.01); percentage of time with pH<4 was also reduced in such patients as compared to baseline values (4.2±1.7 vs 6.7±2.7, p<0.05); no difference was detected in the group receiving placebo. Heartburn was reduced in patients assuming alpha-galactosidase as compared to baseline (1.2±0.4 vs 2±0.6, p<0.05) with no differences in the placebo group. Regurgitation showed a trend toward a decrease after alpha-galactosidase which did not reach statistical significance (1.2±0.4 vs 1.5±0.3, n.s.). Summary and Conclusions: chronic assumption of alpha-galactosidase is associated to a decreased amount of gastro-esophageal reflux episodes in GERD patients. Such patients also experienced an initial improvement in clinical features of the disease. It seems likely that this change in esophageal pH pattern could depend on the modulation of TLESRs due to the reduced fermentation of FOS in the colon.
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