[Helicobacter pylori infection and chronic gastritis as extra-esophageal factors in gastroesophageal reflux disease].

INTRODUCTION Some substances, for example amoniac, that appear during an infection caused by Helicobacter Pylori (HP), can neutralise acid. It is assumed that a HP infection can attribute to the worsening of GERB disease with antral predominant gastritis and a defensive factor eith corpus-predominant gastrytis or esofagitis. AIMS The aim of this study is to ascertain the role of HP infection in the modification of GORD through a prospective study, that is to see does a HP infection prospectively influence the disease or not, with a special focus on symptomatology with pathohistological findings of the antrum and the corpus of the gaster through a monitoring period of 12 months. MATERIALS AND METHODS 50 patients of the main group were involved in this prospective study with symptoms of GORD, or that eventually had a black stool. A control group of 47 patients was formed that had Gerb positive symptomatology, identical to the first group. During endoscopic act eventual changes in oesophagus in view of GORD, so they have been graduated according to Sawary-Millerov graduation from 1991: via Standard Olympus byoptic tongs byoptic specimens were taken with changes in view of GORD, and corpus and antrum mucosac of gaster and they were put into 2% formalin, so analyses has been done at Institute for pathology in Sarajevo. A special attention has been made to the graduation of gastritis, so Sydney classification has been followed. A modification lasted for four weeks since dg has been made, so two groups were formed, one with eradicated HP and second with HP presence. In the second part of this study both groups were followed without treatment in the period of 12 months, meaning that the natural course of illness has been followed up. RESULTS The results of tests of significant differences between treated and control group after 12 months gr. I Sawary-Miller: normal differences n.s. (t = 0.122); chronic differences n.s. (t = 0.724), reflux esophagitis difference n.s.t = 0.733). Tests of differences between treated and control group of pts according to topographic classification of gastritis for GORD gr. I (X2 = 1.076)-n.s.; za GORD gr. II (X2 = 0.999) non significant. Tests between groups of PTS for treated group (X2 = 1.4) n.s., for control group (X2 = 5.073) significant result for p < 0.05; GORD gr. II for treated group (X2 = 1.051) n.s. The results of tests of significant difference between pathohistological findings of corpus antrum treated and control group within gr. I Sawary-Miller: the difference is not statistically significant t = 0.816. The results of test significant differences of antrum after 12 months between treated and control group: within gr. I X2 = 1.623 difference n.s.; within gr. II t = 0.015 difference n.s. CONCLUSION This study proved that eradication of HP infection acts to GORD course by improvement of endoscopic findings by Sawary-Miller and pathohistological findings on oesophagus, as well as with decrease of activity predominant antral atrophic gastritis in I degree of GORD 12 months after and by decreasing daily acid symptoms. The eradication of HP infection in GORD do not influence on activity of predominant corpus gastritis, as well as on heartburn symptom, weekly acid symptom nor chest pain.