Mucosal protective effects of ecabet sodium: pepsin inhibition and interaction with mucus

Pepsin, acid and Helicobacter pylori are major factors in the pathophysiolo gy of peptic ulcer disease and reflux oesophagitis. Ecabet sodium reduces t he survival of H. pylori in the stomach and inhibits pepsin activity in the gastric juice of experimental animals. Here we have investigated the effec ts of ecabet sodium on some of the factors involved in the dynamics of the mucosal barrier, i.e. pepsins and mucins. This study used gastric juice obt ained from 12 nonsymptomatic volunteers and nine patients with reflux oesop hagitis. Ecabet sodium significantly inhibited pepsin activity in human gas tric juice, with a maximum inhibition of 78%. Pepsin I, the ulcer-associate d pepsin, was inhibited to the greatest extent. The ability of gastric juic e to digest mucin was significantly inhibited by ecabet. As with gastric ju ice proteolytic activity, the inhibitory effect of ecabet on mucolysis was greater in gastric juice from patients with reflux oesophagitis than in tha t from controls. Ecabet sodium showed a positive interaction with gastric m ucin, as assessed by an increase in viscosity. Thus ecabet sodium may reduc e the aggressive potential of gastric juice towards the mucosa, which may b e relevant in the treatment of reflux oesophagitis and peptic ulcer disease . In addition, it may strengthen the mucus barrier in peptic ulcer disease and gastritis.