Gastritis in the alcoholic: relationship to gastric alcohol metabolism and Helicobacter pylori.

Abstract

Chronic gastritis is common in the alcoholic. It is characterized by histological inflammation of the gastric mucosa and is associated with variable symptomatology. Its etiology is still the subject of debate. Recently, a new alcohol dehydrogenase isoenzyme, called sigma ADH, absent from the liver but predominant in the upper GI tract, has been fully characterized, its gene cloned, and it appears to play a major role in gastric ethanol metabolism. Indeed, it has now been established, both in vivo in experimental animals and in vitro in cultured human gastric cells, that alcohol is metabolized in the gastric mucosa, resulting in the production of acetaldehyde, a toxic metabolite. In addition, Helicobacter pylori infection is common in the alcoholic, resulting in the breakdown of urea to ammonia, another toxic product. A number of studies carried out over the last 40 years revealed that antibiotic treatment eradicates ammonia production and results in histological and symptomatic improvement in the majority of patients with alcoholic gastritis. Non-invasive tests for the detection of H. pylori are now available which will facilitate the large scale studies needed to confirm whether, in H. pylori -positive patients, antibiotics should become routine treatment for alcoholic gastritis.