The role of pepsinogen assays as surrogate markers of gastritis dynamics in population studies

Abstract

Untreated Helicobacter pylori (H. pylori) infection results in atrophic gastritis in up to half of affected patients during their lifetime1–3. In most of these patients, atrophic gastritis is multifocal and affects the antrum, or antrum and corpus simultaneously. Autoimmune disease is a cause of atrophic corpus gastritis in some patients, most of these cases occurring in Northern Europe. In these patients, atrophic gastritis develops rather quickly, leads to a severe hypo- or achlorhydric stomach, and results in deficiency of vitamin B12 and a high serum homocysteine2’4. The H. pylori infection may, however, precede and trigger the autoimmune corpus gastritis as well5. In a population-based survey of 22000 elderly men in Finland, H. pylori infection defined by the presence of antibodies of the IgG class in the circulation, was associated with advanced atrophic corpus gastritis (serum PGI < 25 µg/L) in approximately 80% of the cases6, suggesting that H. pylori infection is a common causal factor also in atrophic gastritis limited to the corpus alone. Moreover, active treatment of the H. pylori led to a decrease in antibody titers and resulted in significant healing of the atrophy in these patients7.