pylori gastritis were dependent on the extent, topography and severity of the infection; e.g. the gastric cancer risk increased exponentially with the progression of gastritis towards an achlorhydric or hypochlorhydric stomach with Staurosporine chemical structure severe mucosal atrophy and intestinal metaplasia. The earlier studies of Strickland and McKay proposed the topographic classification of atrophic gastritis into types A and B which constituted the core issue of the System. The A type indicating a corpus limited atrophic gastritis of autoimmune origin in patients with achlorhydria and with serological signs of the autoimmunity.8

Type B indicated atrophic gastritis without an autoimmune background and with atrophy limited to the antrum. This B subtype was considered “idiopathic” but was, after the discovery of H. pylori, realized to be typically related to H. pylori infection. It corresponds with the type of atrophic gastritis considered multifocal (MAG; multifocal atrophic gastritis) by Pelayo Correa in his reports from the 80s,14 or atrophic gastritis of the AB type by Glass and Pitchumoni from the 70s.15 In 1988, gastritis of “C type” was proposed by Wyatt and Dixon indicating reactive gastric lesions that were neither H. pylori associated nor autoimmune, and believed to be “chemical”

(reactive) or drug induced in nature.16 see more An important morphological parameter incorporated into the Sydney System from the literature was the “activity” of the gastritis. The activity of gastritis was first proposed and emphasized by Whitehead, Truelove and Gear in 1972.17 In their classification Dipeptidyl peptidase of gastritis, the Schindler—Glass-Pitchumoni—type topographical pattern of chronic gastritis was accepted but was complemented with the

concept of the “activity”. The “activity” indicated the co-existence of polymorphonuclear inflammation alongside the mononuclear one. This phenomenon we now consider to reflect the reaction of the host against the infection and to be strongly associated with the risk of the progression of gastritis to an atrophic pattern which is also related to the acquisitions of cytotoxic H. pylori strains. It is noteworthy that the guidelines presented in the Sydney System are still valid and applicable some 20 years later. In our view this is because the Sydney System was an appropriate synthesis at the time of the old knowledge on chronic gastritis mentioned above with the new data and knowledges about H. pylori acquisition and its consequences. It must be said the Sydney System was not a classification in strict terms but more a practical guideline that provided what we hoped might become a flexible universal gastritis reporting grid. It allowed for a standard rapid documentation of the extent and severity of the gastritis at the time of examination of the patient. H.