Risk for gastric neoplasias in patients with chronic atrophic gastritis: A critical reappraisal

Abstract

Chronic atrophic gastritis (CAG) is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue (non-metaplastic atrophy) or by glandular structures inappropriate for location (metaplastic atrophy). Epidemiological data suggest that CAG is associated with two different types of tumors: Intestinal-type gastric cancer (GC) and type I gastric carcinoid (TIGC). The pathophysiological mechanisms which lead to the development of these gastric tumors are different. It is accepted that a multistep process initiating from Helicobacter pylori-related chronic inflammation of the gastric mucosa progresses to CAG, intestinal metaplasia, dysplasia and, finally, leads to the development of GC. The TIGC is a gastrin-dependent tumor and the chronic elevation of gastrin, which is associated with CAG, stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of TIGC. Thus, several events occur in the gastric mucosa before the development of intestinal-type GC and/or TIGC and these take several years. Knowledge of CAG incidence from superficial gastritis, its prevalence in different clinical settings and possible risk factors associated with the progression of this condition to gastric neoplasias are important issues. This editorial intends to provide a brief review of the main studies regarding incidence and prevalence of CAG and risk factors for the development of gastric neoplasias.

Gastric cancer in patients with type I gastric carcinoids

“…These patients should therefore be monitored also for this neoplasia by using a standardized biopsy protocol including the sampling of the gastric body and antral mucosa [18,40]. Indeed, in our case series three out of the four gastric cancers were localized in the gastric antrum.…”

Cytokine-Producing Potential of Blood Cells and Serum Cytokines in Patients With Chronic Atrophic Gastritis

“…15, 3 2013 Введение Считается, что развитие аденокарцином же-лудка представляет взаимосвязанные между со-бой патогенетические звенья (каскад Correa): поверхностный (неатрофический) гастрит -атрофический гастрит -кишечная метапла-зия -дисплазия -рак [7], поэтому хронический атрофический гастрит (ХАГ), являющийся рас-пространенным заболеванием желудочно-ки-шечного тракта, относят к предраковым состо-яниям желудка [26,29]. ХАГ характеризуется, помимо атрофии, воспалительными изменени-ями в слизистой оболочке желудка (СОЖ) [2], которые сопровождаются продолжительной ста-дией регенерации в условиях длительно сохра-няющейся гипоксии и активации внеклеточного протеолиза с ускорением процесса мобилизации и деления незрелых эпителиальных клеток, с бло-кированием их созревания и увеличением гене-тической нестабильности с нарастанием числа мутаций [3,25].…”

Laboratory screening markers in gastroenterology - state of the art

“…This is because invasive gastric carcinomas are preceded by a cascade of precancerous laesions, multifocal atrophic gastritis, and intestinal metaplasia. The multistep process initiates from Helicobacter pylori-related chronic inflammation of the gastric mucosa, progresses to CAG, intestinal metaplasia, dysplasia, and finally leads to the development of gastric cancer 59,60 . The diagnosis of Helicobacter pylori infections is now simple and easy, with a high sensitivity and specificity 92 -98%, using both the urea breath test and stool antigen tests 61,62 .…”