Autoimmune Atrophic Gastritis

Currently, the diagnosis of gastritis has no commonly accepted classification. The classification called the Sydney System is still used by physicians, and it was developed in 1990. The first detailed classification occurred after the discovery of Helicobacter pylori, a bacteria involved in the etiology of gastritis. In 1994, scientists made further distinctions between atrophic and non-atrophic gastritis.

The updated Sydney System breaks down atrophic gastritis further into multifocal (H. pylori, specific diet, environmental factors) and corpus-predominant (autoimmune). Frequently, metaplasia plays a part in autoimmune gastritis, thus the word has been added in the classification for autoimmune metaplastic atrophic gastritis (AMAG). Let’s take a further look at the causes, manifestations, and treatment of AMAG, for which H. pylori is the most common cause for the development of gastritis worldwide.

Epidemiology

Pernicious anemia (PA) is a key manifestation of AMAG. Physicians used to believe that PA was a disease that affected only elderly females of Northern European descent. However, it is now recognized that the prevalence is similar across all populations. Like other autoimmune disorders, AMAG is more common in females than in males with a 3:1 ratio. Scientists believe that both AMAG and PA are significantly underdiagnosed around the globe. One explanation may be that doctors treat microcytic and macrocytic anemia with iron, folic acid, and cobalamin without identifying the cause of the anemia.

Pathogenesis

Researchers are still working to understand how AMAG develops as a disease. This is due to several reasons, notably the low prevalence of AMAG, coexisting H. pylori-induced gastritis, and very limited symptoms during the early stages. Still, they have identified both genetic and environmental factors that are key to the development of autoimmune gastritis. Genes have been identified that make an individual susceptible to AMAG, and they are located close to diabetes mellitus susceptibility genes in mice. This may explain the strong association between AMAG and diabetes mellitus.

Despite the lack of in-depth knowledge about how AMAG develops, scientists have identified some features like the infiltration of oxyntic mucosa by plasma cells and lymphocytes. The random destruction of parietal cells leaves small “islands” of normal oxyntic mucosa. This phenomenon is known as gastric pseudopolyposis, and it is similar to lesions in patients with ulcerative colitis. The result includes hypochlorhydria, which is a loss or decrease of hydrochloric acid secretion, which sets off a chain of events. This can lead to spasmolytic polypeptide-expressing metaplasia (SPEM). Inflammatory and hyperplastic polyps develop in the later stages of AMAG. Oxyntic mucosa can be completely absent in the advanced stages of AMAG.