Autoimmune disorders: gastrointestinal manifestations and endoscopic findings.

The gastrointestinal tract can be involved in many autoimmune disorders, and women are affected more than men in most of the disease processes discussed. As this article outlines, gastrointestinal manifestations can be either part of the clinical presentation or complications of treatment. Depending on the disease process and the severity of symptoms, gastrointestinal evaluation and treatment can have an important role in the management of these diseases.

Gastric mucosa-associated lymphoid tissue lymphoma.

The connection between Helicobacter pylori and gastric mucosa-associated lymphoid tissue (MALT) lymphoma is well established. H. pylori infection causes an immunological response, leading to chronic gastritis with formation of lymphoid follicles within the stomach. These lymphoid follicles resemble nodal tissues found throughout the body and are composed of reactive T cells and activated plasmal cells and B cells. The B cells are responsible for initiating a clonal expansion of centrocyte-like cells that form the basic histology of MALT lymphoma. Early diagnosis of MALT lymphoma is difficult but essential for adequate treatment. Clinical symptoms are vague and varied, with abdominal pain being a common presenting complaint. The endoscopic appearance of this tumor is varied and can be infiltrative, exophytic, or ulcerative. In addition, the tumor can have a multifocal distribution, and therefore aggressive tissue sampling is crucial for diagnosis. Endoscopic ultrasound is essential to document the extent of disease and is more accurate than CT scan in detection of spread to perigastric lymph nodes. Lesions that are confined to the mucosa or submucosa of the gastric wall are believed to be dependent on H. pylori stimulation and therefore can be successfully treated with H. pylori eradication. Those MALT lymphomas that present at more advanced stages require more aggressive management and can be treated with surgical resection, radiation, or chemotherapy. Follow-up is critical in all patients who have been treated with H. pylori eradication and consists of multiple endoscopic biopsies for histological and molecular studies as well as endoscopic ultrasound at 3, 6, and 12 months after treatment. The reappearance of MALT lymphomas has been seen years after treatment, and therefore follow-up of these patients should be indefinite.

Multifocal atrophic gastritis and gastric carcinoma.

Gastric carcinoma remains a major cause of morbidity and mortality worldwide despite its significant decline in recent years. H. pylori infection begins with nonatrophic gastritis, and most individuals continue to have nonatrophic H. pylori gastritis throughout their lifetime. A minority of those with severe antral inflammation will develop a duodenal ulcer, and a few, for unknown reasons, may develop gastric MALT lymphoma. Others, who acquired the H. pylori infection in early childhood, develop progressive multifocal atrophic gastritis with loss of gastric glands. A small proportion of these individuals develop extensive, incomplete (type III) intestinal metaplasia, and an even smaller proportion will progress to dysplasia and intestinal-type gastric carcinoma. H. pylori-associated gastritis is also a risk factor for diffuse-type gastric carcinoma, which is not preceded by atrophy, intestinal metaplasia, or dysplasia. Appropriate screening and preventive measures should be considered in high-risk groups. It is also crucial to identify cofactors such as genetic susceptibility and environmental factors that might interact with H. pylori infection to increase gastric cancer risk. To make an impact on gastric cancer incidence and mortality, serious consideration should be given to early H. pylori eradication in high-risk groups and endoscopic surveillance according to the updated Sydney system in some patients with high-risk preneoplastic lesions, whereas dysplastic lesions should be removed without delay. Studies currently in progress may tell us whether H. pylori eradication can prevent later development of gastric carcinoma and thus eliminate a major cause of mortality worldwide.