Helicobacter pylori infection and gastric lymphoma

Abstract

Gastric lymphoma of mucosa associated lymphoid tissue (MALT) has characteristic clinicopathological features that are different from nodal-type B cell lymphomas. Before a lymphoma can arise within the stomach, MALT has to be acquired as part of a response to an immunological stimulus. In most instances, gastric MALT is acquired in response to infection by Helicobacter pylori. There are several features of MALT lymphoma, such as plasma cell differentiation and follicular colonisation, that suggest that these lymphomas, although demonstrated on the basis of clonality studies to be neoplastic, retain some immunological drive. In vitro studies have shown that co-culturing cells derived from low grade MALT lymphomas with H. pylori results in tumour cell proliferation in a T cell dependant manner. Clinical studies have taken this discovery further and shown that patients with early low grade gastric MALT lymphoma treated with anti-Helicobacter therapy can show regression of their tumours. It is now generally accepted that eradication of H. pylori is a central component of the management of MALT lymphoma.