With the help of many clinical studies, the diagnosis and therapy of gastric MALT lymphoma have evolved. Major progress has been seen in this area, including improvement of biopsy diagnosis, better histologic classification, new information concerning pathogenesis, and, especially, the start of a revolution in the treatment of low-grade gastric MALT lymphomas by eradicating H. pylori. About 12 clinical studies with almost 400 patients and case reports have shown that cure of H. pylori infection is associated with complete remission in approximately 80% of patients with low-grade MALT lymphoma in an early clinical stage. To establish H. pylori eradication as the primary choice in low-grade gastric MALT lymphoma further, it is necessary to select patients before therapy who are most likely to benefit from this single treatment modality. An excellent histologic workup of obtained biopsy specimens and comprehensive clinical staging are necessary. Because of the supposition that H. pylori-related growth support may play a role only in the early stages of low-grade gastric MALT lymphoma, the importance of determining the depth of lymphoma infiltration in the gastric wall is evident. Examinations by endosonographic ultrasonography have been shown to be the most reliable method to differentiate the layers of the gastric wall and to determine the infiltration depth of lymphomas. Eradication of H. pylori has to be considered as a first-line and single treatment modality in patients with low-grade gastric MALT lymphoma in clinical stage EI1. As a therapy with fewer side effects than radiation, surgery, or chemotherapy and as a stomach-conserving treatment, eradication of H. pylori in patients with low-grade gastric MALT lymphoma should be the treatment of the choice within clinical trials because there are no long-term results available thus far. Besides pretreatment patient selection, careful follow-up with endoscopy, biopsies, and clinical staging including endoscopic ultrasonography is necessary. A 5- to 10-year follow-up is necessary before the definitive value of H. pylori eradication can be established, but long-term results are excellent thus far. There are many questions to be addressed: What are the exact mechanisms that lead to the malignant transformation of a reactive infiltrate? Why do approximately 20% of low-grade MALT lymphomas not regress after H. pylori eradication? Is there a molecular-genetic or immunologic point of no return? What is the biologic significance of the immunoglobulin rearrangement detected with PCR? What will be the 5- and 10-year relapse-free survival rates of patients suffering from low-grade MALT lymphoma treated with H. pylori eradication alone as first and only treatment? The wave of new data each year about the role of H. pylori in gastric MALT lymphoma may help many of these questions to be answered.
