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One-third of the patients with esophageal achalasia treated by PD will experience symptomatic recurrence during a 4-yr period. Long-term remission can be achieved in virtually all the patients treated by repeated PD according to an "on-demand" strategy based on symptom recurrence.

Helicobacter pylori has been associated with the development of two malignant diseases: gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Although the cag pathogenicity island, especially the cagA gene, has been linked with adenocarcinoma, few data concerning H. pylori pathogenic factors involved in low-grade gastric MALT lymphoma are available. The goal of this study was to analyze the prevalence of and correlation between genes coding for seven H. pylori virulence factors (cagA, cagE, vacA, iceA, babA, hopQ, and oipA) and two novel adhesins (sabA and hopZ) by comparing a collection of 43 H. pylori strains isolated from patients with low-grade gastric MALT lymphoma to 39 strains isolated from age-matched patients with gastritis only. Our results show that taken individually, none of the nine genes tested can be considered associated with MALT strains and allow us to conclude that MALT pathogenesis is not linked with more proinflammatory H. pylori strains. We demonstrated that in patients infected with strains harboring the iceA1 allele, sabA functional status, and hopZ "off" status, the odds of developing a MALT lymphoma were 10 times higher. However, the low prevalence of such strains (10 of 43 MALT strains) renders this triple association a low-sensitivity marker for MALT strains. Our data confirmed that H. pylori virulence factors are correlated with one another. If the involvement of H. pylori in MALT lymphoma is well established, the pathomechanism by which gastric lymphoma occurs remains to be identified.Helicobacter pylori infection is the essential etiological factor of type B chronic gastritis and peptic ulcer disease (29,35). It is also the first bacterium discovered to be involved in the development of malignant diseases: i.e., gastric carcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma (14,21,40). Following H. pylori colonization, inflammation occurs. Untreated gastritis may persist for years with different grades of severity. In some individuals, immunological stimulation induces lymphoid follicles in the gastric mucosa and provides the background for MALT lymphoma development (11), the polyclonal lymphoid hyperplasia evolving further toward a monoclonal lymphoid population (36). The reasons for this evolution, which is accompanied by genetic abnormalities, remain to be elucidated (33, 37). MALT lymphoma induction and growth are probably antigen driven, and it has been shown that H. pylori could be the trigger (18,23,24,26). Moreover, there is a demonstrated causal association between H. pylori infection and MALT-type lymphoma development, because it is possible to cure this cancer by eradicating H. pylori, suggesting that bacterial virulence factors exist and are associated with the disease development. H. pylori is the cause of approximately 80% of MALT lymphomas (8,57).Among the factors that may be linked to the outcome of infection, bacterial virulence factors such as cytotoxins and the cag pathogenicity island (PAI) have been extensively ...

Background and aims: Gastric extranodal marginal zone B cell lymphoma of the mucosa associated lymphoid tissue (MALT)-type (MZBL) is a rare complication of Helicobacter pylori infection. Currently, no bacterial factor has been associated with the development of this disease. Our aim was to identify genes associated with lymphoma development. Methods: We used subtractive hybridisation as a tool for comparative genomics between H pylori strains isolated from a patient with gastric MZBL and from a patient with gastritis only. Results: When gastric MZBL strains were compared with gastritis strains, two open reading frames (ORFs) were significantly associated with gastric MZBL: JHP950 (74.4% v 48.7%, respectively; p = 0.023) and JHP1462 (25.6% v 2.6%, respectively; p = 0.004). The prevalence of JHP950 was 48.8% (p = 0.024) in duodenal ulcer strains and 39.3% (p = 0.006) in gastric adenocarcinoma strains, which makes this ORF a specific marker for gastric MZBL strains. In contrast, the prevalence of JHP1462 was 16% (p = 0.545) and 35.7% (p = 0.429) in duodenal ulcer and adenocarcinoma strains, respectively. These ORFs were present in reference strain J99 but not in reference strain 26695. JHP950 is located in the plasticity zone whereas the other, JHP1462, is located outside. Both encode for H pylori putative proteins with unknown functions. Conclusion: Despite its low prevalence, the ORF JHP1462 can be considered a candidate marker for H pylori strains involved in severe gastroduodenal diseases. In contrast, the ORF JHP950 has a high prevalence, and is the first candidate marker for strains giving rise to an increased risk of gastric MZBL strains. Further confirmation in other studies is needed.

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