[Pathophysiology of Helicobacter pylori infections].

Helicobacter pylori is the causative factor of chronic gastritis and ulcers of duodenum and stomach and relates to mucosa-associated lymphoid tissue (MALT) lymphomas. Host factors, bacterial factors and dietary habits conceivably play a part in the more severe mucosal lesions induced by H. pylori. H. pylori is a heterogeneous bacterial species, the various types differing in possession of a locus with genes coding for products that may intensify the inflammatory reaction. The cytotoxin-associated gene (cagA) protein is a marker for this locus; this protein and the vacuolating-associated cytotoxin A are clearly related to the ulcerative disease. Patients may be colonized by a mixed population of H. pylori consisting of cagA-positive and cagA-negative H. pylori. Also, a patient may be infected by a mixed population of H. pylori sensitive and resistant to metronidazole. Accordingly, a substantial part of the H. pylori population in a patient should be examined to arrive at an adequate conclusion concerning the production of H. pylori factors that may relate to a particular clinical picture and to the sensitivity to antibiotics of the H. pylori.