Helicobacter pylori and allergic disease.

Since 1983 when patients with type B gastritis were found to be infected by a hitherto unknown type of bacteria showing a certain similarity to Campylobacter, the prognosis of this disease has changed considerably with the availability of highly effective antibiotics. The Gram-negative bacterium was identified as Helicobacter pylori, which causes most cases of gastritis and of peptic and duodenal ulcer. It has also been found in patients with gastric adenocarcinoma and B-cell lymphoma of mucosa-associated lymphoid issue (MALT) type. H. pylori has certain properties than enable it to cross the gastric mucosa easily, stimulating the production of inflammatory cytokines due to the activity of urease, which is present in large quantities in the bacterial membrane. The mucosal lesion is mediated by mucinase and phospholipase, which alter mucous secretion, and the action of a vacuolizing cytosine. H. pylori also produces factors that stimulate interleukin-8 secretion, production of platelet-activating factor, which causes gastric acid hypersecretion, and programmed cell death of epithelial cells, all of which contributes to the epithelial lesion. Subsequently, H. pylori infection was related to particular allergic diseases when Kolibasova et al achieved remission of chronic urticaria in H. pylori-infected patients through antibiotics against this infection. Since then, numerous studies have been published confirming or disconfirming this initial experience. To date, the causative role of H. pylori in the etiology of chronic urticaria has not been confirmed and this criterion has predominated, despite clinical experiences relating chronic urticaria with H. pylori infection. However, the possibility that an immunological mechanism related to H. pylori is involved in some cases of chronic urticaria has not been ruled out. Thus, Bakos et al studied 33 H. pylori-infected patients with chronic urticaria and mild gastric symptoms. All patients showed high concentrations of IgG antibodies against H. pylori and in 31 of these (93.9%) specificity was to lipoprotein 20 (Lpp20; molecular weight: 19 kDa) of the bacterial surface. Thirteen patients also showed IgA antibodies against H. pylori and 6 of these (46.1 %) showed anti-Lpp20 antibodies. These results were compared with those in another group with chronic urticaria and without H. pylori infection who were seronegative. These authors suggest that there may be an underlying autoimmune mechanism that remains to be investigated.