IgA and IgG tTGA occur in a large number of EmA-negative patients with end-stage heart failure, and their presence is unlikely to be caused by concomitant CD.

It has been suggested that there may be a correlation between Helicobacter pylori (Hp) infection and precancerous lesions of the stomach. However, histological evaluation of bacterial colonization in chronic atrophic gastritis shows a relatively low prevalence of the microorganism, which does not support the hypothesis. The aim of our study was to investigate the Hp serology in 95 patients with chronic gastritis with antral atrophy, with (27 cases) and without (68 cases) intestinal metaplasia, and without Helicobacter-like organisms in antral and corpus biopsy specimens. For all subjects, serum anti-Hp immunoglobulin IgG was identified by a fluorescent immunoenzymatic method (Helori-test; Eurospital), and mucosal atrophy and activity were graded histologically (Sydney System score). The serum Hp-antibody status documented the presence of current bacterial infections in 64 of 95 (67.4%) patients and previous infections in another 17 subjects. In only 14.7% of cases was there no evidence of current or previous infection. These subjects had less severe mucosal atrophy and lower inflammatory scores. In addition, there were no cases of intestinal metaplasia in such subjects. The high prevalence of Hp infection confirms the primary role of the microorganism in the pathogenesis of chronic gastritis with antral atrophy, although the bacterium is no longer present in the advanced stages of such disease. The histological evaluation of Hp colonization following the criteria of the Sydney System appears from our study to underestimate the true prevalence of the infection in the stomach when there is mucosal atrophy.

An increased prevalence of celiac disease has been reported in neurological disorders of unknown etiology. A large proportion of Alzheimer's cases is still of unexplained etiology. Thirty-three Alzheimer's patients and 24 elderly controls were screened for celiac disease. IgA and IgG antigliadin antibodies were assayed in serum samples with enzyme-linked immunoassay. Confirmation of celiac disease in positive subjects was made by assaying IgA anti-endomysium antibodies by indirect immunofluorescence. Two Alzheimer's patients and 2 controls were positive for antigliadin antibodies (6 versus 8%; NS). None was positive for anti-endomysium antibodies. We conclude that the prevalence of celiac disease in Alzheimer's disease is not higher than in cognitively unimpaired elders, suggesting that the immune changes in celiac disease are unlikely to play a role in Alzheimer's disease.