Infection by viral or bacterial pathogens has been suspected in playing a role in the development of autoimmune thyroid disease. Because Helicobacter pylori might be involved in the development of nongastrointestinal conditions such as rosacea, ischemic heart disease, and diabetes mellitus, we evaluated the prevalence of H. pylori infection in patients with autoimmune thyroid disease. Fifty-nine patients with autoimmune thyroid disease were included: autoimmune atrophic thyroiditis (n=21), Hashimoto's thyroiditis (n=18), and Graves' disease (n=20). Twenty patients with nontoxic multinodular goiter served as controls for nonautoimmune thyroid disease, and 11 patients with Addison's disease served as controls for nonthyroid endocrine autoimmune disease. The levels of anti-H. pylori immunoglobulin G (IgG) were determined, and a radiolabeled urea breath test were performed. The prevalence of H. pylori infection was markedly increased in the patients with autoimmune atrophic thyroiditis (85.7%), compared with the controls with nontoxic multinodular goiter (40%) and Addison's disease (45.4%). Infection by H. pylori resulted in increased levels of gastrin, pepsinogen I, and pepsinogen II in the H. pylori-positive groups, compared with the H. pylori-negative groups. A positive linear regression was found between the levels of microsomal autoantibodies and those of anti-H. pylori IgG in patients with autoimmune atrophic thyroiditis (n=21; r=0.79; p < 0.01). Finally, and although the overall prevalence of H. pylori infection was not increased, the anti-H. pylori IgG levels and the results from the breath test were higher in the patients with Graves' disease and Hashimoto's thyroiditis patients than in the controls. Clearly, the prevalence of H. pylori infection is increased in autoimmune atrophic thyroiditis and results in abnormalities of gastric secretory function. The strong relation between the levels of anti-H. pylori IgG and the levels of microsomal antibodies suggests that H. pylori antigens might be involved in the development of autoimmune atrophic thyroiditis or that autoimmune function in autoimmune atrophic thyroiditis may increase the likelihood of H. pylori infection.

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Aim: adherence to therapy is important to ensure success. We wanted to explore this feature in patients with inflammatory bowel disease. Patients and methods: we explored adherence to treatment and its modifiers in 40 patients with inflammatory bowel disease using a battery of tests. Results: a 67% of patients (95% CI: 51-81%) acknowledged a certain degree of involuntary nonadherence, and 35% (95% CI: 20-51%) of voluntary nonadherence. Overall, 72% (95% CI: 56-85%) of patients had some form of nonadherence. An objective correlation of these self-reported data was assessed by the determination of urine salicylate levels in the subset of patients treated with mesalazine or its derivatives (15 cases). Two of them (13%) had no detectable urinary drug levels, indicating complete nonadherence. Voluntary nonadherence was higher in patients with lower scores in the intestinal (p = 0.02) and social areas (p = 0.015) of IBDQ-32, as well as in those with less active Crohn's disease (p < 0.005), patients with high depression scores and high patientphysician discordance (p = 0.01), patients with long-standing disease (p = 0.057), patients who considered themselves not to be well informed about the treatment they were getting (p = 0.04) or who trusted their attending physicians less (p = 0.03). Conclusions: intentional nonadherence to therapy is prevalent among patients with inflammatory bowel disease. A correction of factors associated to poor adherence could lead to higher therapeutic success.

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Our data indicate a possible association of H. pylori infection and the development of coronary heart disease, thrombo-occlusive cerebral disease, or both, in diabetic patients. The importance of this link is highlighted by the possibility of an effective intervention against H. pylori infection.