Similar results were also reported by Ozkasap et al. [36] who demonstrated that H. pylori eradication significantly reduces the levels of hepcidin, possibly by increasing the response to iron therapy. On the other hand, Kim et al. [37] did not find any significant association between H. pylori infection and serum levels of prohepcidin, while this biomarker was decreased in patients with atrophic gastritis. Finally, the results of three recent studies did not support any association between H. pylori infection and IDA [38-40]; however, the occurrence of some biases, such as the exact definition of IDA or the absence of information concerning the specific gastric histologic

patterns shown by patients, may, in our selleck chemical opinion, affect the results of studies performed on this important issue. The role of H. pylori on idiopathic thrombocytopenic purpura (ITP), via the modulation of Fcγ-receptor balance of monocytes/macrophages or molecular mimicry mechanisms between platelet and H. pylori peptides, is well defined [41]. A study by Payandeh et al. [42] clearly reported a significant beneficial effect of H. pylori eradication in patients with mild thrombocytopenia, but a poor response in patients with severe thrombo-cytopenia was noted. In a similar study, Teawtrakul et al. [43] showed a significant platelet count response

in approximately 80% of GSK-3 cancer adults with ITP after H. pylori eradication within a median time of 4 months. Nevertheless, some authors

reported negative findings. Samson et al. [44] did not show any significant difference between infected and noninfected patients concerning the platelet count, while Gan et al. [45] reported a low prevalence of H. pylori infection in patients with ITP and the absence of any significant effect of H. pylori eradication on the platelet count. Differences in the definition MCE of ITP may be the cause of those findings, at least in our opinion. A meta-analysis by Shi et al. [46] conducted on patients with autoimmune thyroid disease (ATD) reported a significant role of H. pylori in Grave’s disease (GD), more than in Hashimoto’s thyroiditis (HT), with an additional increased risk in the case of infection sustained by CagA-positive strains. Another study by Aghili et al. [47] reported a significant epidemiological association between H. pylori infection and HT in patients from Iran. Similarly, Zekry et al. [48] demonstrated a significant association between H. pylori infection and autoimmune thyroiditis in patients affected by type 1 DM. An additional interesting study clearly showed a significant association between GD, CagA positivity, and negative HLA-DQA1 0201 or positive HLA-DQA1 0501 [49]. Finally, Jafarzadeh et al. [50] reported higher serum levels of rheumatoid factor and antinuclear antibodies in H.