The findings of Mason et al. 1 on diabetes mellitus and hepatitis C are similar to our own, reported at the 8th European Congress of Clinical Microbiology and Infectious Diseases. 2 In our study, diabetes was found in 34.7% and 2.7% of chronic hepatitis C and chronic hepatitis B patients, respectively (P Ͻ .001). On the other hand, in a diabetic cohort the anti-HCV positivity (6%) was significantly higher than the control (0.6%) (P Ͻ .05), but the HBsAg positivity (5%) was similar to the control. A notable difference, however, is that even after elimination of patients with predisposing factors, diabetes was found in a higher percentage (11%) of chronic hepatitis B patients in Mason' s study compared with our own (2.7%). Also, when the cirrhotic patients and those with predisposing factors to diabetes were eliminated, the prevalence of diabetes in patients with chronic hepatitis C virus and hepatitis B virus infection did not differ significantly (11% vs. 16%; P ϭ .26 [ Fig. 1B in Mason 1 ]). Perhaps the prevalence of known predisposing factors (e.g., Asian descent, age, alcohol abuse) were higher in their cohorts with hepatitis B.

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HP infection increases the proliferative rate of gastric foveolar cells in conjunction with an increased apoptotic rate and activation of MAPK(ERK). MAPK activation seems to be a significant and persistent event in the HP-induced neoplastic transformation.

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