Helicobacter pylori masks differences in homocysteine plasma levels between controls and type 2 diabetic patients

Background Data in the literature have not clarified whether type 2 diabetes mellitus affects homocysteine plasma levels. Different variables able to influence homocysteine could be the cause of these controversial findings. An important but neglected confounding factor is Helicobacter pylori, which has been demonstrated to be a cause of elevated levels of homocysteine and which is prevalent in the Caucasian population, ranging from 30 to 40% incidence. Starting from these findings we wanted to verify whether differences in homocysteine levels exist between a type 2 diabetic population and a control group, taking into account the presence/absence of Helicobacter pylori. Design The study was carried out on a group of uncomplicated and normotensive type 2 diabetic patients (n = 30, 55.7 +/- 9.7 years) and on a control group (n = 43, 51.2 +/- 11.3 years). On these subjects we evaluated: main parameters of glyco- and lipometabolic balance, presence of Helicobacter pylori by C-13 Urea Breath Test, plasma homocysteine, vitamin B-12, folate and genetic polymorphism of methylenetetrahydrofolate reductase. Results Evaluating the two groups as a whole, significant differences in homocysteine were found when considering Helicobacter pylori presence/absence (14.0 +/- 6.5 vs. 10.6 +/- 4.7 mumol L-1, respectively, P < 0.01) without differences of vitamins and the genetic polymorphism. of methylenetetrahydrofolate reductase. The positive interaction found among Helicobacrer pylori, diabetes and homocysteine (P = 0.03) taking into account all the other evaluated confounding factors, demonstrates that a significant difference in homocysteine plasma levels exists between diabetics and controls (Helicobacter pylori-negative: diabetics 12.5 +/- 5.6 mu mol L-1, controls 9.4 +/- 38 mu mol L-1; Helicobacter pylori-positive: diabetics 13.6 +/- 5.8 mu mol L-1 controls 14.3 +/- 7.0 mu mol L-1). Conclusions Type 2 diabetes seems to induce per se higher levels of homocysteine, which appears to be one of the factors responsible for the increased risk of vascular damage.