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

S. Cenerelli, P. Bonazzi, R. Galeazzi, I. Testa, A. R. Bonfigli, C. Sirolla, S. Giunta, L. Galeazzi, D. Fumelli, Roberto Testa

Research output: Contribution to journalArticlepeer-review

Abstract

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 13C Urea Breath Test, plasma homocysteine, vitamin B12, 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 μmol L-1, respectively, P <0.01) without differences of vitamins and the genetic polymorphism of methylenetetrahydrofolate reductase. The positive interaction found among Helicobacter 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 μmol L-1, controls 9.4 ± 3.8 μmol L-1; Helicobacter pylori-positive: diabetics 13.6 ± 5.8 μmol L-1, controls 14.3 ± 7.0 μmol 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.

Original languageEnglish
Pages (from-to)158-162
Number of pages5
JournalEuropean Journal of Clinical Investigation
Volume32
Issue number3
DOIs
Publication statusPublished - 2002

Keywords

  • Helicobacter pylori
  • Homocysteine
  • Type 2 diabetes mellitus

ASJC Scopus subject areas

  • Medicine(all)

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