title: Helicobacter pylori masks differences in homocysteine plasma levels between controls and type 2 diabetic patients.
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.
  
  
  METHODS
  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 lipo-metabolic 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 micromol 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 micromol L-1, controls 9.4 +/- 3.8 micromol L-1; Helicobacter pylori-positive: diabetics 13.6 +/- 5.8 micromol L-1, controls 14.3 +/- 7.0 micromol 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.
authors.affiliation: Institute of Internal Medicine, University of Ancona, INRCA, via Birarelli 8, I-60121 Ancona, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Cenerelli
authors.forename: P
authors.initials: P
authors.lastname: Bonazzi
authors.forename: R
authors.initials: R
authors.lastname: Galeazzi
authors.forename: I
authors.initials: I
authors.lastname: Testa
authors.forename: A R
authors.initials: AR
authors.lastname: Bonfigli
authors.forename: C
authors.initials: C
authors.lastname: Sirolla
authors.forename: S
authors.initials: S
authors.lastname: Giunta
authors.forename: L
authors.initials: L
authors.lastname: Galeazzi
authors.forename: D
authors.initials: D
authors.lastname: Fumelli
authors.forename: R
authors.initials: R
authors.lastname: Testa
mesh_terms: D000328:Adult; D000368:Aged; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000235:genetics / Q000382:microbiology*; D016481:Helicobacter Infections / Q000097:blood* / Q000150:complications / Q000235:genetics; D016480:Helicobacter pylori; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics; D017354:Point Mutation
chemical_list: D006710:Homocysteine; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)