title: Asymptomatic Helicobacter pylori infection increases asymmetric dimethylarginine levels in healthy subjects.
abstract: BACKGROUND
  Chronic infections have been demonstrated to be early factors of atherosclerosis and cardiovascular diseases, and their relevance increases when they are caused by agents with extremely broad spectrum of disease outcome such as Helicobacter pylori. The consequent endothelial impairment leads to a reduced bioavailability of nitric oxide. Increasing evidences have pointed out that the endogenous inhibitor of nitric oxide synthase, asymmetric dimethylarginine, defined as a risk factor for cardiovascular disease, may increase in infections and plays an important role impairing the vascular functions of the endothelium. Starting from these findings, we aim to investigate whether H. pylori may affect asymmetric dimethylarginine levels.
  
  
  METHODS
  The study was carried out on a group of 186 subjects (age 46.2 +/- 14.9 years). We evaluated asymmetric dimethylarginine, symmetric dimethylarginine, L-arginine, presence of H. pylori by 13C-urea breath test, and the main parameters of glyco and lipo metabolic balance.
  
  
  RESULTS
  Increased levels of asymmetric dimethylarginine were found in H. pylori-positive subjects with respect to H. pylori-negative subjects (0.46 x/ / 1.13 versus 0.42 x/ / 1.23 mol/l, p < .001, respectively). No differences were detected in L-arginine levels between the two groups. Multiple regression analysis performed in H. pylori-positive subjects and H. pylori-negative subjects showed profound differences in the variables related to asymmetric dimethylarginine (R2 = 66.9%, p < .01 versus 34.3%, p < .01, respectively) and symmetric dimethylarginine (R2 = 39.2%, p < .01 versus 20.6%, p = .09, respectively) levels.
  
  
  CONCLUSIONS
  Our data clearly demonstrate that H. pylori infection increases asymmetric dimethylarginine levels. Moreover, this infection causes a profound metabolic modification that alters the role of the known determinants of asymmetric dimethylarginine levels. We conclude that H. pylori infection must be taken into account as a cause of increased asymmetric dimethylarginine levels and that the eradication of H. pylori may therefore lead to a decrease in asymmetric dimethylarginine levels, which is a further reason for the reduction of the risk for cardiovascular disease in this large portion of population.
authors.affiliation: Department of Gerontological Research, Diabetology Unit, INRCA, Ancona, Italy. m.marra@inrca.it
authors.forename: Maurizio
authors.initials: M
authors.lastname: Marra
authors.forename: Anna Rita
authors.initials: AR
authors.lastname: Bonfigli
authors.forename: Patrizia
authors.initials: P
authors.lastname: Bonazzi
authors.forename: Renato
authors.initials: R
authors.lastname: Galeazzi
authors.forename: Cristina
authors.initials: C
authors.lastname: Sirolla
authors.forename: Ivano
authors.initials: I
authors.lastname: Testa
authors.forename: Stefano
authors.initials: S
authors.lastname: Cenerelli
authors.forename: Massimo
authors.initials: M
authors.lastname: Boemi
authors.forename: Roberto
authors.initials: R
authors.lastname: Testa
mesh_terms: D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism; D005260:Female; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D015854:Up-Regulation
chemical_list: C487735:dimethylarginine; D001120:Arginine