title: Helicobacter pylori eradication lowers serum asymmetric dimethylarginine levels.
abstract: BACKGROUND
  Microbial pathogens, one of them is Helicobacter pylori (H. pylori), have frequently been implicated in the atherogenesis. Endothelium-derived nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS) and plays a pivotal role in the regulation of vascular tone. Asymmetric dimethylarginine (ADMA) is the most potent endogenous NOS inhibitor. Elevated levels of ADMA have been reported in many circumstances associated with a high cardiovascular risk. The aim of the present study was to investigate whether the eradication of H. pylori infection affects serum ADMA levels.
  
  
  METHODS
  Forty-two H. pylori-positive patients were enrolled in the study. Triple therapy for 14 days were given to all patients. Serum ADMA levels were measured at baseline and 2 months after therapy.
  
  
  RESULTS
  Eradication was achieved in 34 (81%) patients. The mean serum ADMA levels before and after therapy were 1, 77 ± 0, 30 and 1, 67 ± 0, 29 ng/mL in the group with H. pylori eradicated and 1, 63 ± 0, 28 and 1, 56 ± 0, 32 ng/mL in the noneradicated, respectively. We detected statistically significant decreased serum ADMA levels after therapy in H. pylori eradicated group.
  
  
  CONCLUSIONS
  These findings have indicated that eradication of H. pylori infection may decrease the risk of atherosclerosis and cardiovascular events.
authors.affiliation: Department of Gastroenterology, Faculty of Medicine, Zonguldak Karaelmas University, 67800 Zonguldak, Turkey. selimaydemir@hotmail.com
authors.forename: Selim
authors.initials: S
authors.lastname: Aydemir
authors.forename: Haci
authors.initials: H
authors.lastname: Eren
authors.forename: Ishak Ozel
authors.initials: IO
authors.lastname: Tekin
authors.forename: Ferda Akbay
authors.initials: FA
authors.lastname: Harmandar
authors.forename: Nejat
authors.initials: N
authors.lastname: Demircan
authors.forename: Mehmet
authors.initials: M
authors.lastname: Cabuk
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000008:administration & dosage; D000328:Adult; D000658:Amoxicillin / Q000008:administration & dosage; D000900:Anti-Bacterial Agents / Q000008:administration & dosage; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control; D018376:Cardiovascular Abnormalities / Q000209:etiology / Q000517:prevention & control; D017291:Clarithromycin / Q000008:administration & dosage; D004791:Enzyme Inhibitors / Q000097:blood; D005260:Female; D016481:Helicobacter Infections / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D064747:Lansoprazole; D008297:Male; D008875:Middle Aged; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors; D055815:Young Adult
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000900:Anti-Bacterial Agents; D004791:Enzyme Inhibitors; D064747:Lansoprazole; C018524:N,N-dimethylarginine; D000658:Amoxicillin; D001120:Arginine; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III; D017291:Clarithromycin