title: Influence of Helicobacter pylori infection and eradication on blood lipids and fibrinogen.
abstract: BACKGROUND
  An association between Helicobacter pylori infection and heart disease has been suggested. A potential mechanism may be inflammation-induced atherogenic changes of lipoproteins, but epidemiological studies have provided conflicting results.
  
  
  METHODS
  In a prospective multicentre study, 830 patients submitted for endoscopy and H. pylori testing were evaluated. Of the 686 H. pylori-positive patients, 487 received and 199 did not receive eradication treatment. Serum lipids and plasma fibrinogen were measured at baseline in all patients and 3 months later in those initially positive for H. pylori.
  
  
  RESULTS
  H. pylori had no influence on baseline lipid or fibrinogen levels. Increases in high-density lipoprotein cholesterol were observed in 368 patients who received eradication treatment and in 193 untreated patients: 0.06 mmol/L (P=0.000) and 0.07 mmol/L (P=0.009), respectively. Similar minor increases in total cholesterol and triglycerides occurred in both groups. Lipid changes were related to symptom relief and a reduction in smoking. Eradication therapy was associated with a minor decrease in plasma fibrinogen irrespective of the resolution of infection.
  
  
  CONCLUSIONS
  H. pylori has no influence on blood lipids or fibrinogen. Both the eradication of infection and symptomatic treatment without eradication are associated with minor lipid changes related to symptom relief and lifestyle modifications. Thus, the inflammatory changes associated with H. pylori are unlikely to affect lipoprotein or fibrinogen metabolism.
authors.affiliation: Gastroenterology Department, Institut Malaties Digestive, Hospital Clínic, Barcelona, Spain.
authors.forename: J I
authors.initials: JI
authors.lastname: Elizalde
authors.forename: J M
authors.initials: JM
authors.lastname: Piqué
authors.forename: V
authors.initials: V
authors.lastname: Moreno
authors.forename: J D
authors.initials: JD
authors.lastname: Morillas
authors.forename: I
authors.initials: I
authors.lastname: Elizalde
authors.forename: L
authors.initials: L
authors.lastname: Bujanda
authors.forename: C M
authors.initials: CM
authors.lastname: De Argila
authors.forename: A
authors.initials: A
authors.lastname: Cosme
authors.forename: A
authors.initials: A
authors.lastname: Castiella
authors.forename: E
authors.initials: E
authors.lastname: Ros
mesh_terms: D000328:Adult; D000368:Aged; D000658:Amoxicillin / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D017291:Clarithromycin / Q000627:therapeutic use; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D016481:Helicobacter Infections / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000302:isolation & purification / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D008055:Lipids; D000658:Amoxicillin; D005340:Fibrinogen; D017291:Clarithromycin; D009853:Omeprazole