Helicobacter pylori is associated with modified lipid profile: Impact on Lipoprotein(a)

G. Chimienti, F. Russo, B. L. Lamanuzzi, M. Nardulli, C. Messa, A. Di Leo, M. Correale, V. Giannuzzi, G. Pepe

Research output: Contribution to journalArticlepeer-review


Objectives: Helicobacter pylori is a controversial risk factor for atherosclerosis. We investigated whether the bacterium persistent inflammation or the expression of the cytotoxin-associated gene A (CagA) may affect serum lipids as well as Lipoprotein(a). Design and methods: Two hundred-eleven healthy volunteers were evaluated for lipids and Lipoprotein(a). Helicobacter pylori was characterized by Urea Breath Test and IgG-anti-CagA. apo(a) Kringle-IV polymorphism was genotyped. Results: Prevalence of the infection was 72%; 43% of subjects expressed CagA reactivity. Infected subjects showed increased levels of cholesterol, LDL-cholesterol, and cholesterol/HDL-cholesterol atherogenic index. Association with the Helicobacter pylori CagA(-) strains persisted after the adjustment for covariates. Significant difference between infected and uninfected subjects was found in Lipoprotein(a) levels. This difference did not arise from the Kringle-IV genotype. Conclusions: The infection per se significantly modified serum lipid and Lipoprotein(a) concentrations. CagA does not seem to be a reliable marker of pathogenicity for the atherogenic complications of H. pylori infection.

Original languageEnglish
Pages (from-to)359-365
Number of pages7
JournalClinical Biochemistry
Issue number5
Publication statusPublished - Jul 2003


  • Atherogenic risk
  • Cag(A) antigen
  • Helicobacter pylori
  • Lipid profile
  • Lp(a)

ASJC Scopus subject areas

  • Clinical Biochemistry


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