Estudio de prevalencia de Helicobacter pylori y Chlamydia pneumoniae en placas de ateroma de pacientes diabéticos y no diabéticos con arteriosclerosis

  1. de Luis, D.A.
  2. Becerra, A.
  3. García Arata, I.
  4. Haurie, J.
  5. de Rafael, L.
  6. González, J.
  7. Martín de Argila, C.
  8. Aller, R.
  9. Boixedac, D.
Journal:
Clínica e investigación en arteriosclerosis

ISSN: 0214-9168 1578-1879

Year of publication: 2001

Volume: 13

Issue: 3

Pages: 103-107

Type: Article

DOI: 10.1016/S0214-9168(01)78777-3 DIALNET GOOGLE SCHOLAR

More publications in: Clínica e investigación en arteriosclerosis

Abstract

Background Atherosclerosis is similar to a chronic inflammatory response. Recent reports have suggested that Chlamydia pneumoniae (Cp) and Helicobacter pylori (Hp) may play a role in thepathogenesis of atherosclerosis in both non-diabetic and diabetic patients. The aim of the studywas to determine, by culture and polymerase chainreaction (PCR), whether Cp and Hp are present in arteries from patients with atherosclerosis. Methods and results The design was a cross-sectional study, with 40 patients (22 diabetic and 18 non-diabetic) scheduled for a revascularization procedure. The methods of detection in atheroma plaques included a PCR assay and culture of atheroma plaques to detect Cp and Hp. Serology was used to evaluate the patients previous contact with both microorganisms. In the overall group, 29 (72,5%) patients had a positive serology to Hp and 20 (50%) had a positive serology to Cp (p < 0,05). In diabetic patients, 77,3% had a positive serology to Hp and 50% to Cp (p < 0,05). In non-diabetic patients, 66,7% had a positive serology to Hp and 50% to Cp (difference non-significant). Cp was detected by PCR in a carotid atheroma of a single non-diabetic patient with positive serology and negative culture, who also had positive serology for Hp but negative PCR and culture. All diabetic and non-diabetic patients had negative PCR and culture for Hp in atheroma plaques. Conclusion This study provides evidence of the presence of Cp, but not Hp, in atheroma plaques. A chronic inflammatory response caused by persistent arterial infection may explain the association between Cp and atherosclerosis. The link between Hp and atherosclerosis may be explained by indirect effects.