Helicobacter pylori infection and arterial stiffness in patients with type 2 diabetes mellitus
Abstract Epidemiologic studies have suggested possible atherogenic roles for such pathogens as Chlamydia pneumoniae , Helicobacter pylori (Hp), cytomegalovirus, and herpes simplex virus. The aim of the present study was to examine the relationship between seropositivity of antibodies to Hp (Hp infec...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2008-12, Vol.57 (12), p.1760-1764 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Epidemiologic studies have suggested possible atherogenic roles for such pathogens as Chlamydia pneumoniae , Helicobacter pylori (Hp), cytomegalovirus, and herpes simplex virus. The aim of the present study was to examine the relationship between seropositivity of antibodies to Hp (Hp infection) and arterial stiffness determined by pulse wave velocity (PWV) in 130 patients (73 men and 57 women) with type 2 diabetes mellitus without a history of cardiovascular disease. The prevalence of Hp infection in patients with type 2 diabetes mellitus was 53.8%. Age (66.7 ± 11.3 vs 60.0 ± 12.2 years, P = .0014) and systolic blood pressure (138 ± 19 vs 131 ± 22 mm Hg, P = .0420) were significantly higher in patients with Hp infection than in those without. Serum C-reactive protein was higher in patients with Hp infection than in those without, although it did not reach statistical significance (0.23 ± 0.27 vs 0.18 ± 0.20 mg/dL, P = .2205). Pulse wave velocity was significantly higher in patients with Hp infection than in those without (1877 ± 550 vs 1585 ± 331 cm/s, P = .0005). Multiple regression analysis demonstrated that age ( β = .388, P < .0001), mean arterial pressure ( β = .289, P = .0006), hypertensive treatment ( β = .185, P = .0282), and presence of Hp infection ( β = .169, P = .0220) were independent determinants of PWV. In conclusion, Hp infection is associated with arterial stiffness determined by PWV in patients with type 2 diabetes mellitus. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1016/j.metabol.2008.08.001 |