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Published on: November 1, 2024
Carotid intima-media thickness and serum paraoxonase-1 activity in patients with Helicobacter pylori
1Department of Gastroenterology, Namik Kemal University Faculty of Medicine, Tekirdag, Turkey. rafetmete@yahoo.com
Aim:
To evaluate serum paraoxonase(PON)-1 activity and carotid intima-media thickness (CIMT) in patients with Cytotoxin-associated antigen(CagA)-positive and negative Helicobacter pylori strains.
Patients And Methods:
The study group included a total of 134 individuals, of whom 103 were H. pylori positive, and 31 were H. pylori negative. Five biopsies were collected from each patient for histological examination: two from the antrum, two from the corpus, and one from the incisura angularis. The presence of H. pylori was determined using a modified Gram staining protocol. Peripheral blood was collected from each patient to determine levels of triglyceride, TC, HDL-cholesterol and LDL-cholesterol. IgG antibodies against CagA protein were analyzed by enzyme immunoassays. PON-1 activity was measured by colorimetric method. Carotid intima-media thickness and atherogenic plaques were measured using a grey scale color Doppler ultrasound. Data were analyzed by descriptive and inferential statistics.
Results:
The right, the left and the mean CIMT were significantly higher in H. pylori (+) group versus H. pylori (-) group (p < 0.001 for all). However, the mean PON-1 concentration was significantly lower in H. pylori (+) group versus H. pylori (-) group (p < 0.001). The right, the left and the mean CIMT of CagA (+) group were significantly higher than that of CagA (-) group and controls, while PON-1 concentrations of CagA (+) group were significantly lower than that of CagA (-) group and controls (for all p = 0.0001). The right, the left and the mean CIMT of CagA (-) group were significantly higher than that of the control group, while the mean PON-1 concentration were significantly lower (for all p = 0.0001).
Conclusions:
Decreased PON-1 activity may be an etiopathogenetic factor in increased atherosclerosis in patients with H. pylori infection, especially in those infected with the CagA positive strain.
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