The influence of chronic Helicobacter pylori infection in serum lipoprotein associated phospholipase A2 level and stability of atherosclerotic plaques in patients with carotid atherosclerosis / 中国医师杂志

ABSTRACT

Objective To explore the influence of Helicobacter pylori (Hp) infection in serum lipoprotein associated phospholipase A2 (Lp-PLA2), carotid intima-media thickness and stability of atherosclerotic plaques in atherosclerosis patients.Methods A total of 393 cases of patients with carotid artery arteriosclerosis confirmed by carotid color uhrasonography, who are informed consent, was selected as objects.The14C urea breath test was used to determine the infection situation of selected objects of helicobacter pylori.Meanwhile, enzyme-linked immunosorbent assay (ELISA) was used to determine the level of serum lipoprotein associated phospholipase A2 (Lp-PLA2).Results Serum Lp-PLA2 levels and carotid intimamedia thickness (IMT) of patients with carotid artery atherosclerosis in Hp infection group were higher than that of Hp non-infection group, and with the degree of Hp infection aggravating in the patients of carotid artery atherosclerosis, their serum Lp-PLA2 levels and carotid IMT were also increased accordingly.F test showed that the differences of serum Lp-PLA2 levels and carotid IMT in different degree of carotid artery atherosclerosis group were statistically significant (P ＜0.01).The incidence of unstable plaque of Hp infection group was obviously higher than that of the Hp non-infection group in the carotid atherosclerosis with plaques with statistical significance (chi square value =4.744, P =0.029).Multivariate linear regression analysis showed that the possibility of complication of unstable plaques in Hp infection group of carotid artery atherosclerosis was 1.82 times than that of non-infection group.With serum Lp-PLA2 every increasing 1 μg/L, the possibility of instability plaque increased by 2％.Conclusions Hp infection may promote the occurrence and development of carotid artery atherosclerosis by increasing serum level of Lp-PLA2 and changing the stability of atherosclerotic plaques.