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Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
Helicobacter pylori infection is associated with the seriousness of carotid atherosclerosis and inflammatory
Hong Zhao1, Yemeng Chu2, Ying Li1
1Department of Neurology, Dalian Central Hospital Affiliated to Dalian University of Technology, No.826 Southwest Road, Shahekou District, Dalian City, Liaoning Province 116033, China.
Insights
Helicobacter pylori (Hp) infection is linked to carotid atherosclerosis and its severity. Hp seropositivity correlates with increased inflammation markers like Lp-PLA2 and MMP-9, suggesting a role in stroke risk.
Area of Science:
- Cardiovascular Science
- Infectious Disease Epidemiology
- Biomarkers in Atherosclerosis
Background:
- Carotid atherosclerosis is a major risk factor for ischemic stroke.
- The role of Helicobacter pylori (Hp) infection in atherosclerosis remains debated.
- This study investigates Hp seroprevalence and its association with carotid atherosclerosis severity.
Purpose of the Study:
- To determine Hp seroprevalence in patients with carotid atherosclerosis.
- To assess the correlation between Hp seropositivity and carotid artery stenosis severity.
- To explore the potential role of inflammatory markers (Lp-PLA2, MMP-9) in Hp-associated atherosclerosis.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) used for Hp IgG detection.
- Participants classified into mild, moderate, and severe carotid stenosis groups.
- Measurement of serum cytokines: lipoprotein-associated phospholipase A2 (Lp-PLA2) and metalloproteinase-9 (MMP-9).
Main Results:
- Hp seropositivity was significantly higher in carotid atherosclerosis patients (62.8%) compared to controls (32.1%).
- Higher Hp seropositivity correlated with increased carotid atherosclerosis severity and elevated Lp-PLA2 and MMP-9 levels.
- Hp-positive patients exhibited higher total cholesterol and LDL-C levels.
Conclusions:
- Hp seropositivity is significantly correlated with the presence and severity of carotid atherosclerosis.
- Chronic Hp infection may contribute to atherosclerosis through lipid alterations and increased pro-inflammatory cytokines.
- Reducing Hp burden could potentially decrease cerebrovascular events.
Background:
Carotid atherosclerosis is an important factor to ischemic stroke. Accumulating evidence indicated that certain viral and bacterial infections may contribute to the initiation and progression of atherosclerotic disease. Hp infection is common in China, however, the role of Hp infection in carotid atherosclerosis is still controversial and inconsistent. In our study, we aimed to determine the seroprevalence of Helicobacter pylori (Hp) in patients with carotid atherosclerosis and the association between Hp seropositivity and the severity of carotid artery stenosis. The inflammatory serum cytokines of lipoprotein-associated phospholipase A2 (Lp-PLA2) and metalloproteinase-9 (MMP-9) were also tested to explore the possible mechanism of Hp linked atherosclerosis.
Method:
94 participants with carotid atherosclerosis (patient group) and 56 individuals without carotid atherosclerosis (control group) whom all confirmed by color Doppler ultrasound were included in this study. According to the degree of carotid artery stenosis, the patient group was classified into three different subgroup: mild stenosis (<50 % stenosis, n = 30), moderate stenosis (50-69 % stenosis, n = 34) and severe stenosis (≥70 % stenosis, n = 30). An enzyme linked immunosorbent assay (ELISA) for immunoglobulin (Ig) G test for Hp diagnosis was used on all enrolled subjects. Values higher than 30 IU/mL were considered Hp seropositivity. They were also divided into Hp seropositive (n = 77) and Hp seronegative group (n = 73) according to Hp test result. Lp-PLA2 and MMP-9 were also measured in all participants as inflammatory markers.
Results:
The seropositivity rate for HP reached 62.8 % in patients with carotid atherosclerosis and it was significantly higher than that in controls 32.1 % (P < 0.001). The Hp-IgG levels in patients group were also significantly higher than those in controls (46.89 ± 22.34 IU/ml vs. 29.84 ± 11.83 IU/ml). Furthermore, the higher HP seropositivity, the more severe the extent of carotid atherosclerosis. Lp-PLA2 and MMP-9 levels in the mild, moderate and severe stenosis of carotid atherosclerosis were statistically higher than in controls. There were 77 (55.7 %) Hp positive and 73 (44.3 %) Hp negative subjects. Hp positive patients had a significantly higher incidence of carotid atherosclerosis (76.6 % vs. 47.9 %), TC levels (5.31 ± 0.7 mmo/l vs. 5.01 ± 0.66 mmo/l) and LDL-C levels (2.62 ± 0.66 mmo/l vs. 2.31 ± 0.61 mmo/l) when compared with Hp negative patients. In addition, Plasma Lp-PLA2 and MMP-9 levels in patients seropositive for Hp were significantly higher than in those seronegative for Hp.
Conclusions:
These results showed evidence that Hp seropositivity had a significantly correlation with carotid atherosclerosis as well as its severity evaluated by ultrasound. Furthermore, chronic infection with Hp might involve the prevalence of carotid atherosclerosis via lipid alterations and increased pro-inflammatory cytokines Lp-PLA2 and MMP-9. The reduction of Hp burden may therefore decrease the emerging of cerebrovascular events.
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