Does Eradication of Helicobacter pylori Infection Help Normalize Serum Lipid and CRP Levels?

Abstract

It is still unclear whether Helicobacter pylori infection is associated with risk factors for coronary artery disease. The aim of this study was to determine whether eradication of H. pylori infection affects serum lipid levels and C-reactive protein (CRP) levels. Seventy-eight patients who had H. pylori antigen positivity in their stools were enrolled. Clarithromycin, 1 g/day, amoxicillin, 2 g/day, and omeprazole, 40 mg/day, were given for 14 days. Serum total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG), and CRP were measured at baseline and 8 weeks after therapy. According to H. pylori stool antigen study after 8 weeks, individuals in whom H. pylori was eradicated were recruited as group A and those in whom H. pylori was not eradicated formed group B. Group A comprised 57 patients, and group B 21 patients. Patients in group A comprised 32 women and 25 men and their ages ranged from 35 to 59 years. Patients in group B included 13 women and 8 men, aged 32-61 years. No significant difference in LDL, TC, or TG serum levels were found between group A and group B. Although CRP and HDL serum levels were found to be the same before and after treatment in group B, CRP levels were found to decrease and HDL levels to increase significantly in group A (P < 0.05). We conclude that H. pylori infection may affect lipid metabolism in a way that could increase the risk of atherosclerosis. Thus H. pylori infection is an independent risk factor for coronary artery disease.

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

“…Furthermore, numerous studies have demonstrated that chronic H. pylori infection upregulates the serum CRP level 88,89) , and the high-sensitivity CRP (hsCRP) levels have been reported to be significantly higher in H. pylori-infected individuals, especially those with CagApositive infection, consistent with the strong correlation between infection with more virulent H. pylori strains and atherosclerosis 78,90) . The effects of H. pylori infection on the CRP level are further corroborated by the observation of a significant reduction in the serum CRP level after H. pylori eradication 79) . CRP may elicit a wide array of pro-atherogenic effects, including the stimulation of leukocyte-endothelium interactions, induction of a prothrombotic state and activation of the complement system 91) .…”

“…Clinical investigations have confirmed correlations between circulating markers of inflammation, such as C-reactive protein (CRP) 28,71,72) , tumor necrosis factor (TNF) 73,74) , interleukin (IL)-6 71,75) and IL-18 76,77) , and the occurrence of atherosclerosis and its cerebrovascular or cardiovascular events. In addition, growing evidence suggests that H. pylori infection, accompanied by persistent low-grade systematic inflammation, contributes to the risk of atherosclerosis by stimulating the production of proinflammatory cytokines, such as CRP 78,79) , IL-6 80) , and IL-18 81) , all of which are predictors of atherosclerosis.…”

The Influence of Chronic Helicobacter Pylori Infection on some Serum Lipid Profile Parameters, Apolipoproteins A-I and B and Lp(a) Lipoprotein

“…Aslan et al (17) and Sung et al (16) reported that serum TG, TC and LDL-C levels in HP seropositive subjects were significantly higher than in HP seronegative ones (all p<0.05). In a study of Kanbay et al (20), normalization in lipid parameters after a successful eradication of HP infection was observed. Majka et al (4) and Kucukazman et al (18) found that plasma levels of TC and LDL-C were significantly higher in HP seropositive subjects, and after 6 months of successful anti-HP therapy those levels were significantly lowered (4).…”

“…Although most authors reported about an association between HP infection and a proatherogenic lipid profile (6,(16)(17)(18)(19) which was normalized after successful eradication of HP (4,20), few studies did not confirm these results (1,2,5,10,21). Therefore, the influence of chronic HP infection on lipid parameter changes and their implication in atherogenic mechanisms of this infection are still unclear.…”

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“…The mean fasting insulin, HOMA-IR, total cholesterol (TC), TG, LDL-C, CRP levels and HDL-C levels in patients with unsuccessful eradication were not significantly changed from pretreatment levels [20]. Other studies also showed positive lipid profile changes and inflammatory marker decrease [21].…”