Helicobacter pylori is associated with modified lipid profile: impact on lipoprotein(a)

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

“…This is in agreement with the previous reports which indicated higher seropositivity in an older population (3,11,16,24). Sung et al (16) who analyzed the seropositivity rate in different age groups of Korean adults found the highest seropositivity rate in participants over 50 and the lowest in subjects younger than 30 years, and also that HP se ro positive participants were significantly older than those sero negative (p<0.05).…”

“…Sung et al (16) who analyzed the seropositivity rate in different age groups of Korean adults found the highest seropositivity rate in participants over 50 and the lowest in subjects younger than 30 years, and also that HP se ro positive participants were significantly older than those sero negative (p<0.05). Chimienti et al (11) found that HP infected subjects were significantly older than un in fected (50.8±8.3 vs. 43.5± 10.5 years; p<0.0001), as well. The reason for this could be a long period of possible exposure to the pathogen, as well as coexistence of other pathological conditions and a weaker defense ability in older persons, which could contri bute to higher proneness to infectious agents.…”

“…It has been reported that HP infection is able to affect the concentrations of both mucosal and circulating proinflammatory cytokines (especially IL-6 (1)) (32) and later has been shown to have a role in modulating (i.e. stimulating) the apolipoprotein (a) (apo (a)) gene expression (33) Chimienti et al (11). They found that HP seropositive subjects infected by the CagA(-) strains showed a reduction and by the CagA(+) strains an increase in the Lp(a) levels when compared with the uninfected ones, suggesting that the variations in the Lp(a) levels might derive from an altered balance between Lp(a) stimulatory and inhibitory cytokines, that could be different for the two strains.…”

“…Recent studies have suggested that chronic HP infection may be associated with an increase of the atherogenic risk (2,3,8,11) and several possible mechanisms of this relationship have been repor ted. Proposed mechanisms involving HP in the atherogenesis are production of excessive amounts of proinflammatory factors (such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-a)) (8) and acute phase reactants (such as fibrinogen and C reactive protein) (12), cross-mimicry between HP and host pro teins (13), immunomediated vascular damage and endothelial dysfunction (2), modifying the serum lipid profile (14) and promotion of the oxidation of LDL-cholesterol (15), abnormalities in haemostasis (9), hyperhomocysteinemia, direct bacterial invasion of atherosclerosis plaques, etc.…”

“…Proposed mechanisms involving HP in the atherogenesis are production of excessive amounts of proinflammatory factors (such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-a)) (8) and acute phase reactants (such as fibrinogen and C reactive protein) (12), cross-mimicry between HP and host pro teins (13), immunomediated vascular damage and endothelial dysfunction (2), modifying the serum lipid profile (14) and promotion of the oxidation of LDL-cholesterol (15), abnormalities in haemostasis (9), hyperhomocysteinemia, direct bacterial invasion of atherosclerosis plaques, etc. Recently, it has been hypothesized that only certain HP strains, which express the cytotoxin-associated gene A (Cag A) encoding the Cag A protein, may have a link with atherosclerosis (3,9), but this is still controversial (11).…”