Abstract
The Influence of Chronic Helicobacter Pylori Infection on some Serum Lipid Profile Parameters, Apolipoproteins A-I and B and Lp(a) Lipoprotein Data on proatherogenic lipid profile alterations due to chronic Helicobacter pylori (HP) infection are contradictory. Aim of this study was to examine the differences in some lipid parameters between 55 subjects of both gender with a chronic HP infection (IgG>50 U/mL and IgA <20 U/mL) and 55 gender matched HP seronegative subjects (IgG and IgA <20 U/mL). Total cholesterol (TC) (p<0.001), triglycerides (TG) (p<0.05), LDL-cholesterol (LDL-C) (p<0.02), non-HDL-cholesterol (non-HDL-C), apolipoprotein (apo) B (p<0.001), Lp(a) and HDL-cholesterol (HDL-C) serum levels were higher in HP seropositive than in seronegative subjects, while there were almost no differences in apo A-I. In HP seropositive subjects, the frequency of pathological TC (p<0.001), TG (p<0.05), LDL-C (p<0.01), non-HDL-C (p<0.01), apo B (p<0.02) and Lp(a) serum levels was higher compared to seronegative. Serum HP IgG titers correlated negatively with TC, LDL-C (p<0.05), non-HDL-C, apo B and Lp(a) levels, and positively with TG, HDL-C and apo A-I levels. Results are similar for both genders. Our results confirm the hypothesis that a chronic HP infection could modify the lipid profile in a proatherogenic way.
Highlights
In the past few years, many studies have indicated that atherosclerosis is associated with several infectious pathogens, including Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus and herpes simplex virus [1,2,3,4,5,6,7,8]
Immunoglobulin G (IgG) titer for Helicobacter pylori (HP) higher than 50 U/mL and immunoglobulin A (IgA) titer for HP lower than 20 U/mL were regarded as chronic HP infection, whereas IgG and IgA titers lower than 20 U/mL were regarded as absence of HP infection
After an overnight fasting period of 12–14 hours, blood samples were taken, serum samples were separated from the cells by centrifugation at 3000 rpm for 10 min, and serum IgG and IgA for HP, total cholesterol (TC), triglycerides (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C) and nonHDL-cholesterol, as well as apolipoprotein A-I, apo B and Lp(a) lipoprotein (Lp(a)) levels were measured
Summary
In the past few years, many studies have indicated that atherosclerosis is associated with several infectious pathogens, including Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus and herpes simplex virus [1,2,3,4,5,6,7,8]. There has been increasing evidence that inflammation and infection could alter some atherogenic vascular factors involved in the development of atherosclerosis and its complications. Helicobacter pylori (HP) is a gram-negative microaerophilic spiral bacterium which causes one of the most prevalent infections in the world, affecting approximately 50% of the world’s population [10]. It is considered to be a causative agent of many gastrointestinal (e.g., peptic ulcer, gastric adenocarcinoma, primary gastric lymphoma of the mucosa-associated lymphoid tissue) and extra-gastric (e.g., atherosclerotic processes, peripheral vascular disorders, skin diseases) manifestations
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