Helicobacter pylori cause a chronic gastric infection, and may cause extra gastrointestinal disease. The association between Helicobacter pylori infection and serum lipid profiles is still controversial. The aim of this study was to investigate any possible relationship between Helicobacter pylori infection and lipid levels.
Methods: The subjects were 400 volunteer referring to medical centers between December 2005 and March 2006. Helicobacter pylori infection status was determined by assaying serum anti-Helicobacter pylori immunoglobulin G antibody. Total cholesterol, HDL-cholesterol, triglyceride concentrations were measured by routine enzymatic methods. The data for H.pylori-seropositive and -seronegative individuals were compared.
Results: Three hundred nineteen subjects (79.8 percent) were Helicobacter pylori-seropositive. The serum triglyceride concentration and total cholesterol/HDL-cholesterol ratio were significantly higher in Helicobacter pylori-seropositive than Helicobacter pylori-seronegative individuals (162.03 vs. 143.88 mg/dl, p<0.05 and 4.27 versus 3.91, P<0.05 respectively).
Conclusion: The findings confirm the existence of a moderate association between H.pylori infection and lipid modulation. It also possible that H.pylori infection promotes atherosclerosis by acting through changes in lipid profile.
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Key words: Helicobacter pylori, lipid profile, coronary heart disease, atherosclerosis, serum lipid levels
Helicobacter pylori infection is the most common chronic bacterial infection in the world. This bacterium colonizes the human stomach and causes chronic and active gastritis, peptic ulcer disease and is associated with increased risk of developing gastric cancer (1;2).
A number of seroepidemiologic studies have suggested that H. pylori infection might be involved in the pathogenesis of several extra digestive diseases, which cardiovascular disease is one of them (3;4). The suspicion about H. pylori involvement in such conditions is based on the following: (i) local inflammation can have systemic effects; (ii) H. pylori gastric infection is a chronic process that lasts for decades; and (iii) persistent infection induces chronic inflammatory and immune responses that can induce lesions both locally and remote from the primary infection site (5). H. pylori infection may cause extradigestive manifestations by potential mechanisms with directly or indirect actions. The direct effects this bacterium has on the vascular wall include endothelial injury and dysfunction related to circulating endotoxins, smooth muscle proliferation, and local inflammation. The indirect effects of this infection are more often pronounced than the direct effects. These include reduction of inflammatory mediators with proinflammatory, procoagulant, and atherogenic action; changes in risk factors (lipid profile, coagulation, levels of oxidative metabolites); production of crossreactive antibodies; malabsorption of nutrients and vitamins; and metabolic factors, such as overproduction of ammonia (6).
Although some authors have demonstrated a positive relationship between H. pylori infection and the risk of cardiovascular disease, whilst others have not found such a relationship (7-10). Acute and chronic infections causing the inflammation of arteries may promote the atherosclerotic cascade (11). H.pylori induces along standing low-grade persistent inflammation stimulus. Some studies have indicated that H.pylori infection can modify the serum lipids concentration (7) being also associated with an atherogenic lipid profile (12;13), but the other studies have not confirmed these findings (14;15). On the basis of these considerations, the present study was designed to investigate whether H.pylori infection is also associated with changes in lipid profile.
Four hundred healthy asymptomatic volunteers (mean age 38±12 years, range 11-83 years, 235 male, 165 female) were included in the study. Subjects were enrolled from Kashan medical centers between December 2005 and March 2006. The majority of people who attended were working, socioeconomically middle class. Individuals with a history of indigestion or gastrointestinal disease were not included in this study. Patients with cardiovascular disease, diabetes mellitus, familial hypercholesterolemia and hypertriglyceridemia and liver disease were also excluded. After obtaining written informed consent for the study, which was carried out in accordance with the Helsinki Declaration, a precise medical history was taken .Hematological and biochemical blood tests were performed in the laboratory. Blood samples were taken after overnight fasting, after clotting, centrifuged and the serum was frozen at -20°c, and then used for quantitative analysis. Triglyceride, total cholesterol and high density lipoprotein cholesterol (HDL-cholesterol) concentrations were measured by routine enzymatic methods using commercial kits. Levels of low density lipoprotein cholesterol (LDL-cholesterol) were calculated by Friedwald formula. Seroprevalence of H.pylori was determined by measurement of the serum anti-H.pylori IgG antibody using an enzyme-linked immunosorbent assay (IgG, EIA, Trinity Biotech, USA). According to the manufacturer's instruction ISR³ 1.1 were regarded as positive.
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Data are demonstrated as mean ± standard deviation (SD) for normally distributed continuous variables, median (minimum-maximum) for skew distributed continuous variables, and frequencies for categorical variables. Comparisons between groups were performed using the unpaired two-tailed student's t-test, c2 test to compare between individuals seropositive and seronegative for H.pylori. Data analysis was performed by using the Statistical Package for Social Science (SPSS for Windows, version 10.0, 1999, SPSS Inc, Chicago, IL). Differences were considered to be statistically significant if the null hypothesis could be rejected with >95% confidence. All P values are 2-tailed.
The subjects were divided into 319(79.8%) H.pylori seropositive and 81(20.2%) seronegative individuals, as shown in Table Ð† .The significant differences were observed between infected and uninfected subjects as regards age: H.pylori seropositive subjects were older the H.pylori seronegative subjects with 39.9±12.6 yrs and 30.6±11.8 yrs as mean as standard deviation, respectively (P<0.0001). The seropositive group had a statistically higher male: female ratio than the seronegative group (1.59 vs. 0.92, P<0.05). Mean Triglyceride in H.pylori seropositive and seronegative individuals were 162 and 143.9 mg/dl, respectively (P<0.05). The geometric mean ratio of total cholesterol to HDL-cholesterol was significantly higher in the H. pylori seropositive than seronegative cases (4.27 vs. 3.91, P<0.05). Total cholesterol and LDL- cholesterol were higher in H.pylori seropositive individuals than H.pylori seronegative, but these differences were not significant (Table Ð†Ð†).
TableI. Characteristics in H.pylori Seropositive and seronegatives
Numbers are mean±SD
Table Ð†Ð†. Serum lipid concentrations in H.pylori seropositive and seronegative subjects.
Serological test of H. pylori
Positive Negative P-value
CH (mg/dl) 170.89±40.05 162.01±39.26 NS*
TG (mg/dl) 162.03±71.43 143.88±79.25 0.04
HDL-CH (mg/dl) 41.87±10.41 43.63±10.32 NS
LDL-CH (mg/dl) 96.62±33.87 89.65±32.54 NS
CH/HDL-CH 4.27±1.24 3.91±1.3 0.02
LDL-CH/HDL-CH 2.43±0.98 2.19±0.98 NS
Data are reported as mean± SD
CH: total cholesterol. TG: triglyceride. HDL-CH: HDL-cholesterol. LDL-CH: LDL-cholesterol. CH/HDL-CH: total cholesterol/HDL-cholesterol ratio. LDL-CH/HDL-CH: LDL-cholesterol/HDL-cholesterol ratio.
In the present study we found that prevalence of H.pylori in our study population was 79.8% and HDL-C level was lower in H.Pylori serpositive than seronegative. Some studies have demonstrated a relationship between H.pylori infection and extra digestive disease (3, 5). In this respect, cardiovascular disease is one of the most important disease suggested to be related to H.pylori infection which maybe due to effect of infection on lipid metabolism (7-8, (16-18). Since some studies have shown that the association might be in directed and related to social class (9;16). Our study population consisted males and females were in a relatively small area in center of Iran (Kashan). The social background of the population is homogenous and thus, the odds of in direct association through social class differences are not probable. According to our results the prevalence of H.pylori was 79.8%. One study in northwest of Iran, a region with the highest mortality rate from gastric cancer throughout the country, reported that H.pylori infection occurs in 89.2% (883/990) of the residents (19). Other surveys in different age groups from various regions of the country reported that H.pylori infection occurs in 57%-91% of the study subjects (20-23). Our findings indicated that, H.pylori infection modified serum lipids. Indeed, the serum triglyceride level was found to be higher in H.pylori seropositive than in negative ones. Although the levels of serum total cholesterol and LDL-cholesterol are increased in H.pylori positive, but these differences are not significant. The data also suggest a negative, although not statically significant, effect of H.pylori positivity on plasma HDL-cholesterol concentration. Concerning the changes in serum lipids in H.pylori positive subjects, the results of our study are similar but not identical to those of studies from other countries (8;17;18;24). Laurila et al reported that the serum triglyceride and total cholesterol concentrations were significantly higher in the males with positive IgG and IgA antibody titres for H.pylori than in the males with no signs of infection (16). Also, Adachi et al reported that after adjustment for sex, age and drinking habits, the HDL-cholesterol levels of seropositive and seronegative groups differed markedly (24). These differences in the influence of H.pylori infection on serum lipids maybe caused by different genetic factors of people from other countries and the subjects in the present study.
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In rodents, during the acute stage of bacterial infection the alteration in triglyceride and HDL-cholesterol concentrations, promoting atherogenesis, have been attributed to the action of lipopolysacchride(LPS) , which is a prominent endotoxin and a typical constituent of the cell wall of Gram-negative bacteria. (14;25) LPS administration activates the production of several cytokines, including the tumor necrosis factor
(TNF-α) which increases plasma triglyceride concentration in animals (15). Continuous production of inflammatory cytokines by cells chronically infected with H.pylori, being Gram-negative bacteria, may therefore contribute to the development of observed changes, in serum lipid pattern.
Upon our results, infected subjects showed an atherogenic profile characterized by an increase in total cholesterol: HDL-cholesterol ratio compared to uninfected subjects. This ratio, represent an absolute value indicating a predisposition to atherosclerotic processes and it is recognized as a reliable indicator for assessment of coronary heart disease risk (13,18).
Our data confirm the existence of a moderate association between H.pylori infection and lipid modulation. It also possible that H.pylori infection promotes atherosclerosis by acting through changes in lipid profile. However, maybe other cofactors are involved in the lipid modulation along with the strain of H.pylori including host genetic and environment factors.