Association of Helicobacter pylori infection with elevated serum lipids

Laurila, Aino; Bloigu, Aini; Näyhä, Simo; Hassi, Juhani; Leinonen, Maija; Saikku, Pekka

doi:10.1016/s0021-9150(98)00194-4

Cited by 161 publications

(142 citation statements)

References 22 publications

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“…Dysfunctional lipid metabolism is a characteristic feature of several infections [33]. Some studies have found an association between H. pylori infection and proatherogenic lipid levels, including a low HDL level [34,35].…”

Section: Discussionmentioning

confidence: 99%

Effect of CD14 promoter polymorphism andH. pyloriinfection and its clinical outcomes on circulating CD14

Karhukorpi¹,

Yan²,

Niemelä

et al. 2002

Clinical and Experimental Immunology

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SUMMARYCD14 is a pattern recognition receptor on the membranes of monocytes and macrophages for several microbial products, of which lipopolysaccharide (LPS) is the best known. A shed form of CD14 is present in serum. As the CD14 gene promoter polymorphism -159C/T and some bacterial infections may affect the sCD14 levels, we compared the impact of both the CD14 promoter polymorphism and Helicobacter pylori infection on serum sCD14 levels in 201 dyspeptic patients (group 1) who had undergone gastroscopy, and 127 staff members (group 2) with no endoscopy. sCD14 was measured from the sera by a commercial enzyme immunoassay (EIA), and CD14 genotyping was carried out with PCR. Helicobacter pylori infection was detected by serology and/or culture or PCR. sCD14 levels were elevated in the subjects carrying the T allele (CT or TT genotype) in both groups when compared with subjects with the CC genotype. Overall, H. pylori-positive subjects tended to have higher sCD14 levels compared with H. pylori-negative subjects. In group 1 consisting of dyspeptic patients, those with gastric ulcer, gastric erosion or duodenal ulcer had significantly elevated levels of sCD14 compared with the patients with normal endoscopic findings or macroscopic gastritis. The recent use of NSAIDs was also associated with enhanced sCD14. Thus, we were able to show several factors, one genetic and the other environmental (H. pylori infection and mucosal lesion), to have an impact on sCD14.

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Section: Discussionmentioning

confidence: 99%

Effect of CD14 promoter polymorphism andH. pyloriinfection and its clinical outcomes on circulating CD14

Karhukorpi¹,

Yan²,

Niemelä

et al. 2002

Clinical and Experimental Immunology

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“…Some infectious diseases, such as Chlamydia pneumoniae infection, have been considered as risk factors for coronary heart disease (18), and several studies have pointed to an association between H. pylori infection and vascular changes due to the alteration of the serum lipid profile (19,38). Previous studies reported that the serum T-Chol, TG, or LDL concentrations in H. pylori-infected persons are significantly elevated over those in noninfected individuals (39,40). On the other hand, several authors described HDL cholesterol levels to be decreased by longterm infection with H. pylori (41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

Toyoda

Tsukamoto²,

Takasu

et al. 2009

Cancer Prevention Research

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Statins are commonly used lipid-lowering drugs that reduce the risk of cardiovascular morbidity and mortality. Although recent studies have pointed to chemopreventive effects of statins against various cancers, their efficacy for gastric cancer is unclear. Here, we examined the effects of pitavastatin, a lipophilic statin, on Helicobacter pylori (H. pylori)-associated stomach carcinogenesis and gastritis using Mongolian gerbil and mouse models. The animals were allocated to H. pylori + N-methyl-N-nitrosourea administration (gerbils, 52 weeks) or H. pylori infection alone groups (gerbils and mice, 12 weeks). After H. pylori infection, they were fed basal diets containing 0 to 10 ppm of pitavastatin. The incidences of H. pylori-associated gastric adenocarcinomas and degrees of chronic gastritis were not decreased by pitavastatin compared with those of control values. Expression of interleukin-1β and tumor necrosis factor-α mRNAs in the pyloric mucosa was markedly up-regulated in pitavastatin-treated animals. Furthermore, in the H. pyloriinfected groups, serum total cholesterol, triglyceride, and low-density lipoprotein levels were significantly increased by pitavastatin treatment, contrary to expectation. In the short-term study, H. pylori-infected gerbils and mice also showed significant up-regulation of serum triglyceride levels by pitavastatin, whereas total cholesterol was markedly reduced and low-density lipoprotein exhibited a tendency for decrease in noninfected animals. These findings indicate pitavastatin to be ineffective for suppressing gastritis and chemoprevention of gastric carcinogenesis in H. pylori-infected gerbils. Our serologic results also suggest that the H. pylori infection and consequent severe chronic gastritis interfere with the cholesterol-lowering effects of pitavastatin.

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“…It is thought that HP induced inflammation can be a trigger to the production of high levels of IL-6 and TNF-a. It is known that IL-6 can increase hepatic gluconeogenesis and TG synthesis and TNF-a inhibits lipoprotein lipase activity and stimulates he patic lipogenesis, leading to lipid mobilisation from ti ssues and to elevated serum TG and lowered HDL-C concentrations (1,10,14). The pathogenic mechanisms underlying the increase in TC and LDL-C levels in HP seropositive subjects are still unclear.…”

Section: Discussionmentioning

confidence: 99%

“…The pathogenic mechanisms underlying the increase in TC and LDL-C levels in HP seropositive subjects are still unclear. A possible suggested mechanism is that the effect of HP might be mediated via certain cytokines that can modulate enzyme activity and receptor expression and induce oxidative stress, affecting cholesterol metabolism (1,14,(25)(26)(27)(28), but this hypo thesis needs more explanation. Reported data concerning HDL-C and apo A-I levels in HP infection are also contradictory.…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

Section: Introductionmentioning

confidence: 99%

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

Kojić-Damjanov¹,

Đerić²,

Eremić³

et al. 2009

Journal of Medical Biochemistry

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Kratak sadr`aj: Podaci o proaterogenim promenama lipidskog statusa u sklopu hroni~ne Helicobacter pylori (HP) infekcije su kontradiktorni. Cilj istra`ivanja bio je da se ispitaju razlike u nekim lipidskim parametrima izme|u 55 osoba oba pola s hroni~nom HP infekcijom (IgG >50 U/mL i IgA <20 U/mL) i 55 HP seronegativnih osoba (IgG i IgA <20 U/mL) oba pola. Serumske koncentracije ukupnog holesterola (TC) (p<0,001), triglicerida (TG) (p<0,05), LDL-holesterola (LDL-C) (p<0,02), non-HDL-holesterola (non-HDL-C), apolipoproteina (apo) B (p<0,001), Lp(a) i HDL-holesterola (HDL-C) bile su vi{e kod HP seropozitivnih u odnosu na seronegativne osobe, dok gotovo da nije bilo razlika u nivoima apo A-I. Kod HP seropozitivnih osoba, u~estalost patolo{kih TC (p<0,001), TG (p<0,05), LDL-C (p<0,01), non-HDL-C (p<0,01), apo B (p<0,02) i Lp(a) vrednosti bila je vi{a u odnosu na seronegativne. Ustanovljena je negativna korelacija serum skih titara HP IgG antitela s TC, LDL-C (p<0,05), non-HDL-C, apo B i Lp(a), a pozitivna s TG, HDL-C i apo A-I nivoima. Rezultati su sli~ni za oba pola. Na{i rezultati idu u prilog hipotezi da bi hroni~na HP infekcija mogla da modifikuje lipidske parametre na proate rogeni na~in.Klju~ne re~i: ateroskleroza, Helicobacter pylori, lipidi, aterogeni rizik Summary: 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.

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Association of Helicobacter pylori infection with elevated serum lipids

Cited by 161 publications

References 22 publications

Effect of CD14 promoter polymorphism andH. pyloriinfection and its clinical outcomes on circulating CD14

Effect of CD14 promoter polymorphism andH. pyloriinfection and its clinical outcomes on circulating CD14

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

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

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