Interleukin-6-174G&gt;C polymorphism and risk of coronary heart disease in west of Scotland coronary prevention study (WOSCOPS)

Basso, Federica; Lowe, G.D.O.; Rumley, Ann

doi:10.1016/s1062-1458(02)00774-2

Cited by 53 publications

(74 citation statements)

References 28 publications

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“…In contrast, in other studies, no effect has been observed (21,44,45 ). Possibly, these findings could be explained by localized tissue-specific IL-6 production modulated by the IL-6 G(Ϫ174)C polymorphism (11 ), whereas systemic IL-6 concentrations remain unaffected.…”

Section: Discussionmentioning

confidence: 78%

The Interleukin-6 G(−174)C Promoter Polymorphism Does Not Determine Plasma Interleukin-6 Concentrations in Experimental Endotoxemia in Humans

Endler¹,

Marsik²,

Joukhadar³

et al. 2004

Clinical Chemistry

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Background: Interleukin 6 (IL-6) is a pleiotropic cytokine that plays an essential role in the pathogenesis of acute and chronic infections. As the role of the IL-6 G(؊174)C polymorphism in determining serum concentrations of IL-6 is controversial, we studied the genotype-specific IL-6 response in a well-standardized model of systemic inflammation. Methods: A total of 76 healthy young males (age range, 19 -35 years) received a single bolus of 2 ng/kg endotoxin [lipopolysaccharide (LPS)] intravenously. Plasma IL-6 was measured by enzyme immunoassay at 0, 2, 6, and 24 h after LPS infusion, and the IL-6 promoter genotype was analyzed by a mutagenic separated PCR assay. Results: IL-6 increased 300-fold 2 h after LPS challenge and returned almost to normal within 24 h. Neither basal IL-6 nor the IL-6 response to LPS was significantly affected by the IL-6 promoter genotype. Conclusions: The IL-6 G(؊174)C promoter polymorphism does not significantly influence basal concentrations of IL-6 or peak IL-6 in human endotoxemia.

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Section: Discussionmentioning

confidence: 78%

The Interleukin-6 G(−174)C Promoter Polymorphism Does Not Determine Plasma Interleukin-6 Concentrations in Experimental Endotoxemia in Humans

Endler¹,

Marsik²,

Joukhadar³

et al. 2004

Clinical Chemistry

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“…The sample set was as previously described [8,9] although here only the pravastatin-treated participants were examined. The trial participants were men aged 45-64 years with mean baseline total cholesterol of 7 mmol l -1 .…”

Section: Samplementioning

confidence: 99%

“…The trial participants were men aged 45-64 years with mean baseline total cholesterol of 7 mmol l -1 . Serum measurements of lipid fractions and CRP were as previously described [7,8]. The ethics committee of the Glasgow Royal Infirmary approved this study.…”

Section: Samplementioning

confidence: 99%

The effects of a single nucleotide polymorphism in SLCO1B1 on the pharmacodynamics of pravastatin

Martin

Murray

et al. 2012

Brit J Clinical Pharma

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WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• The SNP rs4149056 is associated with altered statin pharmacokinetics and increased risk of statin intolerance. LDL-cholesterol lowering by simvastatin is also affected by rs4149056 but differences between the genotypes are small. Studies of the effect of rs4149056 on pravastatin pharmacodynamics have been inconclusive. WHAT THIS PAPER ADDS• rs4149056 was not associated with an altered lipid or CRP response to 40 mg day -1 pravastatin in more than 600 high risk men from Scotland, suggesting that the rs4149056 genotype does not significantly affect pravastatin efficacy. AIMTo determine whether the SNP rs4149056 in SLCO1B1 alters the pharmacodynamics of pravastatin. METHODSrs4149056 was genotyped in 626 pravastatin-treated participants in the WOSCOPS trial and the response after 1 year of treatment was compared between the different genotypes. RESULTSPravastatin reduced serum LDL cholesterol by 22.2% in TT homozygotes, by 22.2% in TC heterozygotes and by 17.7% in CC homozygotes (TT + TC vs. CC P value 0.33). There were no significant differences in the response of total cholesterol, LDL, HDL, triglycerides or CRP to pravastatin between the genotypes. CONCLUSIONThe rs4149056 SNP did not significantly affect the pharmacodynamics of pravastatin.

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“…The healthy Ϫ174G allele carriers turned out to be high IL-6 producers after vaccination with Salmonella typhii vaccine (4). It was documented that patients with the Ϫ174GG genotype run a risk of an earlier onset and more serious outcome of cardiovascular and cerebrovascular diseases (5)(6)(7)(8)(9). Also, the IL-6 promoter polymorphism seems to have influence on various postoperative short-term (10 -12) and longterm complications (13,14) as well as on the frequency and severity of different cardiovascular events (15,16).…”

mentioning

confidence: 99%

The −174GG Interleukin-6 Genotype Is Protective From Retinopathy and Nephropathy in Juvenile Onset Type 1 Diabetes Mellitus

et al. 2009

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ABSTRACT:The aim of our study was to determine an association between the Ϫ174GϾC IL-6 polymorphism (rs1800795) and occurrence of retinopathy and nephropathy in type 1 diabetes mellitus (T1DM) patients. Two hundred ten children/adolescents with longstanding T1DM (16.5 Ϯ 3.8 y; with diabetes duration of 8.4 Ϯ 3.0 y) were enrolled into the study. A group of 170 healthy young (16.9 Ϯ 5.2 y) sex-matched volunteers was qualified as the control. The IL-6 polymorphism was genotyped with the PCR-RFLP method. Serum and urine IL-6 concentrations were measured by the ultra-sensitive ELISA tests. The Ϫ174GG genotype was under represented in the diabetic patients compared with the controls. Patients with this genotype were free from nephropathy and retinopathy. The group of Ϫ174GG carriers was characterized by the highest urine IL-6 concentrations in relation to other genotypes. In the multivariate logistic regression analysis adjusted for age, duration of the disease, age of disease onset, HbA1c, and albumin excretion rate, the Ϫ174GG genotype was the only independent variable that significantly decreased the risk of jointly analyzed retinopathy and nephropathy [OR ϭ 0.65; 95% CI ϭ 0.52-0.82; p ϭ 0.0003]. We propose that the Ϫ174GG patients are protected from late diabetic complications by different IL-6 dependent mechanisms. (Pediatr Res 66: 341-345, 2009)

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Interleukin-6-174G>C polymorphism and risk of coronary heart disease in west of Scotland coronary prevention study (WOSCOPS)

Cited by 53 publications

References 28 publications

The Interleukin-6 G(−174)C Promoter Polymorphism Does Not Determine Plasma Interleukin-6 Concentrations in Experimental Endotoxemia in Humans

The Interleukin-6 G(−174)C Promoter Polymorphism Does Not Determine Plasma Interleukin-6 Concentrations in Experimental Endotoxemia in Humans

The effects of a single nucleotide polymorphism in SLCO1B1 on the pharmacodynamics of pravastatin

The −174GG Interleukin-6 Genotype Is Protective From Retinopathy and Nephropathy in Juvenile Onset Type 1 Diabetes Mellitus

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