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Conference Paper: Mendelian randomisation analysis suggests that plasma interleukin-6 is raised in hypertension but does not cause its development

TitleMendelian randomisation analysis suggests that plasma interleukin-6 is raised in hypertension but does not cause its development
Authors
Issue Date2011
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk
Citation
The 16th Medical Research Conference (MRC 2011), The University of Hong Kong, Hong Kong, China, 22 January 2011. In Hong Kong Medical Journal, 2011, v. 17 n. 1 suppl. 1, p. 18, abstract no. 17 How to Cite?
AbstractIntroduction: Interleukin-6 (IL-6) plays a central role in inflammation and insulin resistance as well as atherogenesis. We investigated the associations of plasma IL-6 and its genetic variants with hypertension in both cross-sectional and prospective study designs. Methods: Plasma IL-6 was measured in 648 normotensive and 294 hypertensive subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) in 2000-2004 and three tagging SNPs in the IL-6 gene (IL6) were genotyped. Among subjects normotensive in CRISPS-2, 515 subjects were followed up in CRISPS-3 in 2005- 2008 and 100 of them had developed hypertension. Results: Plasma IL-6 correlated with systolic blood pressure (r=0.128, P<0.001), pulse pressure (r=0.144, P<0.001), and mean arterial pressure (r=0.086, P=0.008). Hypertensive subjects have significantly higher plasma IL-6 level after adjusting for age and sex (geometric mean [95% CI]=0.60 [0.54-0.65] vs 0.47 [0.44-0.50] pg/mL, P=0.021). In stepwise logistic regression, plasma IL-6 was associated with hypertension in women (P=0.004), but not in men. The SNP rs1800796 was associated with plasma IL-6 (beta= –0.098, P=0.002) in stepwise linear regression. However, this SNP was not associated with hypertension or blood pressure. Among subjects normotensive in CRISPS-2, plasma IL-6 was not associated with the development of hypertension in CRISPS-3. Conclusion: Elevated plasma IL-6 is associated with hypertension, especially in women. Plasma IL-6 is influenced by the SNP rs1800796. However, this SNP is not associated with hypertension, suggesting that hypertension is caused by other factors that elevate plasma IL-6. Acknowledgement: This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.
Persistent Identifierhttp://hdl.handle.net/10722/140171
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorCheung, BMYen_US
dc.contributor.authorOng, KLen_US
dc.contributor.authorTso, AWKen_US
dc.contributor.authorLeung, YHen_US
dc.contributor.authorCherny, SSen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorThomas, GNen_US
dc.contributor.authorLam, THen_US
dc.contributor.authorLam, KSLen_US
dc.date.accessioned2011-09-23T06:08:06Z-
dc.date.available2011-09-23T06:08:06Z-
dc.date.issued2011en_US
dc.identifier.citationThe 16th Medical Research Conference (MRC 2011), The University of Hong Kong, Hong Kong, China, 22 January 2011. In Hong Kong Medical Journal, 2011, v. 17 n. 1 suppl. 1, p. 18, abstract no. 17en_US
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/140171-
dc.description.abstractIntroduction: Interleukin-6 (IL-6) plays a central role in inflammation and insulin resistance as well as atherogenesis. We investigated the associations of plasma IL-6 and its genetic variants with hypertension in both cross-sectional and prospective study designs. Methods: Plasma IL-6 was measured in 648 normotensive and 294 hypertensive subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS-2) in 2000-2004 and three tagging SNPs in the IL-6 gene (IL6) were genotyped. Among subjects normotensive in CRISPS-2, 515 subjects were followed up in CRISPS-3 in 2005- 2008 and 100 of them had developed hypertension. Results: Plasma IL-6 correlated with systolic blood pressure (r=0.128, P<0.001), pulse pressure (r=0.144, P<0.001), and mean arterial pressure (r=0.086, P=0.008). Hypertensive subjects have significantly higher plasma IL-6 level after adjusting for age and sex (geometric mean [95% CI]=0.60 [0.54-0.65] vs 0.47 [0.44-0.50] pg/mL, P=0.021). In stepwise logistic regression, plasma IL-6 was associated with hypertension in women (P=0.004), but not in men. The SNP rs1800796 was associated with plasma IL-6 (beta= –0.098, P=0.002) in stepwise linear regression. However, this SNP was not associated with hypertension or blood pressure. Among subjects normotensive in CRISPS-2, plasma IL-6 was not associated with the development of hypertension in CRISPS-3. Conclusion: Elevated plasma IL-6 is associated with hypertension, especially in women. Plasma IL-6 is influenced by the SNP rs1800796. However, this SNP is not associated with hypertension, suggesting that hypertension is caused by other factors that elevate plasma IL-6. Acknowledgement: This study was funded by Hong Kong Research Grant Council grants (HKU7229/01M and HKU7626/07M) and the Sun Chieh Yeh Heart Foundation.-
dc.languageengen_US
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk-
dc.relation.ispartofHong Kong Medical Journalen_US
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleMendelian randomisation analysis suggests that plasma interleukin-6 is raised in hypertension but does not cause its developmenten_US
dc.typeConference_Paperen_US
dc.identifier.emailCheung, BMY: mycheung@hku.hken_US
dc.identifier.emailOng, KL: okl2000@hku.hken_US
dc.identifier.emailTso, AWK: awktso@hku.hken_US
dc.identifier.emailLeung, YH: yhleung@hkucc.hku.hken_US
dc.identifier.emailCherny, SS: cherny@hku.hken_US
dc.identifier.emailSham, PC: pcsham@hku.hken_US
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hken_US
dc.identifier.emailLam, KSL: ksllam@hku.hken_US
dc.identifier.authorityCheung, BMY=rp01321en_US
dc.identifier.authorityTso, AWK=rp00535en_US
dc.identifier.authorityCherny, SS=rp00232en_US
dc.identifier.authoritySham, PC=rp00459en_US
dc.identifier.authorityLam, TH=rp00326en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros194407en_US
dc.identifier.volume17-
dc.identifier.issue1 suppl. 1-
dc.identifier.spage18, abstract no. 17-
dc.identifier.epage18, abstract no. 17-
dc.publisher.placeHong Kong-

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