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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, Department of Medicine, The University of Hong Kong, Hong Kong, China, 22 January 2011. In the 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
2014 Impact Factor: 0.872
2013 SCImago Journal Rankings: 0.293

 

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, Department of Medicine, The University of Hong Kong, Hong Kong, China, 22 January 2011. In the 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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