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Extended Release-Niacin increases anti-ApoA-I antibodies that block the anti-oxidant effect of HDL-C: the EXPLORE clinical trial.

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dc.contributor.authorBatuca, JR
dc.contributor.authorAmaral, M
dc.contributor.authorFavas, C
dc.contributor.authorPaula, F
dc.contributor.authorAMES, PR
dc.contributor.authorPapoila, AL
dc.contributor.authorAlves, JD
dc.date.accessioned2017-01-11T16:01:12Z
dc.date.available2017-01-11T16:01:12Z
dc.date.issued2016
dc.description.abstractExtended Release-Niacin (ERN) is the most effective agent for increasing high-density lipoprotein-cholesterol (HDL-C). Having previously identified anti-HDL antibodies, we investigated whether ERN affected the antioxidant capacity of HDL and whether ERN was associated with the production of antibodies against HDL (aHDL) and apolipoprotein A-I (aApoA-I). METHODS: Twenty-one patients older than 18 years, with HDL-C ≤ 40 mg/dL (men) or ≤ 50 mg/dL (women) were randomly assigned to receive daily ERN (n = 10) or placebo (n = 11) for two sequential 12-week periods, with 4 weeks of wash-out before cross-over. Primary outcome was change of paraoxonase-1 (PON1) activity and secondary outcomes were changes in aHDL and aApoA-I antibodies. Clinical Trial Unique Identifier: EudraCT 2006-006889-42. RESULTS: The effect of ERN on PON1 activity was non-significant (coefficient estimate 20.83U/L, 95% CI -9.88 to 51.53; p = 0.184). ERN was associated with an increase in HDL-C levels (coefficient estimate 5.21 mg/dL, 95% CI 1.16 to 9.25; p = 0.012) and its subclasses HDL2 (coefficient estimate 2.46 mg/dL, 95% CI 0.57 to 4.34; p = 0.011) and HDL3 (coefficient estimate 2.73 mg/dL, 95% CI 0.47 to 4.98; p = 0.018). ERN was significantly associated with the production of aApoA-I antibodies (coefficient estimate 0.25 µg/mL, 95% CI 0.09-0.40; p = 0.001). aApoA-I titres at baseline were correlated with decreased PON activity. CONCLUSIONS: The rise in HDL-C achieved with ERN was not matched by improved anti-oxidant capacity, eventually hampered by the emergence of aApoA-I antibodies. These results may explain why Niacin and other lipid lowering agents fail to reduce cardiovascular risk.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationBr J Clin Pharmacol. 2016 Nov 27. [Epub ahead of print]pt_PT
dc.identifier.doi10.1111/bcp.13198pt_PT
dc.identifier.issn1365-2125
dc.identifier.urihttp://hdl.handle.net/10400.10/1789
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWiley-Blackwellpt_PT
dc.subjectCholesterol HDLpt_PT
dc.subjectNiacinpt_PT
dc.subjectAntioxidantspt_PT
dc.subjectAutoantibodiespt_PT
dc.subjectColesterol HDLpt_PT
dc.titleExtended Release-Niacin increases anti-ApoA-I antibodies that block the anti-oxidant effect of HDL-C: the EXPLORE clinical trial.pt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceOxfordpt_PT
oaire.citation.titleBritish Journal of Clinical Pharmacologypt_PT
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT

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