Publication
Extended-release niacin increases anti-apolipoprotein A-I antibodies that block the antioxidant effect of high-density lipoprotein-cholesterol: the EXPLORE clinical trial.
| dc.contributor.author | Batuca, J | |
| dc.contributor.author | Amaral, M | |
| dc.contributor.author | Favas, C | |
| dc.contributor.author | Paula, F | |
| dc.contributor.author | Ames, P | |
| dc.contributor.author | Papoila, A | |
| dc.contributor.author | Alves, JD | |
| dc.date.accessioned | 2019-03-06T16:24:43Z | |
| dc.date.accessioned | 2019-03-06T16:24:48Z | |
| dc.date.available | 2019-03-06T16:24:43Z | |
| dc.date.available | 2019-03-06T16:24:48Z | |
| dc.date.issued | 2017 | |
| dc.description.abstract | Extended-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-1 (men) or ≤50 mg dl-1 (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 nonsignificant (coefficient estimate 20.83 U l-1 , 95% confidence interval [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-1 , 95% CI 1.16 to 9.25; P = 0.012) and its subclasses HDL2 (coefficient estimate 2.46 mg dl-1 , 95% CI 0.57 to 4.34; P = 0.011) and HDL3 (coefficient estimate 2.73 mg dl-1 , 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-1 , 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 antioxidant 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.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Br J Clin Pharmacol. 2017 May;83(5):1002-1010 | pt_PT |
| dc.identifier.doi | 10.1111/bcp.13198 | pt_PT |
| dc.identifier.issn | 1365-2125 | |
| dc.identifier.uri | http://hdl.handle.net/10400.10/2147 | |
| dc.language.iso | eng | pt_PT |
| dc.peerreviewed | yes | pt_PT |
| dc.publisher | Wiley | pt_PT |
| dc.relation.publisherversion | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5401980/pdf/BCP-83-1002.pdf | pt_PT |
| dc.subject | Antibodies | pt_PT |
| dc.subject | Antioxidants | pt_PT |
| dc.subject | Cholesterol HDL | pt_PT |
| dc.subject | Niacin | pt_PT |
| dc.title | Extended-release niacin increases anti-apolipoprotein A-I antibodies that block the antioxidant effect of high-density lipoprotein-cholesterol: the EXPLORE clinical trial. | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.conferencePlace | Oxford | pt_PT |
| oaire.citation.endPage | 1010 | pt_PT |
| oaire.citation.startPage | 1002 | pt_PT |
| oaire.citation.title | British Journal of Clinical Pharmacology | pt_PT |
| oaire.citation.volume | 83 | pt_PT |
| rcaap.rights | openAccess | pt_PT |
| rcaap.type | article | pt_PT |