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Familial hypercholesterolaemia: a global call to arms

2015-09-18Journal article Restricted access
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dc.contributor.authorVallejo-Vaz, A.J.
dc.contributor.authorKondapally Seshasai, S.R.
dc.contributor.authorCole, D.
dc.contributor.authorHovingh, G.K.
dc.contributor.authorKastelein, J.J.
dc.contributor.authorMata, P.
dc.contributor.authorRaal, F.J.
dc.contributor.authorSantos, R.D.
dc.contributor.authorSoran, H.
dc.contributor.authorWatts, G.F.
dc.contributor.authorAbifadel, M.
dc.contributor.authorAguilar-Salinas, C.A.
dc.contributor.authorAkram, A.
dc.contributor.authorAlnouri, F.
dc.contributor.authorAlonso, R.
dc.contributor.authorAl-Rasadi, K.
dc.contributor.authorBanach, M.
dc.contributor.authorBogsrud, M.P.
dc.contributor.authorBourbon, M.
dc.contributor.authorBruckert, E.
dc.contributor.authorCar, J.
dc.contributor.authorCorral, P.
dc.contributor.authorDescamps, O.
dc.contributor.authorDieplinger, H.
dc.contributor.authorDurst, R.
dc.contributor.authorFreiberger, T.
dc.contributor.authorGaspar, I.M.
dc.contributor.authorGenest, J.
dc.contributor.authorHarada-Shiba, M.
dc.contributor.authorJiang, L.
dc.contributor.authorKayikcioglu, M.
dc.contributor.authorLam, C.S.
dc.contributor.authorLatkovskis, G.
dc.contributor.authorLaufs, U.
dc.contributor.authorLiberopoulos, E.
dc.contributor.authorNilsson, L.
dc.contributor.authorNordestgaard, B.G.
dc.contributor.authorO'Donoghue, J.M.
dc.contributor.authorSahebkar, A.
dc.contributor.authorSchunkert, H.
dc.contributor.authorShehab, A.
dc.contributor.authorStoll, M.
dc.contributor.authorSu, TC
dc.contributor.authorSusekov, A.
dc.contributor.authorWidén, E.
dc.contributor.authorCatapano, A.L.
dc.contributor.authorRay, K.K.
dc.date.accessioned2015-09-30T12:12:29Z
dc.date.available2015-09-30T12:12:29Z
dc.date.issued2015-09-18
dc.description.abstractFamilial Hypercholesterolaemia (FH) is the commonest autosomal co-dominantly inherited condition affecting man. It is caused by mutation in one of three genes, encoding the low-density lipoprotein (LDL) receptor, or the gene for apolipoprotein B (which is the major protein component of the LDL particle), or in the gene coding for PCSK9 (which is involved in the degradation of the LDLreceptor during its cellular recycling). These mutations result in impaired LDL metabolism, leading to life-long elevations in LDLcholesterol (LDL-C) and development of premature atherosclerotic cardiovascular disease (ASCVD) [1e3]. If left untreated, the relative risk of premature coronary artery disease is significantly higher in heterozygous patients than unaffected individuals, with most untreated homozygotes developing ASCVD before the age of 20 and generally not surviving past 30 years [2e5]. Although early detection and treatment with statins and other LDL-C lowering therapies can improve survival, FH remains widely underdiagnosed and undertreated, thereby representing a major global public health challenge.pt_PT
dc.identifier.citationAtherosclerosis. 2015 Nov;243(1):257-9. doi: 10.1016/j.atherosclerosis.2015.09.021. Epub 2015 Sep 18.pt_PT
dc.identifier.doi10.1016/j.atherosclerosis.2015.09.021
dc.identifier.issn0021-9150
dc.identifier.urihttp://hdl.handle.net/10400.18/3174
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S0021915015301301pt_PT
dc.subjectFamilial Hypercholesterolaemiapt_PT
dc.subjectDoenças Cardio e Cérebro-vascularespt_PT
dc.titleFamilial hypercholesterolaemia: a global call to armspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage259pt_PT
oaire.citation.startPage257pt_PT
oaire.citation.titleAtherosclerosispt_PT
oaire.citation.volume243(1)pt_PT
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT

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