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dc.creatorCorral, Pablo-
dc.date2015-
dc.date.accessioned2016-05-20T22:54:56Z-
dc.date.accessioned2021-11-26T17:51:31Z-
dc.date.available2016-05-20T22:54:56Z-
dc.date.available2021-11-26T17:51:31Z-
dc.date.issued2015-
dc.identifier.urihttp://redi.ufasta.edu.ar:8082/jspui/handle/123456789/1133-
dc.descriptionFamilial 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 . 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.es_ES
dc.descriptionFil: Corral, Pablo. Universidad FASTA. Facultad de Ciencias Médicas; Argentina.-
dc.formatapplication/pdfes_ES
dc.languagespaes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/deed.es_ARes_ES
dc.sourceinstname:Universidad FASTAes_ES
dc.sourcereponame:REDIes_ES
dc.titleFamilial hypercholesterolaemia: a global call to armses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.typeinfo:ar-repo/semantics/artículoes_ES
dc.typeinfo:eu-repo/semantics/publishedVersiones_ES
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