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Editorial
Lipoprotein (a): Is its systematic determination indicated?
Lipoproteína (a): ¿está indicada su determinación sistemática?
Manuel Antonio Botana López
Sección de Endocrinología, Hospital Universitario Lucus Augusti, Lugo, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The addition of highly potent hypolipidemic tools has allowed for significant reductions in cardiovascular risk &#40;CVR&#41;&#46; While apolipoprotein B &#40;ApoB&#41;-bearing proteins are primarily responsible for arteriosclerotic lesions&#44; we can find residual CVR involving other contributing factors&#46; Among these factors is lipoprotein &#40;a&#41; &#91;Lp&#40;a&#41;&#93;&#46; Initial epidemiological studies&#44; genome-wide association studies&#44; and data from Mendelian randomization demonstrate a causal relationship between Lp&#40;a&#41; and ischemic heart disease&#44;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> ischemic cerebrovascular disease&#44; and aortic valve stenosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#8211;4</span></a> Doubling the level of Lp&#40;a&#41; is associated with a nearly 20&#37; increase in the risk of myocardial infarction&#44; and elevated levels of Lp&#40;a&#41; are also associated with an accelerated progression of aortic stenosis&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Once a relationship was postulated between elevated levels of Lp&#40;a&#41; and an increased risk of venous thrombosis&#44; which has not yet been confirmed5&#46; However&#44; an inverse relationship between the prevalence of lipoprotein&#40;a&#41; hyperlipoproteinemia and the incidence of type 2 diabetes does seem to be the case&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The Lp&#40;a&#41; molecule results from the fusion&#44; through covalent bonds&#44; of an ApoB particle with another apolipoprotein called apolipoprotein&#40;a&#41; &#91;Apo&#40;a&#41;&#93;&#46; Both are synthesized in the liver&#44; but it is yet to be elucidated whether their assembly occurs inside the hepatocyte or on its surface&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> By the structure of its gene &#40;LPA&#41;&#44; it is known that this is the result of the ancestral splitting of the plasminogen gene &#40;PLG&#41;&#44; with which it shares significant homology&#44; which could help explain some of the pathophysiological characteristics of Lp&#40;a&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The PLG encodes 5 kringles &#40;triple loop protein structures&#44; 80&#8211;90 amino acids long&#44; resembling the shape of a Scandinavian pastry and numbered from I to V&#41;&#44; and a fibrinolytic protease region&#46; LPA lacks kringles I to III&#44; specific to PLG&#44; but encodes 10 subtypes of kringle IV &#40;KIV-1 to KIV-10&#41; and a kringle V-like domain&#44; as well as an inactive protease activity region&#46; Apo&#40;a&#41; molecules and&#44; consequently&#44; Lp&#40;a&#41; molecules&#44; exhibit considerable interindividual variability in their size and density&#44; because the gene may have a highly variable number of copies of the kringle IV-2 subtype&#46; Heterogeneity is also increased due to variable degrees of interindividual glycosylation&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#8211;4</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The larger the Apo&#40;a&#41; molecule&#44; due to a greater number of kringle IV-2 copies&#44; the lower its plasma levels&#46; This heterogeneity explains between 20&#37; and 70&#37; of the variability in Lp&#40;a&#41; concentrations&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Additionally&#44; single nucleotide polymorphisms also frequently influence concentration&#44; unrelated to molecular size &#40;more than 500 of these genetic variants of Lp&#40;a&#41; have been identified&#44; some of which have significant effects on its concentration&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#44;5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Plasma levels of Lp&#40;a&#41; arise from the co-dominant expression of 2 LPA alleles&#44; resulting in 2 detectable circulating Lp&#40;a&#41; isoforms of potentially different sizes&#44; and the levels we measure correspond to the sum contributed by each allele&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The smallest isoform tends to be present at higher levels&#46; A threshold value of 50&#160;mg&#47;dL or 105&#160;nmol&#47;L &#40;&#62;80th percentile&#41; has been established as clinically relevant&#44; but even levels &#62; 30&#160;mg&#47;dL can increase CVR&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;6</span></a> The relationship between Lp&#40;a&#41; concentration and CVR is continuous&#44; without a threshold&#58; higher concentrations imply greater risk&#46; Compared to individuals with mean Lp&#40;a&#41; concentrations of 16&#160;nM&#44; individuals with levels of 70&#44; 115&#44; 175&#44; 230&#44; and 350&#160;nmol&#47;L have 1&#46;22&#44; 1&#46;40&#44; 1&#46;65&#44; 1&#46;95&#44; and 2&#46;72 times higher risk of developing arteriosclerotic vascular disease &#40;ASVD&#41;&#44; respectively&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> With Lp&#40;a&#41; concentrations &#62;180&#160;mg&#47;dL &#40;430&#160;nmol&#47;L&#41;&#44; the CVR is that of familial hypercholesterolemia &#40;FH&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The population distribution of Lp&#40;a&#41; is not normal&#44; so the value ranges discussed are always in terms of &#34;median&#34; and not &#34;arithmetic mean&#34;&#46; Elevated concentrations are the most common form of hyperlipidemia&#46; It is estimated that high Lp&#40;a&#41; affects between 10&#37; and 30&#37; of the world&#39;s population &#40;approximately 1&#46;42&#160;&#215;&#160;109 people worldwide&#41; and 20&#37; of Europeans&#44;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;6</span></a> and having Lp&#40;a&#41; levels &#62;100&#160;nmol&#47;L &#40;48&#160;mg&#47;dL&#41; accounts for 5&#46;7&#37; of all cardiovascular events reported&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Since more than 90&#37; of Lp&#40;a&#41; concentration is conditioned by the LPA gene&#44;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;8</span></a> its values are reasonably constant throughout life&#44; and therefore&#44; a single determination might be enough&#46; However&#44; there is an individual variability of up to 20&#37;&#44;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> and there are also non-genetic factors that can modify the concentration &#40;inflammatory processes&#44; chronic kidney disease&#44; especially nephrotic syndrome&#44; liver diseases&#44; among others&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#44;6&#44;9</span></a> Therefore&#44; sometimes it is recommended to obtain a mean of 2 Lp&#40;a&#41; determinations at different times&#44; in stable phases of the patient&#39;s life&#44; to refine CVR stratification&#46;<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4&#44;6</span></a> In any case&#44; Lp&#40;a&#41; should be measure while the patient remains in a stable vital phase and without intercurrent illness&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Determining Lp&#40;a&#41; levels is achieved through immunoassays that use specific antibodies for Apo&#40;a&#41;&#46; However&#44; there are 2 problems affecting the accuracy of the results and their clinical interpretation&#46; The first one has to do Apo&#40;a&#41; size variability&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Due to an inverse association between the number of kringle IV-2 repeats and Lp&#40;a&#41; particle concentrations&#44; polyclonal immunoassays that recognize epitopes in Apo&#40;a&#41; may tend to underestimate high Lp&#40;a&#41; concentrations and overestimate low concentrations depending on whether the isoforms are small or large&#44; respectively&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> More recent methods commercially available reduce this error factor if the assay calibrators are well validated&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The second problem is that there are 2 different approaches to immunoassay calibration&#44; resulting in 2 different units for reporting Lp&#40;a&#41; results&#46; The first highly sensitive analysis for measuring Lp&#40;a&#41; established results in mg&#47;dL&#44; while the current standard is calibrated in nmol&#47;L&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Given the heterogeneity among the molecular sizes of different Lp&#40;a&#41; isoforms&#44; determining their plasma levels expressed in mass units &#40;mg&#47;dL&#41; may not be accurately representative of the number of particles we are actually measuring&#46; This may be especially important when considering that each Lp&#40;a&#41; particle is 6 times more atherogenic than each ApoB&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Hence&#44; recommendations for Lp&#40;a&#41; measurement indicate expressing its concentration in terms of molarity&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> The existence of two different units to express Lp&#40;a&#41; levels is confusing for physicians and patients alike&#44; and there is no good conversion factor from mg&#47;dL to nmol&#47;L&#44; or vice versa&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> In any case&#44; whatever determination method is used&#44; if properly calibrated&#44; it allows us to identify patients with higher CVR due to elevated Lp&#40;a&#41; levels&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Measuring Lp&#40;a&#41; allows us to identify individuals with very high inherited plasma levels&#46; It also enables better stratification of patients&#39; CVR and improved management of cardiovascular disease by helping optimize the medical treatment of other CVR factors&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In certain situations where Lp&#40;a&#41; is elevated&#44; the LDL value should be corrected using the formula&#58;<elsevierMultimedia ident="eq0005"></elsevierMultimedia><elsevierMultimedia ident="eq0010"></elsevierMultimedia></p><p id="par0055" class="elsevierStylePara elsevierViewall">This Lp&#40;a&#41; correction of the LDL value is not routinely recommended except for some situations&#58; patients of sub-Saharan origin&#44; patients with nephrotic syndrome or on peritoneal dialysis&#44; or when the drop in LDL-C is insufficient after receiving lipid-lowering treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> Also&#44; when FH is suspected&#44; if correcting the LDL value can avoid the need for genetic diagnostic testing&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Since inheritance is autosomal&#44; dependent on a single gene&#44; detecting a case of hyperlipoproteinemia&#40;a&#41; allows us to cascade screening and initiate treatments at earlier ages if necessary&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> Regarding the spending associated with measuring Lp&#40;a&#41;&#44; considering that it would only need to be measured once in a lifetime&#44; and the improvement it would represent in adjusting the treatment of CVR factors in people with elevated levels&#44; it is expected to be efficient&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">The European Atherosclerosis Society &#40;EAS&#41; and individual cardiology societies from other countries &#40;e&#46;g&#46;&#44; France&#44; Germany&#44; UK&#44; Canada&#44; Australia&#41; have developed clinical practice guidelines that include recommendations for the population in which Lp&#40;a&#41; should be determined&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;6&#44;15&#8211;18</span></a> Although all recommend the routine measurement of Lp&#40;a&#41; in individuals with certain characteristics &#40;elevated CVR&#44; FH&#44; first-degree relatives of individuals with very high Lp&#40;a&#41;&#44; family history of premature cardiovascular disease&#44; calcified aortic stenosis&#44; or when the LDL drop is not as expected after the established treatment&#41;&#44; not all recommend measuring Lp&#40;a&#41; universally&#46; This universal determination only appears in the guidelines of the EAS&#44; the Spanish Society of Atherosclerosis&#44; the German guidelines &#40;which replicate those of the EAS&#41;&#44; and the Canadian ones&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;6&#44;15&#44;17</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Since CVR is associated with elevated Lp&#40;a&#41;&#44; the efficiency of measuring it&#44; and the currently available methodologies&#44; the recommendations from the EAS are perfectly assumable and acceptable for our setting&#44; and we would summarize them as follows<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a>&#58;</p><p id="par0075" class="elsevierStylePara elsevierViewall">&#8226; Lp&#40;a&#41; should be measured&#44; at least&#44; once in adults to identify those with high CVR&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">&#8226; Detection is also recommended in young people with a history of ischemic stroke or premature ASVD&#44; or high Lp&#40;a&#41; and without other identifiable risk factors&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">&#8226; Cascade testing is recommended to detect high Lp&#40;a&#41; in FH environments&#44; family history of high Lp&#40;a&#41;&#44; and personal or family history of ASVD&#46;</p><span id="sec0041" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0101">Conflicts of interest</span><p id="par0095" class="elsevierStylePara elsevierViewall">None declared&#46;</p></span></span>"
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Article information
ISSN: 25300180
Original language: English
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