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Clinical report
Vascular lesions in patient with Takayasu arteritis and massive elevated lipoprotein (a) levels. Residual involvement or premature aterosclerosis?
Lesiones vasculares en paciente diagnosticada de arteritis de Takayasu y elevación masiva de lipoproteína (a). ¿Afectación residual o arterioesclerosis prematura?
José Carlos Alarcón García
Corresponding author
jc.alarc88@gmail.com

Corresponding author.
, Santiago Rodríguez Suárez, Ovidio Muñiz Grijalvo, Salvador García Morillo
Unidad de Colagenosis y Enfermedades Minoritarias, Unidad Experimental de Riesgo Cardiovascular, Servicio de Medicina Interna, Hospital Universitario Virgen del Rocío, Sevilla, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Lipoprotein&#40;a&#41; &#91;Lp&#40;a&#41;&#93; has been one of the main areas of focus in cardiovascular pathology in recent decades&#46; Despite not fully understanding its atherogenic role&#44; its importance in the development of premature atherosclerosis and its role as a risk factor for developing cardiovascular disease &#40;CVD&#41; have been proven&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">1</span></a> The case that we present shows how atherosclerosis stimulated by a massive Lp&#40;a&#41; elevation may cast doubt on a clinical diagnosis of vasculitis&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case report</span><p id="par0010" class="elsevierStylePara elsevierViewall">We present the case of a 38-year-old female patient with no known cardiovascular risk factors&#44; diagnosed in 2008 at the age of 31 with Takayasu&#39;s arteritis &#40;TAK&#41; at another centre&#46; The symptoms began with chest pain and severe hypertension&#46; The diagnosis was based on a difference in blood pressure &#40;BP&#41; in both arms along with radiological abnormalities observed in the MR and CT angiography considered compatible&#46; Stenosis of the left common carotid artery and the left subclavian artery was observed&#46; The patient received first-line therapy of intravenous cyclophosphamide per protocol and corticosteroids&#46; She was then placed on maintenance therapy with methotrexate 10<span class="elsevierStyleHsp" style=""></span>mg administered once weekly for 5 years&#46; The patient was seen at our centre for a second opinion&#46; She did not bring any imaging tests except for an echocardiogram&#44; which showed severe&#44; non-obstructive septal hypertrophy&#46; The last imaging test was in 2008&#44; the year of diagnosis&#46; Her family history included a parent who had a stroke at the age of 49 and a sister with severe LP&#40;a&#41; elevation&#44; with figures at 156<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The physical examination showed a left arm BP&#58; 105&#47;70<span class="elsevierStyleHsp" style=""></span>mmHg&#59; right arm BP&#58; 175&#47;85<span class="elsevierStyleHsp" style=""></span>mmHg&#46; Bilateral ankle-brachial index of 0&#46;95&#46; HR&#58; 85<span class="elsevierStyleHsp" style=""></span>bpm&#46; Cardiopulmonary auscultation was normal&#46; No murmurs were present in the abdomen&#46; There was no oedema in the lower limbs&#44; with the pulses present and symmetric&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The basic blood work and chest X-ray were normal&#46; A thoracic CT angiogram was performed which showed complete blockage of the left subclavian and carotid arteries along with calcified atherosclerosis of the thoracic and abdominal aorta &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; The MRA showed stenosis of the left internal carotid artery&#44; likely affecting the cervical carotid artery&#46; The supra-aortic vessels were unable to be visualised as the patient did not tolerate the test&#46; An abdominal and supra-aortic vessel arteriography was performed which showed diffuse atherosclerosis of the abdominal aorta&#44; 50&#37; stenosis of the left renal artery&#44; occlusion from the origin of the left common carotid&#44; subclavian&#44; and vertebral arteries&#44; reduced calibre of the common carotid artery&#44; and obstruction of the right external carotid artery &#40;<a class="elsevierStyleCrossRefs" href="#fig0010">Figs&#46; 2 and 3</a>&#41;&#46; No lesion was considered to be suitable for endovascular treatment&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">Given these findings&#44; the diagnosis of TAK was called into question&#44; and we began to investigate causes for premature vascular disorder&#46; Tests for autoimmune disorders&#44; thrombophilia&#44; and antiphospholipid antibodies were normal&#46; Homocysteine 11&#46;7<span class="elsevierStyleHsp" style=""></span>&#956;mol&#47;L&#46; Urine sediment was normal&#46; A lipid profile was ordered which showed the following values&#58; total cholesterol 197<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; triglycerides 74<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; HDL-c 68<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; LDL-c 114<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; Lp&#40;a&#41; 277<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; apoA 176<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; apoB 102<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">With the aim of discerning whether we were faced with premature atherosclerosis due to a massive elevation of Lp&#40;a&#41; or TAK with residual established lesions&#44; a PET-CT was ordered which showed no signed of active inflammatory disease&#46; Lastly&#44; a coronary CT angiogram was ordered&#44; which showed diffuse mixed atherosclerosis along the entire aorta trajectory with discontinuous calcification in the ascending and descending trajectory&#44; involvement of both coronary ostia&#44; with an estimated 70&#37; stenosis of the right ostium and marked calcified atherosclerosis of the rest of the trajectory of the right coronary artery&#46; In line with the rest of the additional tests ordered&#44; the findings were interpreted as having an atherosclerotic origin&#44; although the TAK diagnosis could not be definitively ruled out&#46; The patient was included in a lipoprotein apheresis programme with sufficient tolerance&#46; Immunosuppressant treatment was withdrawn and the patient is currently asymptomatic&#46; The clinical judgement according to the findings was premature atherosclerosis due to massive Lp&#40;a&#41; elevation affecting the aorta&#44; coronary&#44; carotid&#44; and renal arteries&#44; without being able to rule out Takayasu&#39;s arteritis in remission&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0035" class="elsevierStylePara elsevierViewall">The presented case report raised the question of whether we were faced with premature atherosclerosis due to massive Lp&#40;a&#41; elevation&#44; residual TAK with no signs of activity&#44; or both diagnoses&#46; Attempts were made to address this issue by using PET-CT&#46; Its utility has been demonstrated for diagnosing and monitoring large-vessel vasculitis&#44; including TAK&#46; A pathological uptake has also been demonstrated in developing atheroma plaques&#46; Using this test we were able to attempt to discern both pathologies by the degree&#44; topography&#44; and morphology of the radiotracer uptake&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">2</span></a> In this case&#44; it is a difficult task to differentiate the two entities given the absence of uptake on the PET-CT&#46; The time the patient has remained asymptomatic&#44; the normality of the acute-phase reactants&#44; the intense vascular calcification&#44; and the coronary artery involvement&#44; rare in TAK&#44; are data that in our judgement do not support the TAK diagnosis&#46; Hypertrophic cardiomyopathy&#44; sometimes related to TAK&#44; is justified by the sustained effects in the time the left ventricular outflow tract was obstructed&#44; or by prolonged high BP figures&#46; The latter is the most plausible in our patient&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">3</span></a> We believe that this is independent of TAK&#46; Furthermore&#44; it is true that the patient does not have any other cardiovascular risk factors &#40;although she has a first-degree family history of premature cerebrovascular disease&#41;&#46; Thus it may be argued that the extensive vascular involvement is due only to the massive LP&#40;a&#41; elevation&#46; This means that the possibility of TAK in remission with residual lesions cannot be ruled out entirely&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">As for the Lp&#40;a&#41;&#44; multiple studies have demonstrated its role as a vascular risk factor associated with both heart disease and stroke&#46; This includes a meta-analysis of 36 prospective studies with a total of 126&#44;634 patients published in JAMA&#44; which concluded that there is a continuous&#44; independent correlation of the Lp&#40;a&#41; concentration and the risk of heart disease and stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">4</span></a> Our patient had very high Lp&#40;a&#41; levels&#44; but the threshold from which the Lp&#40;a&#41; concentration increases cardiovascular risk has not yet been fully established&#44; and many studies do not estimate the vascular risk given extreme levels of Lp&#40;a&#41;&#44; as in our case&#46; Nevertheless&#44; the published analysis performed on a cohort study of heart disease in Copenhagen&#44; an increased risk of myocardial infarction in proportion to the Lp&#40;a&#41; levels was observed&#46; A threshold effect was not found and there was a three- to four-fold increase of the risk of acute myocardial infarction at extreme levels &#40;&#8805;120<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#41; of Lp&#40;a&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">5</span></a> We have not found a case in the literature as explicit as this one that shows as extensive a level of involvement&#46; The mechanism by which Lp&#40;a&#41; induces the development of atherosclerosis is still unknown&#46; Given its similarity with the plasminogen domain&#44; a prothrombotic mechanism has been suggested for the development of atherosclerosis&#46; The VLDL receptor expressed in macrophages present in the atheroma plaque may be implicated in its metabolism&#44; enabling LP&#40;a&#41; endocytosis and promoting deposits in the lesion zone&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">6</span></a> The wide heterogeneity in the size of the gene coding for apoA would be responsible for the wide range of Lp&#40;a&#41; concentrations found in different individuals&#44; and the size of the apoA isoforms&#46; There is a correlation between the size of the isoforms and cardiovascular risk&#44; with the smaller forms conferring greater atherogenic power&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">7</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The European Consensus for handling patients with LP&#40;a&#41; elevation suggests it be determined in the following cases&#58; premature CVD&#44; familial hypercholesterolaemia&#44; family history of premature CVD or LP&#40;a&#41; elevation&#44; recurrent CVD despite statin treatment&#44; &#8805;3&#37; and &#8805;10&#37; risk at 10-years of fatal CVD according to European and American clinical practice guidelines&#44; respectively&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">There are currently few available therapeutic options&#46; Hygiene and dietary measures have not been shown to influence the Lp&#40;a&#41; levels and statins do not lower its concentration&#46; One of the drugs that has been demonstrated to reduce the LP&#40;a&#41; level is nicotinic acid &#40;niacin&#41;&#44; with a reduction of up to 40&#37; at the highest tolerated dose&#46; Anti-PCSK9 monoclonal antibodies can reduce LP&#40;a&#41; levels by up to 30&#37;&#44; although its main effect is to reduce LDL-c levels&#46; Mipomersen&#44; an antisense oligonucleotide against apoB100&#44; may reduce the Lp&#40;a&#41; concentrations by 19&#8211;31&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">9</span></a> Studies on an antisense oligonucleotide against apoA are currently starting Phase 2 trials&#46; The last currently available step is one of the most effective measures for reducing Lp&#40;a&#41; levels&#44; lipoprotein apheresis&#46; This method achieves decreases up to 70&#37;&#46; Leebmann et al&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">10</span></a> included 170 patients with increased LP&#40;a&#41; levels and progressive CVD with the maximum tolerated doses of lipid-lowering therapy&#46; The study proved not only that lipoprotein apheresis is safe and effective for reducing Lp&#40;a&#41; levels&#44; but it also reduced the incidence of cardiovascular episodes&#46; It should be taken into account that LDL-c levels were reduced in parallel&#44; which may explain the reduction of episodes as LDL-c also decreased&#46; In our case&#44; LP&#40;a&#41; levels were reduced by 71&#37; &#40;pre- and post-apheresis levels were 257 and 86<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#44; respectively&#41;&#46; The desired LP&#40;a&#41; level established by European consensus is &#60;50<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">8</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusion</span><p id="par0055" class="elsevierStylePara elsevierViewall">Increased blood LP&#40;a&#41; values represent an independent cardiovascular risk factor&#44; with an important role in the development of premature atherosclerosis&#46; It may be advisable to measure it in patients who present or atypically develop large-vessel vasculitis&#46; A useful tool for differentiating vascular involvement due to atherosclerosis or vasculitis is PET-CT&#46; In this case&#44; given the absence of uptake and symptoms&#44; it is not possible to label the patient with a concrete diagnosis&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Ethical responsibilities</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Protection of human and animal subjects</span><p id="par0060" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were conducted on human beings or animals for this research&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Confidentiality of data</span><p id="par0065" class="elsevierStylePara elsevierViewall">The authors declare that they have followed the protocols of their work site regarding the publication of patient data&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Right to privacy and informed consent</span><p id="par0070" class="elsevierStylePara elsevierViewall">The authors declare that no patient data is contained in this article&#46;</p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Authorship</span><p id="par0075" class="elsevierStylePara elsevierViewall">All the authors mentioned have contributed to this manuscript&#44; both by providing ideas as well as in preparing the draft and its final approval&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Conflicts of interest</span><p id="par0080" class="elsevierStylePara elsevierViewall">The authors of this manuscript declare that they have no conflicts of interest&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Lipoprotein &#40;a&#41; &#91;Lp&#40;a&#41;&#93; is a lipoprotein defined by presenting a specific apolipoprotein&#44; ApoA&#44; linked to the ApoB-100 by different types of chemical bonds&#44; including a disulfide bridge&#46; Despite their atherogenic mechanism is not fully understood&#44; its importance has been demonstrated in the development of premature aterosclerosis&#46; Multiple studies have shown its role as a cardiovascular risk factor associated with heart disease and stroke&#46; We report the case of a patient with a diagnosis of Takayasu arteritis in which a massive elevation of Lp&#40;a&#41; was detected&#46; We emphasise its diagnostic and therapeutic implications&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La lipoprote&#237;na &#40;a&#41; &#91;Lp&#40;a&#41;&#93; es una lipoprote&#237;na definida por presentar una apolipoprote&#237;na espec&#237;fica&#44; la apoA&#44; unida a la apoB-100 por diversos tipos de enlaces qu&#237;micos&#44; entre ellos un puente disulfuro&#46; A pesar de que su mecanismo aterog&#233;nico no es completamente conocido&#44; est&#225; demostrada su importancia en el desarrollo de ateroesclerosis prematura&#44; mostrando m&#250;ltiples estudios su papel como factor de riesgo cardiovascular asociado a enfermedad coronaria e ictus&#46; Presentamos el caso de una paciente con diagn&#243;stico de arteritis de Takayasu en la que se detect&#243; una elevaci&#243;n masiva de Lp&#40;a&#41;&#44; y abordamos las implicaciones diagn&#243;sticas y terap&#233;uticas que tuvo este hallazgo&#46;</p></span>"
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Article information
ISSN: 25299123
Original language: English
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es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos