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Um novo alvo para a terapêutica com estatinas?" 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Nunes, Susana Sampaio, Ana Cerqueira, Ziya Kaya, Nuno Pardal Oliveira" "autores" => array:5 [ 0 => array:2 [ "nombre" => "José Pedro L." "apellidos" => "Nunes" ] 1 => array:2 [ "nombre" => "Susana" "apellidos" => "Sampaio" ] 2 => array:2 [ "nombre" => "Ana" "apellidos" => "Cerqueira" ] 3 => array:2 [ "nombre" => "Ziya" "apellidos" => "Kaya" ] 4 => array:2 [ "nombre" => "Nuno" "apellidos" => "Pardal Oliveira" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S0870255115000025" "doi" => "10.1016/j.repc.2014.08.018" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0870255115000025?idApp=UINPBA00004E" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S217420491500029X?idApp=UINPBA00004E" "url" => "/21742049/0000003400000002/v2_201502270337/S217420491500029X/v2_201502270337/en/main.assets" ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial comment</span>" "titulo" => "Autoantibodies to cardiac troponin in patients after renal transplant: A new target for statins?" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "91" "paginaFinal" => "93" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "João Morais" "autores" => array:1 [ 0 => array:3 [ "nombre" => "João" "apellidos" => "Morais" "email" => array:1 [ 0 => "jaraujomorais@mail.telepac.pt" ] ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Centro Hospitalar de Leiria, Leiria, Portugal" "identificador" => "aff0005" ] ] ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Autoanticorpos antitroponina cardíaca em doentes após transplante renal. Um novo alvo para a terapêutica com estatinas?" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">There have been few studies on the immune response to myocardial damage and their findings are of little practical value. Even in myocardial infarction (MI), the classic example of myocardial injury not due to inflammation or infection, the clinical impact of research is limited.</p><p id="par0010" class="elsevierStylePara elsevierViewall">An example of what we would hope for from such research, with potential application to clinical practice, is the recent publication of an interesting study by Savukoski et al., who have developed a new immunoassay for troponin measurement that is free from interference from circulating anti-troponin autoantibodies.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">In another study by the same group, the prevalence of troponin-specific autoantibodies in a cohort of 510 patients with suspected MI was 9.2%, but they found no correlation with 12-month outcome.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The practical relevance of this observation is that the presence of these antibodies can lead to false negative readings for serum troponin in patients with MI and thus delay diagnosis.</p><p id="par0025" class="elsevierStylePara elsevierViewall">The presence of these antibodies has also been reported in apparently healthy individuals. Adamczyk et al.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">3</span></a> reported a 12.7% prevalence of both troponin T and I in healthy blood donors.</p><p id="par0030" class="elsevierStylePara elsevierViewall">This immune response can be partly neutralized by nasal administration of the three troponin isoforms (C, I and T), and such vaccination reduces infarct size when administered prior to or one hour after ischemia/reperfusion injury.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Another area of interest to researchers is the presence of these autoantibodies in patients with dilated cardiomyopathy (DCM), such as those with Emery-Dreifuss muscular dystrophy (EDMD). This rare disease is sometimes diagnosed through the presence of a clinical picture of DCM in which involvement of cardiac muscle precedes that of skeletal muscle. In a study of 10 patients with EDMD and 10 healthy age-matched normal controls, there was no clear relationship between antibody levels and cardiac symptoms, although the authors admit that the detection of anti-troponin I antibodies may be a marker of early stages of DCM in EDMD.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">5</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Autoimmunity plays a part in the pathogenesis of several entities, including DCM, myocarditis, rheumatic fever and even atherosclerosis. However, whether it has a causal relationship with DCM is still the subject of debate.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">6</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Shmilovich et al.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">7</span></a> tested three groups, two with DCM (33 ischemic and 32 non-ischemic) and 42 healthy individuals, and found IgG anti-troponin autoantibodies in 18.2% of the ischemic DCM group and 15.5% of the non-ischemic group, as compared to none in the healthy subjects. However, attempts to bind these antibodies to cultured cardiomyocytes failed and they exhibited no measurable effects on calcium transients, leaving open the question of a possible causal connection.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Daniela Nunes et al.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">8</span></a> studied patients with Chagas disease and found no correlation with left ventricular ejection fraction; however, when grouped as low and high antibody producers, ejection fraction was lower in the group with higher levels of anti-troponin antibodies (p=0.042), and the correlation was even stronger with anti-myosin antibodies (p=0.013). The authors concluded that it may one day be possible to use the production of autoantibodies to troponin T and myosin as markers for the early detection of this disease of long-term evolution, which would have considerable clinical impact.</p><p id="par0055" class="elsevierStylePara elsevierViewall">The study by José Nunes et al.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">9</span></a> published in this issue of the <span class="elsevierStyleItalic">Journal</span> presents a new approach to this subject, focusing on renal transplant patients with end-stage chronic renal disease. In 2013, the same group reported the case of a female patient with DCM and ejection fraction of 30% in which ventricular function improved after renal transplant, although without regaining previous end-diastolic volume.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">10</span></a> Very high levels of anti-troponin antibodies were found in this patient (IgG 1:640 and IgM 1:80), which presumably prompted the authors to continue their investigation.</p><p id="par0060" class="elsevierStylePara elsevierViewall">In the article published here, a study of 48 renal transplant patients under immunosuppressive therapy, low titers (<1:40) of anti-troponin I autoantibodies were detected in most cases (n=30); only eight patients had IgG titers ≥1:80, and there was a single value of 1:160. In only one patient were both anti-troponin I antibody IgG and IgM titers ≥1:80. Clinical cardiac disease was seen in nine patients, but this was not associated with antibody levels. The authors found an interesting correlation between anti-troponin antibodies and statin use, with high levels being detected in only 3/26 patients under statin therapy as opposed to 10/22 of those not under statin therapy (p=0.008 by the chi-square test), suggesting that the immune response is weakened by statin therapy.</p><p id="par0065" class="elsevierStylePara elsevierViewall">The non-lipid effects of statins have been the subject of much research over the past twenty years, with heated debate between opposing viewpoints. However, statins’ anti-inflammatory effects, for which evidence is accumulating, are more generally accepted.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">11</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">The long history of investigation into the clinical effects of statins includes their marked reduction of contrast-induced nephropathy, as shown in a meta-analysis published in 2014,<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">12</span></a> with 46% lower relative risk (RR) (RR 0.54, 95% confidence interval 0.38–0.78, p=0.001).</p><p id="par0075" class="elsevierStylePara elsevierViewall">Various hypotheses have been put forward concerning the mechanisms behind this effect, but they are merely speculative. The anti-inflammatory effect of statins has been invoked once more, but there are other possibilities, including protection against the cytotoxic effects of contrast agents. A subgroup analysis of the Novel Approaches for Preventing or Limiting Events (NAPLES II) trial<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">13</span></a> showed that a high loading dose of atorvastatin in vitro reduced the activation of the intrinsic apoptotic pathway seen in situations of extreme metabolic or hemodynamic stress.</p><p id="par0080" class="elsevierStylePara elsevierViewall">The authors of the present study consider some of these possibilities from a hypothetical standpoint in the discussion of their results. The idea that renal transplant patients should undergo chronic statin therapy remains controversial. However, while there are clear benefits from statins in patients with chronic renal disease not requiring dialysis, reducing mortality by around 20%,<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">14</span></a> there is less agreement concerning patients on dialysis. A recent meta-analysis of studies in renal transplant recipients<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">15</span></a> was inconclusive due to the heterogeneity in the methodologies used.</p><p id="par0085" class="elsevierStylePara elsevierViewall">Nevertheless, until there is solid evidence either way, the severe vascular disease normally seen in end-stage renal disease, and the attendant higher risk of MI, are in the opinion of this author sufficient reason to consider statin therapy in these patients.</p><p id="par0090" class="elsevierStylePara elsevierViewall">Only further studies can demonstrate whether a reduction in antibody levels is an additional protective factor. We look forward to the results of future studies by the authors of the article published here in their search for answers to these questions.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0095" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflicts of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Morais J. Autoanticorpos antitroponina cardíaca em doentes após transplante renal. Um novo alvo para a terapêutica com estatinas? Rev Port Cardiol. 2015;34:91–93.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib0080" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Novel sensitive cardiac troponin I immunoassay free from troponin I-specific autoantibody interference" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:3 [ 0 => "T. Savukoski" 1 => "J. Jacobino" 2 => "P. 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Year/Month | Html | Total | |
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2024 November | 6 | 5 | 11 |
2024 October | 28 | 33 | 61 |
2024 September | 49 | 24 | 73 |
2024 August | 29 | 33 | 62 |
2024 July | 28 | 31 | 59 |
2024 June | 29 | 22 | 51 |
2024 May | 32 | 34 | 66 |
2024 April | 22 | 22 | 44 |
2024 March | 27 | 20 | 47 |
2024 February | 21 | 23 | 44 |
2024 January | 19 | 25 | 44 |
2023 December | 19 | 26 | 45 |
2023 November | 29 | 31 | 60 |
2023 October | 20 | 15 | 35 |
2023 September | 16 | 24 | 40 |
2023 August | 18 | 15 | 33 |
2023 July | 19 | 12 | 31 |
2023 June | 21 | 21 | 42 |
2023 May | 32 | 24 | 56 |
2023 April | 11 | 8 | 19 |
2023 March | 19 | 22 | 41 |
2023 February | 27 | 23 | 50 |
2023 January | 12 | 18 | 30 |
2022 December | 20 | 17 | 37 |
2022 November | 25 | 27 | 52 |
2022 October | 25 | 26 | 51 |
2022 September | 20 | 47 | 67 |
2022 August | 22 | 36 | 58 |
2022 July | 25 | 34 | 59 |
2022 June | 20 | 23 | 43 |
2022 May | 23 | 39 | 62 |
2022 April | 28 | 24 | 52 |
2022 March | 26 | 35 | 61 |
2022 February | 15 | 30 | 45 |
2022 January | 26 | 20 | 46 |
2021 December | 11 | 27 | 38 |
2021 November | 25 | 33 | 58 |
2021 October | 36 | 30 | 66 |
2021 September | 9 | 24 | 33 |
2021 August | 22 | 25 | 47 |
2021 July | 18 | 27 | 45 |
2021 June | 14 | 16 | 30 |
2021 May | 18 | 23 | 41 |
2021 April | 22 | 51 | 73 |
2021 March | 38 | 13 | 51 |
2021 February | 62 | 20 | 82 |
2021 January | 19 | 10 | 29 |
2020 December | 19 | 7 | 26 |
2020 November | 37 | 10 | 47 |
2020 October | 9 | 10 | 19 |
2020 September | 57 | 9 | 66 |
2020 August | 15 | 12 | 27 |
2020 July | 63 | 9 | 72 |
2020 June | 22 | 7 | 29 |
2020 May | 28 | 13 | 41 |
2020 April | 37 | 6 | 43 |
2020 March | 52 | 10 | 62 |
2020 February | 55 | 53 | 108 |
2020 January | 42 | 7 | 49 |
2019 December | 29 | 6 | 35 |
2019 November | 38 | 11 | 49 |
2019 October | 29 | 3 | 32 |
2019 September | 26 | 11 | 37 |
2019 August | 28 | 3 | 31 |
2019 July | 49 | 10 | 59 |
2019 June | 33 | 3 | 36 |
2019 May | 32 | 5 | 37 |
2019 April | 42 | 13 | 55 |
2019 March | 192 | 12 | 204 |
2019 February | 149 | 13 | 162 |
2019 January | 89 | 8 | 97 |
2018 December | 94 | 13 | 107 |
2018 November | 170 | 7 | 177 |
2018 October | 268 | 10 | 278 |
2018 September | 79 | 15 | 94 |
2018 August | 45 | 7 | 52 |
2018 July | 56 | 4 | 60 |
2018 June | 80 | 11 | 91 |
2018 May | 118 | 16 | 134 |
2018 April | 91 | 17 | 108 |
2018 March | 123 | 8 | 131 |
2018 February | 70 | 3 | 73 |
2018 January | 90 | 2 | 92 |
2017 December | 166 | 12 | 178 |
2017 November | 34 | 14 | 48 |
2017 October | 28 | 9 | 37 |
2017 September | 40 | 23 | 63 |
2017 August | 35 | 15 | 50 |
2017 July | 34 | 13 | 47 |
2017 June | 49 | 23 | 72 |
2017 May | 52 | 17 | 69 |
2017 April | 25 | 5 | 30 |
2017 March | 31 | 31 | 62 |
2017 February | 24 | 3 | 27 |
2017 January | 34 | 5 | 39 |
2016 December | 45 | 18 | 63 |
2016 November | 29 | 11 | 40 |
2016 October | 29 | 8 | 37 |
2016 September | 28 | 8 | 36 |
2016 August | 13 | 1 | 14 |
2016 July | 19 | 11 | 30 |
2016 June | 15 | 4 | 19 |
2016 May | 16 | 2 | 18 |
2016 April | 26 | 2 | 28 |
2016 March | 38 | 25 | 63 |
2016 February | 43 | 35 | 78 |
2016 January | 37 | 28 | 65 |
2015 December | 37 | 21 | 58 |
2015 November | 35 | 19 | 54 |
2015 October | 43 | 27 | 70 |
2015 September | 34 | 17 | 51 |
2015 August | 44 | 15 | 59 |
2015 July | 33 | 8 | 41 |
2015 June | 24 | 5 | 29 |
2015 May | 38 | 12 | 50 |
2015 April | 47 | 43 | 90 |
2015 March | 117 | 65 | 182 |
2015 February | 11 | 5 | 16 |