Letter to the Editor
Anemia and iron in heart failure – A brief comment
Anemia e ferro na insuficiência cardíaca – um breve comentário
José Pedro Lopes Nunes
Faculdade de Medicina da Universidade do Porto, Porto, Portugal
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Porto, Portugal" "identificador" => "aff0005" ] ] ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Anemia e ferro na insuficiência cardíaca – um breve comentário" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">I read with interest a letter mentioning our paper on “Anti-troponin I antibodies in renal transplant patients”, recently published.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">1</span></a> Since the text is on a different topic, iron metabolism in heart failure, I will start by briefly commenting on this latter theme.</p><p id="par0010" class="elsevierStylePara elsevierViewall">Medical textbooks have traditionally paid a considerable degree of attention to anemia and to iron deficiency. The underlying line of reasoning is that as iron is an essential element for the production of erythrocytes, insufficient body iron stores may lead to anemia, a situation that can be corrected by the administration of iron. Conventional medical wisdom has been that it is better to have a hemoglobin concentration in the normal range, rather than a lower one.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Data obtained in chronic renal failure patients with the use of erythropoiesis-stimulating agents (compared to placebo) caused a shift in medical thinking on the subject under consideration. Studies by Singh et al.,<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">2</span></a> Drueke et al.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">3</span></a> and Pfeffer et al.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">4</span></a> have clearly shown that normal or near-normal values for hemoglobin lead to worse outcomes in patients with chronic renal failure, compared to lower values, leading to the current policy of avoiding hemoglobin values greater than 11.5 g/dl in these patients (therefore, normal is not always better).</p><p id="par0020" class="elsevierStylePara elsevierViewall">It was not until the turn of the millennium that an important regulator of iron metabolism<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">5</span></a> was discovered – hepcidin.<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">6,7</span></a> As iron is important not only for human cells but also for invading microbial cells, the human body has a hepcidin-based mechanism to withdraw iron from the circulation in the presence of infection.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">5</span></a> Many inflammatory states would appear to be interpreted as stimuli for the action of hepcidin – giving rise to the so-called anemia of chronic disease. In a study carried out in preschool children in Africa (in a region with a high incidence of malaria), Sazawal et al. showed that routine prophylactic supplementation with iron and folic acid resulted in an increased risk of severe illness and death.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">8</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">With regard to heart failure, a condition frequently associated with anemia (and also with inflammation<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">9</span></a>), Swedberg et al. showed that darbepoetin alfa did not improve clinical outcomes in this setting.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">10</span></a> Adverse thromboembolic events were in fact increased in the intervention patient group.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">10</span></a> Anemia in heart failure may have different types of causes, one of which is the action of angiotensin-converting enzyme inhibitors.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">11</span></a> Enalapril has been shown to increase the incidence of anemia in patients with heart failure.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">11</span></a> Hepcidin was shown to be decreased in patients with heart failure and anemia,<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">12</span></a> and has an uncertain role in this disease (unlike the case of hemodialysis patients, who have increased hepcidin levels<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">13</span></a>).</p><p id="par0030" class="elsevierStylePara elsevierViewall">Anemia is associated with increased mortality in patients with heart failure, however it is unclear whether it is a marker or a mediator of increased mortality risk in this setting.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">14</span></a> Ferric carboxymaltose has been used in patients with heart failure and “iron deficiency”, with improvement in symptoms, functional capacity, and quality of life.<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">15,16</span></a> However, data are available for only up to one year of therapy, and the longer-term effects of ferric carboxymaltose are unclear. Iron deficiency was diagnosed if ferritin <100 ng/ml or 100–299/300 ng/ml if transferrin saturation <20%, meaning that it is uncertain whether total body iron stores were decreased in all patients studied.<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">15,16</span></a> “Iron deficiency”, under the same criteria, has been shown to act as a marker for an unfavorable prognosis in patients with heart failure.<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">17,18</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Getting back to the comment on our text,<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">1</span></a> we did not report that “the levels of antibodies were associated with reduced left ventricular ejection fraction”, neither did we state that “inflammatory mediators such as antibodies can be used as a marker of cardiac dysfunction”.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Moreover, I would certainly not agree with the concept that erythropoietin “seems to be an efficient therapy” for heart failure (as the data presented above<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">10</span></a> show).</p><p id="par0045" class="elsevierStylePara elsevierViewall">However, we did publish a case report,<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">19</span></a> mentioned in our text, in which high titers of anti-troponin I antibodies were associated with the partial reversibility of a clinical picture of dilated cardiomyopathy, after immunosuppressive drugs were used. We presented the hypothesis that “the syndrome of reversible cardiomyopathy seen after renal transplantation is associated with immunosuppression therapy acting on immunological mechanisms previously at play”.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">19</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">The speculation that anti-troponin I antibodies, acting as inflammatory mediators, could “lead to the inhibition of iron absorption at the duodenal level” – and this would seem to be the major point to be considered in the text – is worthy of consideration, in my view.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:19 [ 0 => array:3 [ "identificador" => "bib0100" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Anti-troponin I antibodies in renal transplant patients" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:3 [ 0 => "J.P.L. 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| Ano/Mês | Html | Total | |
|---|---|---|---|
| 2024 Novembro | 6 | 2 | 8 |
| 2024 Outubro | 34 | 23 | 57 |
| 2024 Setembro | 42 | 22 | 64 |
| 2024 Agosto | 42 | 32 | 74 |
| 2024 Julho | 36 | 33 | 69 |
| 2024 Junho | 34 | 19 | 53 |
| 2024 Maio | 44 | 23 | 67 |
| 2024 Abril | 33 | 20 | 53 |
| 2024 Maro | 39 | 23 | 62 |
| 2024 Fevereiro | 31 | 30 | 61 |
| 2024 Janeiro | 22 | 37 | 59 |
| 2023 Dezembro | 31 | 29 | 60 |
| 2023 Novembro | 35 | 12 | 47 |
| 2023 Outubro | 38 | 21 | 59 |
| 2023 Setembro | 33 | 32 | 65 |
| 2023 Agosto | 24 | 14 | 38 |
| 2023 Julho | 50 | 13 | 63 |
| 2023 Junho | 74 | 18 | 92 |
| 2023 Maio | 43 | 23 | 66 |
| 2023 Abril | 19 | 5 | 24 |
| 2023 Maro | 21 | 21 | 42 |
| 2023 Fevereiro | 17 | 20 | 37 |
| 2023 Janeiro | 17 | 11 | 28 |
| 2022 Dezembro | 19 | 19 | 38 |
| 2022 Novembro | 24 | 27 | 51 |
| 2022 Outubro | 23 | 16 | 39 |
| 2022 Setembro | 21 | 26 | 47 |
| 2022 Agosto | 19 | 25 | 44 |
| 2022 Julho | 26 | 18 | 44 |
| 2022 Junho | 19 | 15 | 34 |
| 2022 Maio | 14 | 32 | 46 |
| 2022 Abril | 25 | 20 | 45 |
| 2022 Maro | 21 | 25 | 46 |
| 2022 Fevereiro | 18 | 14 | 32 |
| 2022 Janeiro | 21 | 23 | 44 |
| 2021 Dezembro | 16 | 32 | 48 |
| 2021 Novembro | 25 | 37 | 62 |
| 2021 Outubro | 31 | 38 | 69 |
| 2021 Setembro | 18 | 27 | 45 |
| 2021 Agosto | 27 | 24 | 51 |
| 2021 Julho | 20 | 36 | 56 |
| 2021 Junho | 17 | 21 | 38 |
| 2021 Maio | 21 | 26 | 47 |
| 2021 Abril | 25 | 22 | 47 |
| 2021 Maro | 34 | 23 | 57 |
| 2021 Fevereiro | 42 | 13 | 55 |
| 2021 Janeiro | 35 | 5 | 40 |
| 2020 Dezembro | 27 | 5 | 32 |
| 2020 Novembro | 31 | 10 | 41 |
| 2020 Outubro | 23 | 5 | 28 |
| 2020 Setembro | 55 | 9 | 64 |
| 2020 Agosto | 18 | 8 | 26 |
| 2020 Julho | 45 | 15 | 60 |
| 2020 Junho | 29 | 4 | 33 |
| 2020 Maio | 37 | 7 | 44 |
| 2020 Abril | 36 | 12 | 48 |
| 2020 Maro | 36 | 7 | 43 |
| 2020 Fevereiro | 40 | 35 | 75 |
| 2020 Janeiro | 28 | 4 | 32 |
| 2019 Dezembro | 22 | 6 | 28 |
| 2019 Novembro | 25 | 9 | 34 |
| 2019 Outubro | 32 | 5 | 37 |
| 2019 Setembro | 14 | 6 | 20 |
| 2019 Agosto | 22 | 7 | 29 |
| 2019 Julho | 25 | 8 | 33 |
| 2019 Junho | 26 | 7 | 33 |
| 2019 Maio | 31 | 6 | 37 |
| 2019 Abril | 12 | 8 | 20 |
| 2019 Maro | 18 | 9 | 27 |
| 2019 Fevereiro | 57 | 15 | 72 |
| 2019 Janeiro | 22 | 8 | 30 |
| 2018 Dezembro | 37 | 10 | 47 |
| 2018 Novembro | 59 | 8 | 67 |
| 2018 Outubro | 101 | 14 | 115 |
| 2018 Setembro | 32 | 10 | 42 |
| 2018 Agosto | 36 | 10 | 46 |
| 2018 Julho | 26 | 7 | 33 |
| 2018 Junho | 35 | 4 | 39 |
| 2018 Maio | 37 | 7 | 44 |
| 2018 Abril | 64 | 3 | 67 |
| 2018 Maro | 66 | 8 | 74 |
| 2018 Fevereiro | 74 | 3 | 77 |
| 2018 Janeiro | 55 | 9 | 64 |
| 2017 Dezembro | 84 | 7 | 91 |
| 2017 Novembro | 58 | 9 | 67 |
| 2017 Outubro | 26 | 13 | 39 |
| 2017 Setembro | 29 | 8 | 37 |
| 2017 Agosto | 24 | 14 | 38 |
| 2017 Julho | 15 | 7 | 22 |
| 2017 Junho | 26 | 11 | 37 |
| 2017 Maio | 33 | 11 | 44 |
| 2017 Abril | 39 | 38 | 77 |
| 2017 Maro | 28 | 7 | 35 |
| 2017 Fevereiro | 23 | 8 | 31 |
| 2017 Janeiro | 20 | 4 | 24 |
| 2016 Dezembro | 19 | 3 | 22 |
| 2016 Novembro | 14 | 5 | 19 |
| 2016 Outubro | 12 | 7 | 19 |
| 2016 Setembro | 11 | 6 | 17 |
| 2016 Agosto | 13 | 0 | 13 |
| 2016 Julho | 6 | 7 | 13 |
| 2016 Junho | 2 | 11 | 13 |
| 2016 Maio | 11 | 0 | 11 |
| 2016 Abril | 11 | 1 | 12 |
| 2016 Maro | 18 | 12 | 30 |
| 2016 Fevereiro | 38 | 14 | 52 |
| 2016 Janeiro | 18 | 13 | 31 |
| 2015 Dezembro | 32 | 10 | 42 |
| 2015 Novembro | 60 | 36 | 96 |
| 2015 Outubro | 73 | 47 | 120 |
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