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Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation

Chronic diseases are characterised by altered autophagy and protein metabolism disarrangement, resulting in sarcopenia, hypoalbuminemia and hypo-haemoglobinaemia. Hypo-haemoglobinaemia is linked to a worse prognosis independent of the target organ affected by the disease. Currently, the cornerstone...

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Autores principales: Pasini, Evasio, Corsetti, Giovanni, Romano, Claudia, Aquilani, Roberto, Scarabelli, Tiziano, Chen-Scarabelli, Carol, Dioguardi, Francesco S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7830481/
https://www.ncbi.nlm.nih.gov/pubmed/33467658
http://dx.doi.org/10.3390/nu13010237
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author Pasini, Evasio
Corsetti, Giovanni
Romano, Claudia
Aquilani, Roberto
Scarabelli, Tiziano
Chen-Scarabelli, Carol
Dioguardi, Francesco S.
author_facet Pasini, Evasio
Corsetti, Giovanni
Romano, Claudia
Aquilani, Roberto
Scarabelli, Tiziano
Chen-Scarabelli, Carol
Dioguardi, Francesco S.
author_sort Pasini, Evasio
collection PubMed
description Chronic diseases are characterised by altered autophagy and protein metabolism disarrangement, resulting in sarcopenia, hypoalbuminemia and hypo-haemoglobinaemia. Hypo-haemoglobinaemia is linked to a worse prognosis independent of the target organ affected by the disease. Currently, the cornerstone of the therapy of anaemia is iron supplementation, with or without erythropoietin for the stimulation of haematopoiesis. However, treatment strategies should incorporate the promotion of the synthesis of heme, the principal constituent of haemoglobin (Hb) and of many other fundamental enzymes for human metabolism. Heme synthesis is controlled by a complex biochemical pathway. The limiting step of heme synthesis is D-amino-levulinic acid (D-ALA), whose availability and synthesis require glycine and succinil-coenzyme A (CoA) as precursor substrates. Consequently, the treatment of anaemia should not be based only on the sufficiency of iron but, also, on the availability of all precursor molecules fundamental for heme synthesis. Therefore, an adequate clinical therapeutic strategy should integrate a standard iron infusion and a supply of essential amino acids and vitamins involved in heme synthesis. We reported preliminary data in a select population of aged anaemic patients affected by congestive heart failure (CHF) and catabolic disarrangement, who, in addition to the standard iron therapy, were treated by reinforced therapeutic schedules also providing essential animo acids (AAs) and vitamins involved in the maintenance of heme. Notably, such individualised therapy resulted in a significantly faster increase in the blood concentration of haemoglobin after 30 days of treatment when compared to the nonsupplemented standard iron therapy.
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spelling pubmed-78304812021-01-26 Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation Pasini, Evasio Corsetti, Giovanni Romano, Claudia Aquilani, Roberto Scarabelli, Tiziano Chen-Scarabelli, Carol Dioguardi, Francesco S. Nutrients Article Chronic diseases are characterised by altered autophagy and protein metabolism disarrangement, resulting in sarcopenia, hypoalbuminemia and hypo-haemoglobinaemia. Hypo-haemoglobinaemia is linked to a worse prognosis independent of the target organ affected by the disease. Currently, the cornerstone of the therapy of anaemia is iron supplementation, with or without erythropoietin for the stimulation of haematopoiesis. However, treatment strategies should incorporate the promotion of the synthesis of heme, the principal constituent of haemoglobin (Hb) and of many other fundamental enzymes for human metabolism. Heme synthesis is controlled by a complex biochemical pathway. The limiting step of heme synthesis is D-amino-levulinic acid (D-ALA), whose availability and synthesis require glycine and succinil-coenzyme A (CoA) as precursor substrates. Consequently, the treatment of anaemia should not be based only on the sufficiency of iron but, also, on the availability of all precursor molecules fundamental for heme synthesis. Therefore, an adequate clinical therapeutic strategy should integrate a standard iron infusion and a supply of essential amino acids and vitamins involved in heme synthesis. We reported preliminary data in a select population of aged anaemic patients affected by congestive heart failure (CHF) and catabolic disarrangement, who, in addition to the standard iron therapy, were treated by reinforced therapeutic schedules also providing essential animo acids (AAs) and vitamins involved in the maintenance of heme. Notably, such individualised therapy resulted in a significantly faster increase in the blood concentration of haemoglobin after 30 days of treatment when compared to the nonsupplemented standard iron therapy. MDPI 2021-01-15 /pmc/articles/PMC7830481/ /pubmed/33467658 http://dx.doi.org/10.3390/nu13010237 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Pasini, Evasio
Corsetti, Giovanni
Romano, Claudia
Aquilani, Roberto
Scarabelli, Tiziano
Chen-Scarabelli, Carol
Dioguardi, Francesco S.
Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation
title Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation
title_full Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation
title_fullStr Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation
title_full_unstemmed Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation
title_short Management of Anaemia of Chronic Disease: Beyond Iron-Only Supplementation
title_sort management of anaemia of chronic disease: beyond iron-only supplementation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7830481/
https://www.ncbi.nlm.nih.gov/pubmed/33467658
http://dx.doi.org/10.3390/nu13010237
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