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2. Hepatocyte-derived biomarkers predict liver-related events at 2 years in Child-Pugh class A alcohol-related cirrhosis

Author

Elkrief, Laure, Ganne-Carrié, Nathalie, Manceau, Hana, Tanguy, Marion, Valainathan, Shantha Ram, Riescher-Tuczkiewicz, Alix, Biquard, Louise, Barget, Nathalie, Chaffaut, Cendrine, Louvet, Alexandre, Paradis, Valérie, Ziol, Marianne, Bæk, Rikke, Jørgensen, Malene Møller, Van Niel, Guillaume, Coly, Pierre-Michael, Hammoutène, Adel, Dujardin, Fanny, Peoc’h, Katell, Poynard, Thierry, Chevret, Sylvie, and Rautou, Pierre-Emmanuel

Published
2023
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3. Evaluation of iron metabolism in hospitalized COVID-19 patients

Author

Lefebvre, Thibaud, Boutten, Anne, Raulet-Bussian, Célia, Raynor, Alexandre, Manceau, Hana, Puy, Hervé, Moulouel, Boualem, Schmitt, Caroline, Timsit, Jean-François, Lefort, Agnès, Weiss, Emmanuel, Lescure, Francois-Xavier, Ricard, Jean-Damien, Sonneville, Romain, and Peoc'h, Katell

Published
2023
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5. Givosiran in acute intermittent porphyria: A personalized medicine approach

Author

Poli, Antoine, Schmitt, Caroline, Moulouel, Boualem, Mirmiran, Arienne, Talbi, Neila, Rivière, Sophie, Cerutti, Diane, Bouchoule, Isabelle, Faivre, Anthony, Grobost, Vincent, Douillard, Claire, Duchêne, Francis, Fiorentino, Valeria, Dupré, Thierry, Manceau, Hana, Peoc'h, Katell, Puy, Hervé, Lefebvre, Thibaud, and Gouya, Laurent

Published
2022
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9. Regulation of globin-heme balance in Diamond-Blackfan anemia by HSP70/GATA1

Author

Rio, Sarah, Gastou, Marc, Karboul, Narjesse, Derman, Raphaёl, Suriyun, Thunwarat, Manceau, Hana, Leblanc, Thierry, El Benna, Jamel, Schmitt, Caroline, Azouzi, Slim, Larghéro, Jérome, Karim, Zoubida, Macias-Garcia, Alejandra, Chen, Jane-Jane, Hermine, Olivier, Courtois, Geneviève, Puy, Hervé, Gouya, Laurent, Mohandas, Narla, and Da Costa, Lydie

Published
2019
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15. Quantification of Urine and Plasma Porphyrin Precursors Using LC–MS in Acute Hepatic Porphyrias: Improvement in Routine Diagnosis and in the Monitoring of Kidney Failure Patients

Author

Poli, Antoine, primary, Manceau, Hana, additional, Nguyen, Anvi Laetitia, additional, Moulouel, Boualem, additional, Dessendier, Nathalie, additional, Talbi, Neila, additional, Puy, Hervé, additional, Junot, Christophe, additional, Gouya, Laurent, additional, Schmitt, Caroline, additional, and Lefebvre, Thibaud, additional

Published
2023
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17. Reversible atransferrinemia in a patient with chronic enteropathy: is transferrin mandatory for iron transport?

Author

Raynor, Alexandre, Stefanescu, Carmen, Bruneel, Arnaud, Puy, Hervé, Peoc’h, Katell, Manceau, Hana, Raynor, Alexandre, Stefanescu, Carmen, Bruneel, Arnaud, Puy, Hervé, Peoc’h, Katell, and Manceau, Hana

Abstract

Herein, we report the case of a 42-year-old woman, hospitalized in a French tertiary hospital for a relapse of a chronic enteropathy, who was found on admission to have no detectable serum transferrin. Surprisingly, she only exhibited mild anaemia. This atransferrinemia persisted for two months throughout her hospitalization, during which her haemoglobin concentration remained broadly stable. Based on her clinical history and evolution, we concluded to an acquired atransferrinemia secondary to chronic undernutrition, inflammation and liver failure. We discuss the investigations performed in this patient, and hypotheses regarding the relative stability of her haemoglobin concentration despite the absence of detectable transferrin.

Published
2023

20. Neglected Comorbidity of Chronic Heart Failure: Iron Deficiency

Author

Manceau, Hana, Ausseil, Jérome, Masson, Damien, Feugeas, Jean-Paul, Sablonniere, Bernard, Guieu, Régis, Puy, Hervé, Peoc’h, Katell, Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre hospitalier universitaire de Nantes (CHU Nantes), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC), CHU Lille, Aix Marseille Université (AMU), ANR-11-LABX-0051,GR-Ex,Biogenèse et pathologies du globule rouge(2011), and ANR-11-IDEX-0005,USPC,Université Sorbonne Paris Cité(2011)

Subjects
iron deficiency, transferrin saturation coefficient, [SDV]Life Sciences [q-bio], serum ferritin, heart failure, ferric carboxymaltose
Abstract

International audience; Iron deficiency is a significant comorbidity of heart failure (HF), defined as the inability of the myocardium to provide sufficient blood flow. However, iron deficiency remains insufficiently detected. Iron-deficiency anemia, defined as a decrease in hemoglobin caused by iron deficiency, is a late consequence of iron deficiency, and the symptoms of iron deficiency, which are not specific, are often confused with those of HF or comorbidities. HF patients with iron deficiency are often rehospitalized and present reduced survival. The correction of iron deficiency in HF patients is associated with improved functional capacity, quality of life, and rehospitalization rates. Because of the inflammation associated with chronic HF, which complicates the picture of nutritional deficiency, only the parenteral route can bypass the tissue sequestration of iron and the inhibition of intestinal iron absorption. Given the negative impact of iron deficiency on HF progression, the frequency and financial implications of rehospitalizations due to decompensation episodes, and the efficacy of this supplementation, screening for this frequent comorbidity should be part of routine testing in all HF patients. Indeed, recent European guidelines recommend screening for iron deficiency (serum ferritin and transferrin saturation coefficient) in all patients with suspected HF, regular iron parameters assessment in all patients with HF, and intravenous iron supplementation in symptomatic patients with proven deficiency. We thus aim to summarize all currently available data regarding this common and easily improvable comorbidity.

Published
2022
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21. Hepatocyte-derived biomarkers concentrations predict liver-related events within 2 years in patients with Child-Pugh class A alcohol-related cirrhosis

Author

Elkrief, Laure, primary, Ganne-Carrié, Nathalie, additional, Manceau, Hana, additional, Tanguy, Marion, additional, Barget, Nathalie, additional, Chaffaut, Cendrine, additional, Valainathan, Shantha, additional, Riescher, Alix, additional, Peoch, Katell, additional, Poynard, Thierry, additional, Chevret, Sylvie, additional, and Rautou, Pierre-Emmanuel, additional

Published
2022
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27. I-FABP is decreased in COVID-19 patients, independently of the prognosis

Author

Guedj, Kevin, primary, Uzzan, Mathieu, additional, Soudan, Damien, additional, Trichet, Catherine, additional, Nicoletti, Antonino, additional, Weiss, Emmanuel, additional, Manceau, Hana, additional, Nuzzo, Alexandre, additional, Corcos, Olivier, additional, Treton, Xavier, additional, and Peoc’h, Katell, additional

Published
2021
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28. A mutation in the iron-responsive element of ALAS2 is a modifier of disease severity in a patient suffering from CLPX associated erythropoietic protoporphyria

Author

Ducamp, Sarah, primary, Luscieti, Sara, additional, Ferrer-Cortès, Xènia, additional, Nicolas, Gaël, additional, Manceau, Hana, additional, Peoc’h, Katell, additional, Yien, Yvette Y., additional, Kannengiesser, Caroline, additional, Gouya, Laurent, additional, Puy, Herve, additional, and Sanchez, Mayka, additional

Published
2021
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31. Fecal let-7b and miR-21 directly modulate the intestinal microbiota, driving chronic inflammation

Author

Casado-Bedmar, Maite, Roy, Maryline, Berthet, Louis, Hugot, Jean-Pierre, Yang, Chunhua, Manceau, Hana, Peoc’h, Katell, Chassaing, Benoit, Merlin, Didier, and Viennois, Emilie

Abstract

ABSTRACTInflammatory bowel diseases (IBD) etiology is multifactorial. Luminal microRNAs (miRNAs) have been suspected to play a role in the promotion of chronic inflammation, but the extent to which fecal miRNAs are interacting with the intestinal ecosystem in a way that contribute to diseases, including IBD, remains unknown. Here, fecal let-7b and miR-21 were found elevated, associated with inflammation, and correlating with multiple bacteria in IBD patients and IL-10–/–mice, model of spontaneous colitis. Using an in vitromicrobiota modeling system, we revealed that these two miRNAs can directly modify the composition and function of complex human microbiota, increasing their proinflammatory potential. In vivoinvestigations revealed that luminal increase of let-7b drastically alters the intestinal microbiota and enhances macrophages’ associated proinflammatory cytokines (TNF, IL-6, and IL-1β). Such proinflammatory effects are resilient and dependent on the bacterial presence. Moreover, we identified that besides impairing the intestinal barrier function, miR-21 increases myeloperoxidase and antimicrobial peptides secretion, causing intestinal dysbiosis. More importantly, in vivoinhibition of let-7b and miR-21 with anti-miRNAs significantly improved the intestinal mucosal barrier function and promoted a healthier host-microbiota interaction in the intestinal lining, which altogether conferred protection against colitis. In summary, we provide evidence of the functional significance of fecal miRNAs in host-microbiota communication, highlighting their therapeutic potential in intestinal inflammation and dysbiosis-related conditions, such as IBD.

Published
2024
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34. Biological response under treatment and prognostic value of protein induced by vitamin K absence or antagonist-II in a French cohort of patients with hepatocellular carcinoma

Author

Payancé, Audrey, primary, Dioguardi Burgio, Marco, additional, Peoc’h, Katell, additional, Achahboun, Mohamed, additional, Albuquerque, Miguel, additional, Devictor, Julie, additional, Chor, Hélène, additional, Manceau, Hana, additional, Soubrane, Olivier, additional, Durand, François, additional, Castera, Laurent, additional, Bouattour, Mohamed, additional, and Paradis, Valérie, additional

Published
2019
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35. This title is unavailable for guests, please login to see more information.

Author

Massachusetts Institute of Technology. Department of Biology, Kardon, Julia R., Baker, Tania, Yien, Yvette Y., Ducamp, Sarah, van der Vorm, Lisa N., Manceau, Hana, Kannengiesser, Caroline, Bergonia, Hector A., Kafina, Martin D., Karim, Zoubida, Gouya, Laurent, Puy, Hervé, Phillips, John D., Nicolas, Gaël, Paw, Barry H., Massachusetts Institute of Technology. Department of Biology, Kardon, Julia R., Baker, Tania, Yien, Yvette Y., Ducamp, Sarah, van der Vorm, Lisa N., Manceau, Hana, Kannengiesser, Caroline, Bergonia, Hector A., Kafina, Martin D., Karim, Zoubida, Gouya, Laurent, Puy, Hervé, Phillips, John D., Nicolas, Gaël, and Paw, Barry H.

Abstract

National Institutes of Health (U.S.) (Grant F32 DK095726), National Institutes of Health (U.S.) (Grant R01 GM049224)

Published
2018

36. From a dominant to an oligogenic model of inheritance with environmental modifiers in acute intermittent porphyria

Author

Lenglet, Hugo, primary, Schmitt, Caroline, additional, Grange, Thomas, additional, Manceau, Hana, additional, Karboul, Narjesse, additional, Bouchet-Crivat, Florian, additional, Robreau, Anne-Marie, additional, Nicolas, Gael, additional, Lamoril, Jerôme, additional, Simonin, Sylvie, additional, Mirmiran, Arienne, additional, Karim, Zoubida, additional, Casalino, Enrique, additional, Deybach, Jean-Charles, additional, Puy, Hervé, additional, Peoc’h, Katell, additional, and Gouya, Laurent, additional

Published
2018
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39. Non syndromic childhood onset congenital sideroblastic anemia: A report of 13 patients identified with an ALAS2 or SLC25A38 mutation.

Author

UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, UCL - (SLuc) Service d'hématologie et d'oncologie pédiatrique, UCL - (SLuc) Centre de malformations vasculaires congénitales, Le Rouzic, Marie-Amelyne, Fouquet, Cyrielle, Leblanc, Thierry, Touati, Mohamed, Fouyssac, Fanny, Vermylen, Christiane, Jäkel, Nadja, Guichard, Jean-François, Maloum, Karim, Toutain, Fabienne, Lutz, Patrick, Perel, Yves, Manceau, Hana, Kannengiesser, Caroline, Vannier, Jean-Pierre, UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, UCL - (SLuc) Service d'hématologie et d'oncologie pédiatrique, UCL - (SLuc) Centre de malformations vasculaires congénitales, Le Rouzic, Marie-Amelyne, Fouquet, Cyrielle, Leblanc, Thierry, Touati, Mohamed, Fouyssac, Fanny, Vermylen, Christiane, Jäkel, Nadja, Guichard, Jean-François, Maloum, Karim, Toutain, Fabienne, Lutz, Patrick, Perel, Yves, Manceau, Hana, Kannengiesser, Caroline, and Vannier, Jean-Pierre

Abstract

The most frequent germline mutations responsible for non syndromic congenital sideroblastic anemia are identified in ALAS2 and SLC25A38 genes. Iron overload is a key issue and optimal chelation therapy should be used to limit its adverse effects on the development of children. Our multicentre retrospective descriptive study compared the strategies for diagnosis and management of congenital sideroblastic anemia during the follow-up of six patients with an ALAS2 mutation and seven patients with an SLC25A38 mutation. We described in depth the clinical, biological and radiological phenotype of these patients at diagnosis and during follow-up and highlighted our results with a review of available evidence and data on the management strategies for congenital sideroblastic anemia. This report confirms the considerable variability in manifestations among patients with ALAS2 or SLC25A38 mutations and draws attention to differences in the assessment and the monitoring of iron overload and its complications. The use of an international registry would certainly help defining recommendations for the management of these rare disorders to improve patient outcome.

Published
2017

44. Erythropoietic Protoporphyric Red Blood Cells Are Resistant to the Growth of Malarial Parasites

Author

McMorran, Brendan John, primary, Smith, Clare M, additional, Jerkovic, Ante, additional, Puy, Hervé, additional, Winship, Ingrid, additional, Deybach, Jean-Charles, additional, Gouya, Laurent, additional, van Dooren, Giel, additional, Goodman, Christopher Dean, additional, Sturm, Angelika, additional, Manceau, Hana, additional, McFadden, Geoffrey Ian, additional, David, Peter, additional, Mercereau-Puijalon, Odile, additional, Burgio, Gaetan, additional, and Foote, Simon J, additional

Published
2014
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46. TSPO2 translocates 5-aminolevulinic acid into human erythroleukemia cells

Author

Caroline Schmitt, Hugo R Sugier, Katell Peoc'h, Sophie D. Lefevre, Laurent Gouya, Hana Manceau, Claude Hattab, Hervé Puy, Mariano A. Ostuni, Arienne Mirmiran, Jean-Jacques Lacapère, Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hôpital Beaujon, Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Biologie Intégrée du Globule Rouge (BIGR (UMR_S_1134 / U1134)), Institut National de la Transfusion Sanguine [Paris] (INTS)-Université Paris Diderot - Paris 7 (UPD7)-Université de La Réunion (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université des Antilles (UA), Centre Français des Porphyries, Hôpital Louis Mourier - AP-HP [Colombes], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Louis Mourier - AP-HP [Colombes], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Laboratoire des biomolécules (LBM UMR 7203), Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Département de Chimie - ENS Paris, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Chimie Moléculaire de Paris Centre (FR 2769), Institut de Chimie du CNRS (INC)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Hôpital Beaujon [AP-HP], Chimie Moléculaire de Paris Centre (FR 2769), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Département de Chimie - ENS Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Manceau, Hana

Subjects
[SDV.BBM.BS] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Structural Biology [q-bio.BM], Green Fluorescent Proteins, Protoporphyrins, Receptors, Cytoplasmic and Nuclear, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Transfection, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Porphobilinogen, Translocator protein, Humans, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], Heme, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, [SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], 030304 developmental biology, 0303 health sciences, biology, Protoporphyrin IX, [SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Structural Biology [q-bio.BM], Cell Membrane, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, [SDV.BBM.MN]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], Biological Transport, Cell Biology, General Medicine, Membrane transport, Isoquinolines, Transmembrane protein, Levulinic Acids, chemistry, Membrane protein, Biochemistry, [SDV.BBM.MN] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular Networks [q-bio.MN], biology.protein, Leukemia, Erythroblastic, Acute, K562 Cells, 030217 neurology & neurosurgery, K562 cells
Abstract

International audience; Background: 5-aminolevulinic acid (ALA) is the first precursor of heme biosynthesis pathway. The exogenous addition of ALA to cells leads to protoporphyrin IX (PPIX) accumulation that has been exploited in photodynamic diagnostic and photodynamic therapy. Several types of ALA transporters have been described depending on the cell type, but there was no clear entry pathway for erythroid cells. The 18 kDa translocator protein (TSPO) has been proposed to be involved in the transport of porphyrins and heme analogs.Results: ALA-induced PPIX accumulation in erythroleukemia cells (UT-7, K562) was impaired by PK 11195, a competitive inhibitor of both transmembrane proteins TSPO (1 and 2). PK 11195 did not modify the activity of the enzymes of heme biosynthesis, suggesting that ALA entry at the plasma membrane was the limiting factor. In contrast, porphobilinogen (PBG)-induced PPIX accumulation was not affected by PK 11195, suggesting that plasma membrane TSPO2 is a selective transporter of ALA. Overexpression of TSPO2 at the plasma membrane of erythroleukemia cells increased ALA-induced PPIX accumulation, confirming the role of TSPO2 in the import of ALA into the cells.Conclusions: ALA-induced PPIX accumulation in erythroid cells involves TSPO2 as a selective translocator through the plasma membrane. Significance: This is the first characterization of molecular mechanisms involving a new actor in ALA transport in ALA-induced PPIX accumulation in erythroleukemia cells, which could be inhibited by specific drug ligands.

Published
2019
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47. Reversible atransferrinemia in a patient with chronic enteropathy: is transferrin mandatory for iron transport?

Author

Raynor A, Stefanescu C, Bruneel A, Puy H, Peoc'h K, and Manceau H

Subjects
Adult, Humans, Hemoglobins, Female, Iron, Transferrin deficiency, Metal Metabolism, Inborn Errors
Abstract

Herein, we report the case of a 42-year-old woman, hospitalized in a French tertiary hospital for a relapse of a chronic enteropathy, who was found on admission to have no detectable serum transferrin. Surprisingly, she only exhibited mild anaemia. This atransferrinemia persisted for two months throughout her hospitalization, during which her haemoglobin concentration remained broadly stable. Based on her clinical history and evolution, we concluded to an acquired atransferrinemia secondary to chronic undernutrition, inflammation and liver failure. We discuss the investigations performed in this patient, and hypotheses regarding the relative stability of her haemoglobin concentration despite the absence of detectable transferrin., Competing Interests: Potential conflict of interest None declared., (Croatian Society of Medical Biochemistry and Laboratory Medicine.)

Published
2023
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48. Neglected Comorbidity of Chronic Heart Failure: Iron Deficiency.

Author

Manceau H, Ausseil J, Masson D, Feugeas JP, Sablonniere B, Guieu R, Puy H, and Peoc'h K

Subjects
Chronic Disease, Comorbidity, Ferric Compounds, Humans, Iron, Maltose, Quality of Life, Anemia, Iron-Deficiency diagnosis, Anemia, Iron-Deficiency epidemiology, Anemia, Iron-Deficiency etiology, Heart Failure complications, Heart Failure diagnosis, Heart Failure epidemiology, Iron Deficiencies
Abstract

Iron deficiency is a significant comorbidity of heart failure (HF), defined as the inability of the myocardium to provide sufficient blood flow. However, iron deficiency remains insufficiently detected. Iron-deficiency anemia, defined as a decrease in hemoglobin caused by iron deficiency, is a late consequence of iron deficiency, and the symptoms of iron deficiency, which are not specific, are often confused with those of HF or comorbidities. HF patients with iron deficiency are often rehospitalized and present reduced survival. The correction of iron deficiency in HF patients is associated with improved functional capacity, quality of life, and rehospitalization rates. Because of the inflammation associated with chronic HF, which complicates the picture of nutritional deficiency, only the parenteral route can bypass the tissue sequestration of iron and the inhibition of intestinal iron absorption. Given the negative impact of iron deficiency on HF progression, the frequency and financial implications of rehospitalizations due to decompensation episodes, and the efficacy of this supplementation, screening for this frequent comorbidity should be part of routine testing in all HF patients. Indeed, recent European guidelines recommend screening for iron deficiency (serum ferritin and transferrin saturation coefficient) in all patients with suspected HF, regular iron parameters assessment in all patients with HF, and intravenous iron supplementation in symptomatic patients with proven deficiency. We thus aim to summarize all currently available data regarding this common and easily improvable comorbidity.

Published
2022
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50. Rare microcytic anemias.

Author

Puy H, Manceau H, Karim Z, and Kan-Nengiesser C

Subjects
Heme biosynthesis, Humans, Iron metabolism, Rare Diseases, Anemia, Iron-Deficiency genetics
Abstract

Microcytic anemia is often due to disorder of globin genes. Here, we focus on rare monogenic microcytic anemias, We describe the diferent congenital forms that are due to mutations in genes implicated in iron homeostasis, the heme biosynthesis pathway, the cluster Fe-S biosynthesis pathway andmitochondrial proteins biosynthesis pathway. Among rare congenital microcytic anemias, most frequent forms are non syndromic sideroblastic anemias and iron refractory iron deficiency anemias (IRIDA). Sideroblastic anemias is characterized by mitochondrial iron overload and presence of ring sideroblasts in patient bone marrow.. IRIDA results from bi-allelic mutations of TMPRSS6 gene encoding Matriptase-2. Matriptase-2 protein is a transmembrane serine protease that plays an essential role in down-regulating hepcidin, the key regulator of iron homeostasis. The next generation sequencing would be helpful to identify the genes implicated in unexplained rare anemias.

Published
2016

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