title: Soluble TNFα receptor type I and hepcidin as determinants of development of anemia in the long-term follow-up of heart failure patients.
abstract: BACKGROUND
  Anemia is common in patients with chronic heart failure (CHF) and is associated with a worse prognosis. This study aims to identify the biological mechanisms which reflect evolutionary changes in the hemoglobin concentrations in heart failure patients who are still not anaemic.
  
  
  METHODS
  Fifty-nine patients (54 ± 14 years, 83% males) with CHF (LVEF 28 ± 10%), who did not have anemia, and had not received any previous transfusions, were included. The parameters studied were: iron metabolism (ferritin, iron, transferrin, soluble transferrin receptor (sTfR), hepcidin); inflammation (C-reactive protein, soluble TNFα receptor I (sTNFRI), interleukin 6); and myocardial stress (NT-proBNP, high sensitivity TnT, growth differentiation factor 15). All parameters were measured on inclusion and 1 year after inclusion.
  
  
  RESULTS
  Baseline hemoglobin (g/dL) was 14.7 ± 1.5 and at 1 year of follow-up it showed a significant decrease of -0.4 (RIC: -0.7 to -0.06) (p=0.02). At baseline, only the sTNFRI was a predictor of a decrease in hemoglobin 1 year later (p=0.007). During follow-up, the increase in sTNFRI (p=0.002, r=-0.39) and hepcidin (p=0.006, r=-0.35) were both associated with a decrease in hemoglobin. Similarly, the patients who became anemic (13%) had higher levels of hepcidin (p=0.001) and sTNFRI (p=0.008). The remaining parameters did not show any relationship with the evolution in the hemoglobin.
  
  
  CONCLUSIONS
  In CHF patients without anemia, the increase in the inflammatory state (sTNFRI) and the following deterioration in the iron metabolism (hepcidin) were the main determinants of a decrease in hemoglobin and the appearance of anemia in the long term follow-up period.
authors.affiliation: Clinical Analysis Department, Virgen de Arrixaca University Hospital, Murcia, Spain. anamr82@gmail.com
authors.forename: A
authors.initials: A
authors.lastname: Martínez-Ruiz
authors.forename: P L
authors.initials: PL
authors.lastname: Tornel-Osorio
authors.forename: J
authors.initials: J
authors.lastname: Sánchez-Más
authors.forename: J
authors.initials: J
authors.lastname: Pérez-Fornieles
authors.forename: J A
authors.initials: JA
authors.lastname: Vílchez
authors.forename: P
authors.initials: P
authors.lastname: Martínez-Hernández
authors.forename: D A
authors.initials: DA
authors.lastname: Pascual-Figal
mesh_terms: D000328:Adult; D000368:Aged; D000740:Anemia / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D023181:Antimicrobial Cationic Peptides / Q000097:blood*; D002908:Chronic Disease; D005260:Female; D005500:Follow-Up Studies; D055436:Growth Differentiation Factor 15 / Q000097:blood; D006333:Heart Failure / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D006454:Hemoglobins / Q000378:metabolism; D064451:Hepcidins; D006801:Humans; D000090463:Iron Deficiencies; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011446:Prospective Studies; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood*; D013318:Stroke Volume; D020107:Troponin T / Q000097:blood
chemical_list: D023181:Antimicrobial Cationic Peptides; C526140:GDF15 protein, human; D055436:Growth Differentiation Factor 15; C578702:HAMP protein, human; D006454:Hemoglobins; D064451:Hepcidins; D047888:Receptors, Tumor Necrosis Factor, Type I; D020107:Troponin T; D020097:Natriuretic Peptide, Brain