Soluble TNFα receptor type I and hepcidin as determinants of development of anemia in the long-term follow-up of heart failure patients

• Published in: Clinical biochemistry Vol. 45; no. 16-17; pp. 1455 - 1458
• Main Authors: Martínez-Ruiz, A., Tornel-Osorio, P.L., Sánchez-Más, J., Pérez-Fornieles, J., Vílchez, J.A., Martínez-Hernández, P., Pascual-Figal, D.A.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01-11-2012; Elsevier
• Subjects: Adult; Aged; Anemia; Anemia - blood; Anemia - etiology; Anemia - physiopathology; Anemias. Hemoglobinopathies; Antimicrobial Cationic Peptides - blood; Biological and medical sciences; Cardiology. Vascular system; Chronic Disease; Diseases of red blood cells; Female; Follow-Up Studies; Growth Differentiation Factor 15 - blood; Heart; Heart failure; Heart Failure - blood; Heart Failure - complications; Heart Failure - physiopathology; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Hematologic and hematopoietic diseases; Hemoglobins - metabolism; Hepcidins; Humans; Inflammation; Investigative techniques, diagnostic techniques (general aspects); Iron - deficiency; Iron metabolism; Linear Models; Male; Medical sciences; Middle Aged; Natriuretic Peptide, Brain - blood; Prospective Studies; Receptors, Tumor Necrosis Factor, Type I - blood; Stroke Volume; Troponin T - blood; CHF; CRP; Heart failure; sTNFRI; IL6; Iron metabolism; Hs TnT; GDF15; Anemia; sTfR; Inflammation; NT proBNP; Human; Cytokine; Cardiovascular disease; Hemopathy; Iron; Soluble form; Metabolism; Long term; Follow up study; Heart disease; Clinical biology; Development; Hepcidin; Tumor necrosis factor α; Biological receptor
• ISSN: 0009-9120; 1873-2933
• DOI: 10.1016/j.clinbiochem.2012.05.011

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.
Fifty-nine patients (54±14years, 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 1year after inclusion.
Baseline hemoglobin (g/dL) was 14.7±1.5 and at 1year 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 1year 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.
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.
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► Patients with heart failure who are still non-anemic were studied. ► Parameters of iron metabolism, inflammation and myocardial stress were measured. ► A higher sTNFRI at baseline predicted a significant decrease in hemoglobin at 1-year. ► The increase in hepcidin over time was also associated with a decrease in hemoglobin. ► Inflammation and iron metabolism were the main determinants of anemia development.