Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy
Autore:
Aukrust, P; Ueland, T; Lien, E; Bendtzen, K; Muller, F; Andreassen, AK; Nordoy, I; Aass, H; Espevik, T; Simonsen, S; Froland, SS; Gullestad, L;
Indirizzi:
Univo,slo, Rikshosp, Dept Med A, Sect Clin Immunol & Infect Dis, N-0027 Osl Univ Oslo Oslo Norway N-0027 Sect Clin Immunol & Infect Dis, N-0027 Osl Univ Oslo, Rikshosp, Dept Med A, Internal Med Res Inst, N-0027 Oslo, Norway Univ Oslo Oslo Norway N-0027 Internal Med Res Inst, N-0027 Oslo, Norway Univ Oslo, Rikshosp, Dept Med B, Cardiol Sect, N-0027 Oslo, Norway Univ Oslo Oslo Norway N-0027 pt Med B, Cardiol Sect, N-0027 Oslo, Norway Norwegianorway Sci & Technol, Inst Canc Res & Mol Biol, N-7034 Trondheim, N Norwegian Univ Sci & Technol Trondheim Norway N-7034 N-7034 Trondheim, N Univmarkenhagen Hosp, Rigshosp, Inst Inflammat Res, DK-2100 Copenhagen, Den Univ Copenhagen Hosp Copenhagen Denmark DK-2100 DK-2100 Copenhagen, Den
Titolo Testata:
AMERICAN JOURNAL OF CARDIOLOGY
fascicolo: 3, volume: 83, anno: 1999,
pagine: 376 - 382
SICI:
0002-9149(19990201)83:3<376:CNICHF>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-BETA; ELEVATED CIRCULATING LEVELS; FACTOR SOLUBLE RECEPTORS; FACTOR-ALPHA; HUMAN SERUM; INTERLEUKIN-10; RELEASE; GP130; INFLAMMATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Aukrust, P Univo,slo, Rikshosp, Dept Med A, Sect Clin Immunol & Infect Dis, N-0027 Osl Univ Oslo Oslo Norway N-0027 Immunol & Infect Dis, N-0027 Osl
Citazione:
P. Aukrust et al., "Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy", AM J CARD, 83(3), 1999, pp. 376-382

Abstract

lnflammatory cytokines may play a pathogenic role in the development of congestive heart failure (CHF). Elevated circulating levels of inflammatory cytokines have been reported in CHF, but most studies have focused on only afew cytokine parameters. However, the activity of these cytokines are modulated by soluble cytokine receptors and cytokines with anti-inflammatory activities, and in the present study several of these interacting factors were examined simultaneously in 38 CHF patients with various degrees of heart failure and in 21 healthy controls. Patients with CHF had increased plasma concentrations of tumor necrosis factor (TNF)alpha, interleukin-6, soluble TNF receptors and the soluble interleukin-6 receptor, glycoprotein (gp)130. They also had elevated ratios of TNF alpha/soluble TNF receptors and interleukin-6/soluble gp130 as well as enhanced interleukin-6 bioactivity in serum, suggesting inflammatory net effects. In addition to raised circulating levels of inflammatory cytokines, CHF patients with severe heart failure also had abnormalities in the levels of anti-inflammatory cytokines, with decreased levels of transforming growth factor beta 1 and inadequately raised interleukin-10 in relation to the elevated TNF alpha concentrations. This dysbalance between inflammatory and anti-inflammatory cytokines was also found in monocyte supernatants from CHF patients. The abnormalities in the cytokine network were most pronounced in patients with the most severe heart failure, and several of the immunologic parameters, in particular soluble gp130, were correlated with variables reflecting deranged hemodynamic status. The present study analyzing the complexity of the cytokine network in CHF,demonstrates profound disturbances in the levels of both inflammatory and antiinflammatory mediators with a marked dysbalance favoring inflammatory effects. (C)1999 by Excerpta Medico, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 10:04:02