Pulmonary cachexia, systemic inflammatory profile, and the interleukin 1ß -511 single nucleotide polymorphism

Broekhuizen, Roelinka, Grimble, Robert F., Howell, W. Martin, Shale, Dennis J., Creutzberg, Eva C., Wouters, Emiel F. and Schols, Annemie M. (2005) Pulmonary cachexia, systemic inflammatory profile, and the interleukin 1ß -511 single nucleotide polymorphism American Journal of Clinical Nutrition, 82, (5), pp. 1059-1064.


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Background: Cachexia is common in chronic obstructive pulmonary disease (COPD) and is thought to be linked to an enhanced systemic inflammatory response.
Objective: We investigated differences in the systemic inflammatory profile and polymorphisms in related inflammatory genes in COPD patients.
Design: A cross-sectional study was performed in 99 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease stages II–IV), who were stratified by cachexia based on fat-free mass index (FFMI; in kg/m2: <16 for men and <15 for women) and compared with healthy control subjects (HCs). Body composition was determined by bioelectrical impedance analysis. Plasma concentrations and gene polymorphisms of interleukin 1ß (IL-1ß –511), IL-6 (IL-6 –174), and the tumor necrosis factor system (TNF- –308 and lymphotoxin- +252) were determined. Plasma C-reactive protein, leptin, and urinary pseudouridine (as a marker of cellular protein breakdown) were measured.
Results: Fat mass, leptin, and pseudouridine were significantly different (P < 0.001) between noncachectic patients (NCPs) and cachectic patients (CPs: n = 35); the systemic inflammatory cytokine profile was not. NCPs had a body compositional shift toward a lower fat-free mass and a higher fat mass compared with HCs. CPs and NCPs had a greater systemic inflammatory response (P < 0.05) than did HCs, as reflected in C-reactive protein, soluble TNF-R75, and IL-6 concentrations. The overall distribution of the IL-1ß –511 polymorphism was significantly different between the groups (P < 0.05).
Conclusions: In COPD patients, who are characterized by an elevated systemic inflammatory response, cachexia is not discriminatory for the extent of increase in inflammatory status. This study, however, indicates a potential influence of genetic predisposition on the cachexia process.

Item Type: Article
Additional Information: Original research communication
ISSNs: 0002-9165 (print)
Related URLs:
Keywords: chronic obstructive pulmonary disease, copd, body composition, inflammation, polymorphism, cachexia, protein breakdown, leptin

ePrint ID: 25280
Date :
Date Event
November 2005Published
Date Deposited: 10 Apr 2006
Last Modified: 16 Apr 2017 22:37
Further Information:Google Scholar
URI: http://eprints.soton.ac.uk/id/eprint/25280

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