|
|
||||||||
ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Respiratory Medicine, University Hospital Maastricht, Netherlands (RB, EFW, and AMS); the School of Medicine, University of Southampton, Southampton, United Kingdom (RFG and WMH); the Section of Respiratory Medicine, Cardiff University, Cardiff, United Kingdom (DJS); and the Asthma Centre Hornerheide, Horn, Netherlands (ECC)
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 IIIV), 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.
Key Words: Chronic obstructive pulmonary disease COPD body composition inflammation polymorphism cachexia protein breakdown leptin
This article has been cited by other articles:
![]() |
J. Smolonska, C. Wijmenga, D. S. Postma, and H. M. Boezen Meta-analyses on Suspected Chronic Obstructive Pulmonary Disease Genes: A Summary of 20 Years' Research Am. J. Respir. Crit. Care Med., October 1, 2009; 180(7): 618 - 631. [Abstract] [Full Text] [PDF] |
||||
![]() |
J-Q He, M G Foreman, K Shumansky, X Zhang, L Akhabir, D D Sin, S F P Man, D L DeMeo, A A Litonjua, E K Silverman, et al. Associations of IL6 polymorphisms with lung function decline and COPD Thorax, August 1, 2009; 64(8): 698 - 704. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. J. H. Sillen, C. M. Speksnijder, R.-M. A. Eterman, P. P. Janssen, S. S. Wagers, E. F. M. Wouters, N. H. M. K. Uszko-Lencer, and M. A. Spruit Effects of Neuromuscular Electrical Stimulation of Muscles of Ambulation in Patients With Chronic Heart Failure or COPD: A Systematic Review of the English-Language Literature Chest, July 1, 2009; 136(1): 44 - 61. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. J. Barnes and B. R. Celli Systemic manifestations and comorbidities of COPD Eur. Respir. J., May 1, 2009; 33(5): 1165 - 1185. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. C. Deans, B. H. Tan, J. A Ross, M. Rose-Zerilli, S. J Wigmore, W M. Howell, R. F Grimble, and K. C. Fearon Cancer cachexia is associated with the IL10 -1082 gene promoter polymorphism in patients with gastroesophageal malignancy Am. J. Clinical Nutrition, April 1, 2009; 89(4): 1164 - 1172. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Laviano, A. Inui, D. L. Marks, M. M. Meguid, C. Pichard, F. Rossi Fanelli, and M. Seelaender Neural control of the anorexia-cachexia syndrome Am J Physiol Endocrinol Metab, November 1, 2008; 295(5): E1000 - E1008. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. D. Wagner Possible mechanisms underlying the development of cachexia in COPD Eur. Respir. J., March 1, 2008; 31(3): 492 - 501. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. H. Remels, P. Schrauwen, R. Broekhuizen, J. Willems, S. Kersten, H. R. Gosker, and A. M. Schols Peroxisome proliferator-activated receptor expression is reduced in skeletal muscle in COPD Eur. Respir. J., August 1, 2007; 30(2): 245 - 252. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. J. Barnes Unexpected Failure of Anti-Tumor Necrosis Factor Therapy in Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., May 1, 2007; 175(9): 866 - 867. [Full Text] [PDF] |
||||
![]() |
E. P. Rutten, F. M. Franssen, M. P. Engelen, E. F. Wouters, N. E. Deutz, and A. M. Schols Greater whole-body myofibrillar protein breakdown in cachectic patients with chronic obstructive pulmonary disease. Am. J. Clinical Nutrition, April 1, 2006; 83(4): 829 - 834. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |