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

Am J Clin Nutr. 2005 Nov;82(5):1059-64. doi: 10.1093/ajcn/82.5.1059.


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 1beta (IL-1beta -511), IL-6 (IL-6 -174), and the tumor necrosis factor system (TNF-alpha -308 and lymphotoxin-alpha +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-1beta -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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism*
  • Body Composition / genetics
  • Body Composition / physiology
  • Body Mass Index
  • C-Reactive Protein / metabolism
  • Cachexia / metabolism*
  • Case-Control Studies
  • Cross-Sectional Studies
  • Electric Impedance
  • Energy Metabolism / genetics
  • Energy Metabolism / physiology
  • Female
  • Genetic Predisposition to Disease
  • Humans
  • Interleukin-1 / blood
  • Interleukin-1 / genetics*
  • Interleukin-6 / blood
  • Interleukin-6 / genetics
  • Leptin / blood
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide*
  • Pseudouridine / urine
  • Pulmonary Disease, Chronic Obstructive / immunology*
  • Pulmonary Disease, Chronic Obstructive / metabolism*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism


  • Interleukin-1
  • Interleukin-6
  • Leptin
  • Tumor Necrosis Factor-alpha
  • Pseudouridine
  • C-Reactive Protein