Broekhuizen Roelinka, Grimble Robert F, Howell W Martin, Shale Dennis J, Creutzberg Eva C, Wouters Emiel F, Schols Annemie M
Department of Respiratory Medicine, University Hospital Maastricht, The Netherlands.
Am J Clin Nutr. 2005 Nov;82(5):1059-64. doi: 10.1093/ajcn/82.5.1059.
Cachexia is common in chronic obstructive pulmonary disease (COPD) and is thought to be linked to an enhanced systemic inflammatory response.
We investigated differences in the systemic inflammatory profile and polymorphisms in related inflammatory genes in COPD patients.
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.
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).
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.
恶病质在慢性阻塞性肺疾病（COPD）中很常见，被认为与全身炎症反应增强有关。
我们研究了COPD患者全身炎症特征及相关炎症基因多态性的差异。
对99例COPD患者（慢性阻塞性肺疾病全球倡议组织II-IV期）进行了一项横断面研究，根据无脂肪质量指数（FFMI；单位为kg/m2：男性<16，女性<15）将患者分为恶病质组和非恶病质组，并与健康对照者（HCs）进行比较。通过生物电阻抗分析测定身体成分。测定白细胞介素1β（IL-1β -511）、IL-6（IL-6 -174）和肿瘤坏死因子系统（TNF-α -308和淋巴毒素-α +252）的血浆浓度和基因多态性。测量血浆C反应蛋白、瘦素和尿假尿苷（作为细胞蛋白分解的标志物）。
非恶病质患者（NCPs）和恶病质患者（CPs：n = 35）之间的脂肪量、瘦素和假尿苷有显著差异（P < 0.001）；全身炎症细胞因子谱无差异。与HCs相比，NCPs的身体成分向较低的无脂肪质量和较高的脂肪量转变。CPs和NCPs的全身炎症反应比HCs更强（P < 0.05），这在C反应蛋白、可溶性TNF-R75和IL-6浓度中得到体现。IL-1β -511多态性的总体分布在各组之间有显著差异（P < 0.05）。
在以全身炎症反应升高为特征的COPD患者中，恶病质对炎症状态增加的程度没有鉴别作用。然而，本研究表明遗传易感性对恶病质过程有潜在影响。
