Rheumatoid cachexia: metabolic abnormalities, mechanisms and interventions

被引:183
作者
Rall, LC
Roubenoff, R
机构
[1] Marshfield Clin Res Fdn, Epidemiol Res Ctr, Marshfield, WI 54449 USA
[2] Millennium Pharmaceut Inc, Cambridge, MA USA
[3] Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA 02111 USA
关键词
rheumatoid arthritis; cachexia; protein metabolism; muscle; body cell mass; interleukin-1; beta; tumour necrosis factor-alpha; exercise;
D O I
10.1093/rheumatology/keh321
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We have previously identified the phrase 'rheumatoid cachexia' to describe the loss of body cell mass (BCM) that may occur among patients with rheumatoid arthritis (RA). Specifically, rheumatoid cachexia is characterized by altered energy and protein metabolism (reduced total energy expenditure, increased resting energy expenditure and increased whole-body protein catabolism) and increased inflammatory cytokine production (interleukin-1beta and tumour necrosis factor-alpha). Patients with rheumatoid cachexia consistently have a diet that appears adequate in protein and calories (based on US Dietary Reference Intakes), but with reduced physical activity. These phenomena are similar to some of the metabolic abnormalities that occur with normal ageing, but the aetiology appears to be different in RA. This review will focus on describing the metabolic abnormalities observed in rheumatoid cachexia, identifying potential mechanisms for loss of BCM and discussing strategies for intervention.
引用
收藏
页码:1219 / 1223
页数:5
相关论文
共 56 条
[1]   Exercise can reverse quadriceps sensorimotor dysfunction that is associated with rheumatoid arthritis without exacerbating disease activity [J].
Bearne, LM ;
Scott, DL ;
Hurley, MV .
RHEUMATOLOGY, 2002, 41 (02) :157-166
[2]   INCREASED INTERLEUKIN-1-BETA IN HUMAN SKELETAL-MUSCLE AFTER EXERCISE [J].
CANNON, JG ;
FIELDING, RA ;
FIATARONE, MA ;
ORENCOLE, SF ;
DINARELLO, CA ;
EVANS, WJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (02) :R451-R455
[3]  
Castagnetta LA, 2003, J RHEUMATOL, V30, P2597
[4]  
CHIKANZA IC, 1995, J RHEUMATOL, V22, P600
[5]   Mechanisms of disease: Cytokine pathways and joint inflammation in rheumatoid arthritis. [J].
Choy, EHS ;
Panayi, GS .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (12) :907-916
[6]   MUSCLE PROTEOLYSIS INDUCED BY A CIRCULATING PEPTIDE IN PATIENTS WITH SEPSIS OR TRAUMA [J].
CLOWES, GHA ;
GEORGE, BC ;
VILLEE, CA ;
SARAVIS, CA .
NEW ENGLAND JOURNAL OF MEDICINE, 1983, 308 (10) :545-552
[7]   Hypothalamic-pituitary-adrenocortical and gonadal functions in rheumatoid arthritis [J].
Cutolo, M ;
Sulli, A ;
Pizzorni, C ;
Craviotto, C ;
Straub, RH .
NEUROENDOCRINE AND NEURAL REGULATION OF AUTOIMMUNE AND INFLAMMATORY DISEASE: MOLECULAR, SYSTEMS, AND CLINICAL INSIGHTS, 2003, 992 :107-117
[8]   Tumor necrosis factor α produces insulin resistance in skeletal muscle by activation of inhibitor κB kinase in a p38 MAPK-dependent manner [J].
de Alvaro, C ;
Teruel, T ;
Hernandez, R ;
Lorenzo, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (17) :17070-17078
[9]   Is a long-term high-intensity safe in patients with exercise program effective and rheumatoid arthritis? Results of a randomized controlled trial [J].
de Jong, Z ;
Munneke, M ;
Zwinderman, AH ;
Kroon, HM ;
Jansen, A ;
Ronday, KH ;
van Schaardenburg, D ;
Dijkmans, BAC ;
Van den Ende, CHM ;
Breedveld, FC ;
Vlieland, TPMV ;
Hazes, JMW .
ARTHRITIS AND RHEUMATISM, 2003, 48 (09) :2415-2424
[10]  
Dessein PH, 2002, J RHEUMATOL, V29, P462