The “Weakness” Link: Can Muscle Impairment Be Identified as a Cause of Disability in Rheumatology Patients?

Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are associated with significant physical disability, which has a substantial negative impact on employment and work productivity, as well as health-related quality of life (1,2). Therefore, a primary goal for many RA and SLE patients is to maintain or improve physical function. To effectively meet this objective, interventions should be targeted toward the underlying causes of a patient’s physical disability. This often proves difficult for health professionals because, almost invariably, multiple factors contribute to their patients’ physical disability (3), and while some may be modified through intervention (e.g., joint pain), many cannot be altered (e.g., joint damage and deformity). Therefore, the challenge for health professionals is to identify, within an individual patient, the modifiable factors that contribute to physical disability. One primary candidate factor in RA and SLE patients that should be considered for physical disability intervention is body composition. Both RA and SLE are associated with accelerated loss of muscle mass and gain in fat mass compared to healthy controls (4,5), and there is growing evidence that these abnormal body composition phenotypes are linked to disability (6,7). Body composition is potentially modifiable, and there is evidence from randomized trials that resistance training can increase lean muscle mass, decrease fat mass, and induce a concomitant improvement in physical function (8). But as mentioned earlier, physical disability is multifactorial and cannot be attributed to abnormal body composition in all patients. So how do we identify those key clinical subgroups of patients who may actually benefit from interventions aimed at maintaining a favorable body composition? In this issue of Arthritis Care & Research, Baker et al build on prior evidence that there are important sex differences in lean mass among RA patients (9). This study included 2 independent cohorts of RA patients with information on height-adjusted total and appendicular (sum of arms and legs) lean mass ascertained by dual x-ray absorptiometry (DXA). Within cohorts, lean mass indices were compared between men and women, and, to compare lean mass in RA patients to a reference population, indices were converted to sexand race-specific Z scores based on DXA data collected in the large, nationally representative National Health and Nutrition Examination Survey (NHANES). Finally, patients were classified as having “sarcopenia” based on 3 previously published criteria for low appendicular lean mass and a fourth, a criterion of lean mass 1 SD below the mean for NHANES adults ages 20–40 years. While men expectedly had greater lean mass than women in the RA cohorts, Z scores for men were significantly lower than the women, indicating greater deficits for men compared to the reference population, even after adjustment for potential confounders. Furthermore, the prevalence of sarcopenia was up to 8 times greater in men compared to women. While a few previous studies have shown similar sex differences in body composition among RA patients, this is the first to utilize published national reference ranges to demonstrate lean mass deficits, and the first to describe the prevalence of “low” lean mass based on previously used definitions. The results of the study by Baker et al (9) suggest that perhaps among male RA patients with physical disability, low lean mass should be assessed as a potential intervention target. But before DXA tests can be recommended for RA patients with physical disability, there are some important questions that still remain. First, what degree of “low” lean mass is meaningful for physical disability? Baker et al used several definitions of sarcopenia to identify low lean mass, yet the low lean mass criteria were all similarly based solely on the distribution lean mass in a healthy reference population. While these cutoffs can identify individuals with “abnormally” low lean mass, the authors point out that they provide no indication of whether this level is associated with the clinical outRobert R. McLean, DSc, MPH: Institute for Aging Research, Hebrew SeniorLife, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts. Address correspondence to Robert R. McLean, DSc, MPH, Institute for Aging Research, Hebrew SeniorLife, 1200 Centre Street, Boston, MA 02131. E-mail: rmclean@hsl.harvard. edu. Submitted for publication June 24, 2014; accepted July 1, 2014. Arthritis Care & Research Vol. 67, No. 1, January 2015, pp 1–3 DOI 10.1002/acr.22397 © 2015, American College of Rheumatology