P S Helliwell1, S Jackson. 1. Rheumatology and Rehabilitation Research Unit, Leeds, United Kingdom.
Abstract
OBJECTIVE: To relate weakness of grip to loss of forearm muscle bulk, hand joint deformity, and hand joint tenderness in patients with rheumatoid arthritis (RA). METHODS: Using anthropometric data we have estimated the anatomical cross-sectional area (CSA) of forearm muscles in 100 subjects with RA compared with 100 aged and sex-matched normal subjects. We also recorded hand joint tenderness using a modification of the Ritchie articular index, and a simple index of hand joint deformity. RESULTS: We found a significant reduction in anatomical CSA in RA (forearm CSA in normal subjects 29.7 cm2 and in RA 25.9 cm2; p = 0.002). In simple linear regression we found that 46.3% of the variation in grip strength in normal subjects was explained by variation in muscle CSA; in RA this figure decreased to 33.4%. Adding terms for joint deformity and pain in a multiple regression model improved the amount of variation explained to 37.9%. CONCLUSIONS: Although there is significant muscle wasting in RA, it is likely that reduction in strength is also attributable to joint deformity and pain leading to inhibition of grip directly and, indirectly, by arthrogenous muscle inhibition. Doubts remain about the quality of muscle in RA.
OBJECTIVE: To relate weakness of grip to loss of forearm muscle bulk, hand joint deformity, and hand joint tenderness in patients with rheumatoid arthritis (RA). METHODS: Using anthropometric data we have estimated the anatomical cross-sectional area (CSA) of forearm muscles in 100 subjects with RA compared with 100 aged and sex-matched normal subjects. We also recorded hand joint tenderness using a modification of the Ritchie articular index, and a simple index of hand joint deformity. RESULTS: We found a significant reduction in anatomical CSA in RA (forearm CSA in normal subjects 29.7 cm2 and in RA 25.9 cm2; p = 0.002). In simple linear regression we found that 46.3% of the variation in grip strength in normal subjects was explained by variation in muscle CSA; in RA this figure decreased to 33.4%. Adding terms for joint deformity and pain in a multiple regression model improved the amount of variation explained to 37.9%. CONCLUSIONS: Although there is significant muscle wasting in RA, it is likely that reduction in strength is also attributable to joint deformity and pain leading to inhibition of grip directly and, indirectly, by arthrogenous muscle inhibition. Doubts remain about the quality of muscle in RA.
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