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Muscle protein synthesis in patients with rheumatoid arthritis: effect of chronic corticosteroid therapy on prostaglandin F 2α availability
Author(s) -
GIBSON J. N. A.,
POYSER N. L.,
MORRISON W. L.,
SCRIMGEOUR C. M.,
RENNIE M. J.
Publication year - 1991
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1991.tb01388.x
Subject(s) - rheumatoid arthritis , medicine , endocrinology , muscle atrophy , atrophy , muscle biopsy , osteoarthritis , leucine , prednisolone , corticosteroid , biopsy , chemistry , pathology , biochemistry , amino acid , alternative medicine
. Using stable‐isotope techniques, we measured rates of quadriceps muscle protein synthesis in twelve women with sero‐positive rheumatoid arthritis. The results were compared to those from the normal limb of seven women with unilateral osteoarthritis of the knee. Six patients had never received corticosteroid immuno‐suppression, but the other six had taken an average of 8 mg Prednisolone per day for 9 years. Quadriceps atrophy was present in both sets of patients with rheumatoid arthritis (normal legs 444 ± 182, rheumatoid 190 ± 40, rheumatoid+steroid 300 ± 110 μg protein/μg DNA, means ± SD, both P < 0·001). Muscle protein synthesis, calculated by comparing the incorporation of 13 C‐leucine into biopsy samples taken after an 8 h L‐[1‐ 13 C] leucine infusion with the time averaged enrichment of blood α‐ketoisocaproate, was 0·056 ± 0·005% h ‐1 in the patients not receiving steroids compared with 0·050 ± 0·002% h ‐1 in normals ( P > 0·05) indicating that muscular atrophy was primarily due to an increase in rate of muscle protein breakdown. Intra‐muscular PGE 2 concentration was increased in these patients (rheumatoid 0·12 ± 0·06 ng mg ‐1 tissue, normals 0·06 ± 0·03 ng mg ‐1 tissue, P <0·05). Patients taking corticosteroids had a markedly depressed rate of muscle protein synthesis (0·035 ± 0·008% h ‐1 , P <0·05) and reduced intra‐muscular PGF 2α concentration ( P <0·01). We conclude that steroid therapy significantly influences the mechanism of skeletal muscle atrophy in patients with rheumatoid arthritis.