RT Journal Article
SR Electronic
T1 Body weight, body composition, and bone turnover changes in patients with spondyloarthropathy receiving anti-tumour necrosis factor α treatment
JF Annals of the Rheumatic Diseases
JO Ann Rheum Dis
FD BMJ Publishing Group Ltd and European League Against Rheumatism
SP 1137
OP 1140
DO 10.1136/ard.2004.028670
VO 64
IS 8
A1 K Briot
A1 P Garnero
A1 A Le Henanff
A1 M Dougados
A1 C Roux
YR 2005
UL http://ard.bmj.com/content/64/8/1137.abstract
AB Objectives: To determine the changes in body weight, body composition, and bone turnover in patients with spondyloarthropathy (SpA) treated with anti-tumour necrosis factor α (TNFα).Patients and methods: 19 patients with SpA (2 women, 17 men), aged 21–71 years, were studied in a 1 year prospective open study. 17 patients received infliximab: 3 or 5 mg/kg/infusion at weeks 0, 2, 6 and infusions in the case of a relapse (n = 14) or systematically (n = 3); 2 patients received etanercept (25 mg twice a week). Body weight, body composition (lean mass, fat mass), and bone mineral density (BMD; using dual energy x ray absorptiometry) were measured at baseline and at months 6 and 12. Serum insulin-like growth factor-I (IGF-I), bone markers (carboxy terminal telopeptide of collagen Ι (CTX) and procollagen type Ι N terminal propeptide (PINP)) were measured at baseline and months 3, 6, and 12.Results: In 1 year there was a significant increase in body weight (mean (SD) 2.24 (3.1) kg, p = 0.0004), and in lean mass (1.4 (1.69) kg, p = 0.005), but no changes in fat mass. BMD increased at the spine (5.6%, p = 0.0005) and total femur (2.6%, p = 0.01). CTX decreased from the third month (−50%, p = 0.005) up to 1 year (−30%, p = 0.012), and a trend for an increase in PINP (10%, p = 0.06) and in IGF-I (15%, p = 0.04) was seen at month 3.Conclusion: These data confirm that treatment with anti-TNFα in SpA is associated with an increase of BMD, which results from a decrease of bone resorption. Increase in body weight and lean mass is observed in parallel with an increase in IGF-1.