Concepedia

Abstract

Summary Background Muscle wasting or sarcopenia arising from chronic inflammation is found in 60% of patients with Crohn's disease. Transcriptional protein NF ‐κB reduces muscle formation through MyoD transcription and increases muscle breakdown by proteolysis. Aim As TNF is a potent activator of NF ‐κB, and anti‐ TNF agent infliximab ( IFX ) prevents NF ‐κB activation, to determine whether or not Crohn's patients treated with IFX gain muscle volume and strength. Methods We performed a prospective, repeated‐measures cohort study in adult Crohn's disease patients with an acute disease flare. Patients were instructed not to vary diet or activity. Concomitant medications were kept stable. At week 1 (pre‐treatment), week 16 (post‐ IFX induction) and week 25 (post‐first IFX maintenance dose), we assessed (i) MRI volume of quadriceps femoris at anatomical mid‐thigh; (ii) maximal concentric quadriceps contractions strength at three specific speeds of contraction; (iii) physical activity by validated instrument ( IPAQ ); (iv) Three‐day food record of intake and composition (food‐weighing method); (v) Serum levels of IL 6. Results Nineteen patients (58% female; mean age 33.2 ± 10.7 years) were recruited. IFX increased muscle volume in both legs from baseline (right, 1505 cm 3 ) to week 25 (right, 1569 cm 3 ; P = 0.010). IFX also increased muscle strength in both legs from baseline (right 30°/s, 184.8 Nm) to week 25 (right 30°/s, 213.6 Nm; P = 0.002). Muscle volume gain correlated with male gender ( P = 0.003). Significant gains in muscle volume and strength were unrelated to prednisolone use. Serum IL 6 levels decreased by week 25 ( P = 0.037). Conclusion The anti‐TNF agent infliximab reverses inflammatory sarcopenia in patients with Crohn's disease.

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