Fat-corrected T2 measurement as a marker of active muscle disease in inflammatory myopathy

We sought to improve the utility of T2 measurement as a marker of active muscle disease in patients with idiopathic inflammatory myopathy by correcting for T2 prolongations caused by fatty replacement of muscle that accompnaies chronic muscle damage. Twenty-one patients with idiopathic inflammatory...

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Veröffentlicht in:American journal of roentgenology (1976) 2012-05, Vol.198 (5), p.W475-W481
Hauptverfasser: Yao, Lawrence, Gai, Neville
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Sprache:eng
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Zusammenfassung:We sought to improve the utility of T2 measurement as a marker of active muscle disease in patients with idiopathic inflammatory myopathy by correcting for T2 prolongations caused by fatty replacement of muscle that accompnaies chronic muscle damage. Twenty-one patients with idiopathic inflammatory myopathy underwent a standardized MRI evaluation of the thighs. Fat fraction maps were calculated from dual-echo gradient-echo images. Fat-corrected T2 maps were generated from multiecho spin-echo images on the basis of a biexponential model that incorporated voxelwise fat fraction estimates. Semiautomated summaries of conventional and fat-corrected muscle T2 values were compared with one another and with standardized visual scores of muscle disease based on T1-weighted spin-echo and STIR images. Fat-corrected muscle T2 maps showed lower mean values and greater histogram entropy than conventional T2 maps, as analyzed over a standardized portion of the thigh muscles. Conventional and fat-corrected T2 values correlated with visual scores of active muscle disease on STIR images and with the varying intensity of disease depicted with STIR in focal muscle regions. MRI T2 maps of muscle can be corrected for varying fat content by combining the information from chemical shift-sensitive gradient-echo and multiecho spin-echo images. Use of this strategy may prove useful in the study of idiopathic inflammatory myopathy and other diseases characterized by both muscle inflammation and atrophy.
ISSN:0361-803X
1546-3141
DOI:10.2214/ajr.11.7113