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Neil Basu, Gabe Cheung, Nicholas Senn, Karen Keenan, Gayle Hutcheon, Lars Erwig, Andrew Schrepf, Paula Dospinescu, Stuart Gray, Gordon Waiter, Jiabao He, 129 Does skeletal muscle mitochondrial dysfunction explain SLE related physical fatigue?, Rheumatology, Volume 57, Issue suppl_3, April 2018, key075.353, https://doi.org/10.1093/rheumatology/key075.353
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Background: Fatigue is considered to be one of the most pervasive and disabling aspects of SLE. The pathogenesis of fatigue is poorly understood and therapeutic options are consequentially limited. Poorly functioning mitochondria - the primary sites of cellular energy generation - may be implicated in fatigue. Since SLE patients commonly describe their fatigue to be physical in nature and attribute this as local to their skeletal muscles, we hypothesised that skeletal muscle mitochondrial dysfunction existed among SLE patients which in turn related to physical fatigue.
Methods: A case control 31P MR Spectroscopy (MRS) study was conducted. Cases were SLE patients who fulfilled 1987 ACR criteria; reported chronic (>three months) clinically relevant fatigue (defined as a score of > 3 on the Chalder fatigue binary scale, CFS) and had inactive disease (defined as BILAG2004=0, excluding the fatigue-constitutional domain). Controls were age/sex matched healthy members of the general population. Participants were scanned on a 3T whole body MR system where resting and dynamic (using within scanner exercise plantar flexion apparatus) MRS of the calf muscles was acquired. Physical fatigue was measured using the CFS Physical domain. In addition, all participants were characterised for co-variates of interest: current pain (VAS); depression (Hospital Anxiety & Depression Scale); sleep disturbance (Jenkins Sleep Scale); inflammation (ESR); and aerobic fitness (Siconolfi Step Test). Measures of ATP metabolism (phosphocreatine (PCr), pH, PCr recovery half time) were computed from the resting and dynamic MRS. These are considered valid markers of mitochondrial dysfunction. Simple descriptive statistics were applied to evaluate differences between cases and controls. Path analyses were undertaken to investigate if physical fatigue (or other co-variates of interest) mediated the relationship between mitochondrial dysfunction and group membership (i.e. case or control).
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