LIPID STORAGE MYOPATHY ASSOCIATED WITH LOW ACYL-COA DEHYDROGENASE ACTIVITIES

Abstract
A man with a painful proximal myopathy had excess lipid deposition in skeletal muscle, excretion of dicarboxylic acids in urine and low acyl-CoA dehydrogenase activities in skeletal muscle mitochondria. In addition he had little immunoreactive short-chain and medium-chain acyl-CoA dehydrogenase enzyme protein compared with normal controls. Following treatment with riboflavin there was considerable improvement in his clinical condition which was confirmed by further biochemical and morphological investigations.

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