TY - JOUR
T1 - Incomplete Palmitate Oxidation
T2 - Possible Source of Human Myopathy
AU - Shumate, Jack B.
AU - Brooke, Michael H.
AU - Carroll, James E.
AU - Choksi, Rati M.
PY - 1982/9
Y1 - 1982/9
N2 - A study of palmitate oxidation in 200 consecutive human muscle biopsy specimens showed 14 patients in whom there was abnormal, incomplete palmitate oxidation when the rate of oxidation of palmitate14C (ul) was compared with that of palmitate14C (at carbon 1). Five patients had denervation as a primary diagnosis, and the remaining nine had a primary muscle disease. Of this latter group, six had clinical similarities, including proximal weakness, necrotic fibers on muscle biopsy, and extreme elevations of serum creatine kinase. With one exception, lipid storage was not part of the syndrome. The possibility of incomplete palmitate oxidation due to a defect in β-oxidation producing a human myopathy is discussed.
AB - A study of palmitate oxidation in 200 consecutive human muscle biopsy specimens showed 14 patients in whom there was abnormal, incomplete palmitate oxidation when the rate of oxidation of palmitate14C (ul) was compared with that of palmitate14C (at carbon 1). Five patients had denervation as a primary diagnosis, and the remaining nine had a primary muscle disease. Of this latter group, six had clinical similarities, including proximal weakness, necrotic fibers on muscle biopsy, and extreme elevations of serum creatine kinase. With one exception, lipid storage was not part of the syndrome. The possibility of incomplete palmitate oxidation due to a defect in β-oxidation producing a human myopathy is discussed.
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U2 - 10.1001/archneur.1982.00510210031007
DO - 10.1001/archneur.1982.00510210031007
M3 - Article
C2 - 7115144
AN - SCOPUS:0019987407
SN - 0003-9942
VL - 39
SP - 561
EP - 564
JO - Archives of Neurology
JF - Archives of Neurology
IS - 9
ER -
