Muscular dystrophies transaminases

The copious muscle enzyme efflux in Duchenne-type muscular dystrophy, giving gross serum elevations despite the rapid serum clearance, may well deplete some muscle enzymes that so much aldolase still remains may indicate a replacement so rapid that, if applied to the transaminases and to lactic dehydrogenase, the muscle content may be maintained or even increased, since their serum elevations, though considerable, are proportionately much less than that of aldolase. 

M18. Murphy, E. G., and Cherniak, M. M., Glutamic oxalacetic transaminase activity in the serum in muscular dystrophy and other neuromuscular disorders in childhood. Pediatrics 22, 1110 (1958). 

P4. Pearson, C. M., Serum enzymes in muscular dystrophy and certain other muscular and neuromuscular diseases. I. Serum glutamic oxalacetic transaminase. New Engl. ]. Med. 256, 1069 (19.57). 

A 7-year-old boy with Duchenne muscular dystrophy and attention deficit hyperactivity disorder (ADHD) developed acute hepatic failure, with features of autoimmune hepatitis (2). The only medications he had taken were pemoline (56 mg/day) and cjrproheptadine (2 mg/day). Pemoline was withdrawn after 8 months as the presumed cause of his raised transaminases. Two weeks later he developed an altered mental state, jaundice, and encephalopathy. The histological features of the liver and his autoimmune antibody panel were consistent with autoimmune hepatitis. He was treated with corticosteroids and azathioprine and recovered. 

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