Valproic acid itself can cause high concentrations of ammonia in the serum
of patients with normal urea cycle enzymes but may also worsen a
pre-existing hyperammonaemia caused by an enzymatic defect of the urea cycle
due to its ability to inhibit ureagenesis. There is an association between
valproate therapy and undiagnosed OCT deficiency. A few references are
attached, but their have been cases where an individual with undiagnosed OCT
deficeincy has been put on valproate and has subsequently presented in a
coma with hyperammonaemia.
Oechsner et al. Hyperammonaemic encephalopathy after initiation of valproate
therapy in unrecognised ornithine transcarbamylase deficiency. Journal of
Neurology, Neurosurgery & Psychiatry. 64(5):680-2, 1998
Straver JS et al. Carbamyl phosphate synthetase-1 deficiency discovered
after valproic acid-induced coma. Acta Neurologica Scandinavica.
86(3):275-9, 1992
Honeycutt D. et al Heterozygote ornithine transcarbamylase deficiency
presenting as symptomatic hyperammonemia during initiation of valproate
therapy. Neurology. 42(3 Pt 1):666-8, 1992
Ian
Dr Ian Godber
Principal Biochemist
Wishaw General Hospital
Wishaw, Lanarkshire
ML2 0DP
01698 366338
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