Exogenous pyridoxine is known to antagonize the neuropharmacologic action of levodopa in Parkinson disease. The metabolic interactions of levodopa, pyridoxine, and carbidopa, a peripheral decarboxylase inhibitor, were studied in 15 long-term, levodopa-treated patients. Pyridoxine reduced plasma dopa levels 67% but enhanced homovanillic acid synthesis 49% Carbidopa potentiated plasma dopa, inhibited homovanillic acid synthesis, and minimized the effects of pyridoxine.
The decarboxylase activity index following pyridoxine administration increased 483% and 136% for plasma and urine respectively. Carbidopa effected a 77% and 94% reduction.
It is suggested that pyridoxine accelerates systemic metabolism of levodopa, thereby decreasing availability of the amino acid to brain parenchyma. The combination of levodopa and carbidopa prevents the loss of levodopa effect produced by exogenous pyridoxine.
Mars H. Levodopa, Carbidopa, and Pyridoxine in Parkinson Disease: Metabolic Interactions. Arch Neurol. 1974;30(6):444–447. doi:10.1001/archneur.1974.00490360020005
Browse and subscribe to JAMA Network podcasts!
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: