Abstract
To the Editor: Vidarabine (adenine arabinoside, ara-A, or 9-β-D-arabinofuranosyladenine), alone or in combination with an adenosine deaminase inhibitor, is used clinically as an antiviral and oncostatic agent.1 , 2 Toxic manifestations occur in a large proportion of treated patients.3 Recently, it has been reported by several investigators that vidarabine administration leads to a severe depression of the activity of the enzyme S-adenosylhomocysteine hydrolase, and therefore could cause an increase in the intracellular levels of S-adenosylhomocysteine, a reduction in the ratio of S-adenosylmethionine to S-adenosylhomocysteine, and possibly an inhibition of several transmethylation reactions.4 , 5 On the basis of these important . . .