Valproic Acid Toxicity

ALLEN, RICHARD J.

doi:10.1001/archpedi.1985.02140090010004

Cited by 6 publications

(1 citation statement)

References 19 publications

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“…Fourteen patients had anecdotal evidence [241][242][243][244][245][246][247][248], 5 patients had recurrent acute pancreatitis upon rechallenge [242,243,245,[249][250][251] and 1 tolerated rechallengc without developing pancreatitis. Acute pancreatitis is not mentioned as a complication of valproic acid therapy in larger studies, but hepatic tox icity occurred frequently [252][253]. Toxicol ogy studies in mice, rats and dogs revealed dose-dependent lobular atrophy, acinar cell vacuolization and interstitial inflammatory infiltrate after 1 year in the rat [254], Based on the well-documented case reports with similar courses in most patients and frequent positive rechallenge the evidence for a causal relation ship of valproic acid therapy and acute pan creatitis appears strong.…”

Section: Valproic Acidmentioning

confidence: 99%

Drug-Induced Acute Pancreatitis: Further Criticism

Frick¹,

Speiser²,

Bimmler³

et al. 1993

Dig Dis

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A comprehensive literature search was performed to collect all available data on drug-induced pancreatitis. Strong evidence for an association with acute pancreatitis has been described for anticholinesterases, calcium 2’,3’-dideoxyinosine, estrogen, L-asparaginase, salicylates, thiazide-diuretics, valproic acid, and vinca alkaloids. Weak evidence has been found for antituberculous agents, azathioprine, biguanides, cisplatinum, cyclosporine A, H2-blocking agents, loop diuretics, 6-mercaptopurine, metronidazole, pentamidine, steroids, sulfonamides, sulindac and tetracycline. Many cases were associated with underlying conditions known to induce acute pancreatitis themselves. It is concluded that for none of the drugs studied the available data are consistent enough to support a definite association with acute pancreatitis. Nevertheless, the data suggest that drugs may be a trigger or a cofactor in inducing pancreatitis.

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