Barbiturates are enzyme inducers. Patients should be monitored when these
drugs are started or stopped for a decreased or increased therapeutic effect
respectively.
Barbiturates may enhance the hepatotoxic potential of overdoses of
acetaminophen
Acetazolamide may decrease absorption of primidone (metabolized to
phenobarbital) and reduce clinical effects
Barbiturates may increase the metabolism of some beta-blockers and decrease
their clinical effect (atenolol and nadolol unlikely to interact given their
renal elimination)
Barbiturates may increase the metabolism of chloramphenicol and
chloramphenicol may inhibit barbiturate metabolism; monitor for altered response
Barbiturates may enhance the metabolism (decrease the efficacy) of
antipsychotics; monitor for altered response; dose adjustment may be needed
Barbiturates may enhance the metabolism of calcium channel blockers,
cimetidine, corticosteroids, cyclosporine, disopyramide, doxycycline,
ethosuximide, furosemide, griseofulvin, lamotrigine, phenytoin, propafenone,
quinidine, tacrolimus, TCAs, theophylline; dose adjustment may be needed
Barbiturates may increase the metabolism of estrogens and reduce the efficacy
of oral contraceptives; an alternative method of contraception should be
considered
Barbiturates, ethanol, and narcotic analgesics have additive CNS depressant
effects
Felbamate may inhibit the metabolism of barbiturates and barbiturates may
increase the metabolism of felbamate
Barbiturates may impair the absorption of griseofulvin
MAOIs may inhibit the metabolism of barbiturates
Barbiturates may enhance the nephrotoxic effects of methoxyflurane
Valproic acid inhibits the metabolism of barbiturates; monitor for excessive
sedation; a dose reduction may be needed
Barbiturates inhibit the hypoprothrombinemic effects of oral anticoagulants
via increased metabolism; this combination should generally be avoided
Barbiturates may enhance the metabolism of methadone resulting in methadone
withdrawal