Comparative Pharmacology
Head-to-head clinical analysis: DILANTIN versus PHENYTOIN.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DILANTIN versus PHENYTOIN.
DILANTIN vs PHENYTOIN
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Phenytoin stabilizes neuronal membranes and decreases seizure activity by increasing efflux or decreasing influx of sodium ions across cell membranes in the motor cortex during generation of nerve impulses. It acts by blocking voltage-dependent sodium channels, thereby inhibiting the spread of seizure activity.
Phenytoin is a hydantoin anticonvulsant that stabilizes neuronal membranes and decreases seizure activity by increasing efflux or decreasing influx of sodium ions across cell membranes in the motor cortex during generation of nerve impulses. It use-dependently blocks voltage-gated sodium channels, prolonging their inactivation phase and reducing high-frequency repetitive firing of action potentials.
300–400 mg/day orally in 2–3 divided doses; IV loading dose 15–20 mg/kg at max 50 mg/min, then 300 mg/day IV divided 2–3 times daily.
Oral: 300-400 mg/day in 3-4 divided doses; IV: 15-20 mg/kg loading dose, then 300 mg/day maintenance.
None Documented
None Documented
Clinical Note
moderatePhenytoin + Digoxin
"The metabolism of Digoxin can be increased when combined with Phenytoin."
Clinical Note
moderateFosphenytoin + Digoxin
"The metabolism of Digoxin can be increased when combined with Fosphenytoin."
Clinical Note
moderatePhenytoin + Digitoxin
"The metabolism of Digitoxin can be increased when combined with Phenytoin."
Clinical Note
moderateFosphenytoin + Digitoxin
"The metabolism of Digitoxin can be increased when combined with Fosphenytoin."
Average 22 hours (range 7-42 hours) in adults. Dose-dependent; increases with higher concentrations due to saturable metabolism. In neonates: 10-15 hours. In chronic use, half-life may increase.
Average terminal half-life 22 hours (range 7–42 hours) in adults; dose-dependent due to saturation of metabolism at therapeutic concentrations (10–20 mg/L). Half-life increases with higher doses.
Primarily hepatic metabolism to inactive metabolites (p-hydroxyphenyltoin and glucuronide conjugate). Less than 5% excreted unchanged in urine. Fecal excretion minimal (<2%).
Primarily hepatic metabolism (>95%); less than 5% excreted unchanged in urine. Renal excretion of metabolites (glucuronides) accounts for ~80% of elimination; biliary/fecal excretion of metabolites ~20%.
Category C
Category D/X
Anticonvulsant
Anticonvulsant