Study on Combined Treatment with Phenobarbital and Diphenylhydantoin

Frey, H.‐H.; Kampmann, Elsemarie; Nielsen, C. K.

doi:10.1111/j.1600-0773.1968.tb00447.x

Cited by 16 publications

(3 citation statements)

References 6 publications

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“…The C max and AUC of zonisamide continued to be low 10 weeks but not 12 weeks after the discontinuation of phenobarbital, suggesting that at least 10 weeks are necessary for the interaction of phenobarbital in dogs to resolve. There was one report which examined the wearing‐off period of phenobarbital with a focus on T 1/2 in dogs: T 1/2 of a single oral administration of phenobarbital decreased in one out of three dogs after repeated administration of phenobarbital, and it took over 7 months to restore the shortened T 1/2 (Frey et al. , 1968).…”

Section: Discussionmentioning

confidence: 99%

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Pharmacokinetics of zonisamide and drug interaction with phenobarbital in dogs

Orito

Saito

Fukunaga

et al. 2008

Vet Pharm & Therapeutics

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The purposes of the present study were to elucidate the pharmacokinetics of zonisamide, determine the presence of a drug interaction with phenobarbital, and evaluate how long any interaction lasted after discontinuation of phenobarbital in dogs. Five dogs received zonisamide (5 mg/kg, p.o. and i.v.) before and during repeated oral administration of phenobarbital (5 mg/kg, bid, for 30-35 days). Zonisamide (5 mg/kg, p.o.) was also administered 8, 10, and 12 weeks after discontinuation of phenobarbital. Blood was sampled until 24 h after each zonisamide administration and serum concentrations of zonisamide were determined. Repeated phenobarbital decreased the maximum serum concentration, area under the serum concentration vs. time curve, apparent elimination half-life, and bioavailability of zonisamide. Total clearance increased. Time to maximum serum concentration and volume distribution were not changed. The maximum serum concentration and area under the serum concentration vs. time curve of zonisamide continued to be low until 10 weeks after the discontinuation of phenobarbital. They were restored to the same serum concentration as before phenobarbital administration 12 weeks after the discontinuation of phenobarbital. These data suggested that repeated administration of a clinical dose of phenobarbital enhanced the clearance of zonisamide and the enhanced clearance lasted at least 10 weeks after the discontinuation of phenobarbital. Caution may be necessary when zonisamide is given with phenobarbital and when antiepileptic therapy is changed from phenobarbital to zonisamide.

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Section: Discussionmentioning

confidence: 99%

“…, 1968). However, it took 3 months to be restored in one other dog, and in the remaining dog, T 1/2 was prolonged after the discontinuation of phenobarbital (Frey et al. , 1968).…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics of zonisamide and drug interaction with phenobarbital in dogs

Orito

Saito

Fukunaga

et al. 2008

Vet Pharm & Therapeutics

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“…These enzymes metabolize PB, and their activity results in a decrease in the serum concentration of PB. 16 The effect of short-term PB administration on cytochrome p450 enzyme in dogs has been established by use of antipyrine clearance. 25 To our knowledge , there are no readily available assays for assessing the activity or function of the cytochrome p450 enzymes after chronic PB administration.…”

Section: Discussionmentioning

confidence: 99%

Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989)

Dayrell-Hart,

Steinberg,

VanWinkle

et al. 1991

javma

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Summary The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration ≤ 2.2 g/dl in 12 dogs, serum alkaline phosphatase activity ≥ 169 U/L in 18 dogs, serum alanine transaminase activity ≥ 57 U/L in 15 dogs, and total bilirubin concentration ≥ 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was ≥ 40 μg/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations > 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration ≥ 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, po. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.

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�berwachung der Langzeitmedikation mit Diphenylhydantoin

Mascher

Bernhardt

1973

Z. Neurol.

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Study on Combined Treatment with Phenobarbital and Diphenylhydantoin

Cited by 16 publications

References 6 publications

Pharmacokinetics of zonisamide and drug interaction with phenobarbital in dogs

Pharmacokinetics of zonisamide and drug interaction with phenobarbital in dogs

Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989)

�berwachung der Langzeitmedikation mit Diphenylhydantoin

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