Biomaterial Database

Rebound of plasma free phenytoin concentration following plasmapheresisin a patient with thrombotic thrombocytopenic purpura. 1995

L I Mansur, and R W Murrow, and J C Garrelts, and G O Minns

Department of Internal Medicine, University of Kansas School of Medicine, Wichita.

OBJECTIVE To measure the total and free serum phenytoin concentrations and phenytoin clearance in a patient with thrombotic thrombocytopenic purpura undergoing plasmapheresis. METHODS A dose of phenytoin 400 mg i.v. was administered daily 2.5 hours after the completion of plasmapheresis. Intravenous samples were obtained to measure the free and total phenytoin concentrations on 4 consecutive days. These samples were obtained before, at the midpoint, upon completion, and 30, 60, and 120 minutes after completion of plasmapheresis. The samples were centrifuged and stored at 4 degrees C until analysis using the same fluorescence polarization immunoassay kit. The free phenytoin was separated by ultracentrifugation. CONCLUSIONS Despite a decrease in total and free serum phenytoin concentrations measured during the procedure, a marked rebound in the free phenytoin concentration was noted 30 minutes after completion of the procedure. However, by 120 minutes after the procedure, the free phenytoin concentration had decreased to the preprocedure value. The total amount of phenytoin removed by the procedure was less than 5%. CONCLUSIONS Despite the decrease in total and free serum phenytoin concentrations observed during plasmapheresis, patients undergoing plasmapheresis may not need supplemental phenytoin, as a rapid reequilibration of the therapeutically active free serum phenytoin occurs following the completion of the procedure. In addition, less than 5% of the total body phenytoin is removed. Second, if the patient experiences symptoms of phenytoin toxicity immediately after the procedure, a free serum phenytoin concentration may be obtained, as this concentration may reflect the reason for toxicity despite a decreased total phenytoin concentration.

UI	MeSH Term	Description	Entries
D008657	Metabolic Clearance Rate	Volume of biological fluid completely cleared of drug metabolites as measured in unit time. Elimination occurs as a result of metabolic processes in the kidney, liver, saliva, sweat, intestine, heart, brain, or other site.	Total Body Clearance Rate,Clearance Rate, Metabolic,Clearance Rates, Metabolic,Metabolic Clearance Rates,Rate, Metabolic Clearance,Rates, Metabolic Clearance
D010672	Phenytoin	An anticonvulsant that is used to treat a wide variety of seizures. It is also an anti-arrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs.	Diphenylhydantoin,Fenitoin,Phenhydan,5,5-Diphenylhydantoin,5,5-diphenylimidazolidine-2,4-dione,Antisacer,Difenin,Dihydan,Dilantin,Epamin,Epanutin,Hydantol,Phenytoin Sodium,Sodium Diphenylhydantoinate,Diphenylhydantoinate, Sodium
D010956	Plasmapheresis	Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use.	Double Filtration Plasmapheresis,Therapeutic Immunoadsorption,Therapeutic Plasma Adsorption,Therapeutic Plasmapheresis,Adsorption, Therapeutic Plasma,Adsorptions, Therapeutic Plasma,Double Filtration Plasmaphereses,Filtration Plasmapheresis, Double,Immunoadsorption, Therapeutic,Plasma Adsorption, Therapeutic,Plasmaphereses,Plasmapheresis, Double Filtration,Plasmapheresis, Therapeutic,Therapeutic Immunoadsorptions,Therapeutic Plasma Adsorptions,Therapeutic Plasmaphereses
D011697	Purpura, Thrombotic Thrombocytopenic	An acquired, congenital, or familial disorder caused by PLATELET AGGREGATION with THROMBOSIS in terminal arterioles and capillaries. Clinical features include THROMBOCYTOPENIA; HEMOLYTIC ANEMIA; AZOTEMIA; FEVER; and thrombotic microangiopathy. The classical form also includes neurological symptoms and end-organ damage, such as RENAL FAILURE. Mutations in the ADAMTS13 PROTEIN gene have been identified in familial cases.	Moschkowitz Disease,Purpura, Thrombotic Thrombopenic,Thrombotic Thrombocytopenic Purpura, Congenital,Thrombotic Thrombocytopenic Purpura, Familial,Congenital Thrombotic Thrombocytopenic Purpura,Familial Thrombotic Thrombocytopenia Purpura,Familial Thrombotic Thrombocytopenic Purpura,Microangiopathic Hemolytic Anemia, Congenital,Moschcowitz Disease,Schulman-Upshaw Syndrome,Thrombotic Microangiopathy, Familial,Thrombotic Thrombocytopenic Purpura,Upshaw Factor, Deficiency of,Upshaw-Schulman Syndrome,Familial Thrombotic Microangiopathy,Microangiopathy, Familial Thrombotic,Schulman Upshaw Syndrome,Thrombocytopenic Purpura, Thrombotic,Thrombopenic Purpura, Thrombotic,Thrombotic Thrombopenic Purpura,Upshaw Schulman Syndrome
D005260	Female		Females
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000293	Adolescent	A person 13 to 18 years of age.	Adolescence,Youth,Adolescents,Adolescents, Female,Adolescents, Male,Teenagers,Teens,Adolescent, Female,Adolescent, Male,Female Adolescent,Female Adolescents,Male Adolescent,Male Adolescents,Teen,Teenager,Youths