Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Primidone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1983

Coma and crystalluria: a massive primidone intoxication treated with haemoperfusion.

The present paper describes a patient who was in danger of dying from a massive primidone overdose. She was comatose, hypotensive and in acute renal failure with crystalluria. Because of her clinical condition and high plasma primidone level (209 mg/l) haemoperfusion was instituted. Both the calculated drug clearances and the remarkable improvement in the patient's clinical condition suggest that haemoperfusion was very effective.

Aged↗
PubMed1980

Primidone in the treatment of the long QT syndrome: QT shortening and ventricular arrhythmia suppression.

We studied a family with the long QT syndrome. The initial case was in a patient who presented with seizures, ventricular fibrillation, and syncope. After a trial of conventional modalities of treatment including left stellate ganglionectomy, primidone (Mysoline) therapy was initiated. This drug has been successful in suppressing ventricular arrhythmias and shortening the QT interval over a 2-year follow-up period. Two additional family members with QT prolongation have been treated with primidone. During an 8-month follow-up, electrocardiographic and Holter recordings showed shortening of the QT interval.

Adolescent↗
PubMed1989

[A clinical case of severe megaloblastic anemia during treatment with primidone].

The case of a patient who developed megaloblastic anemia caused by folate deficiency during treatment with primidone is reported. The serum level of folic acid was significantly low. Two causes able to produce folate deficiency have been discovered: chronic assumption of primidone, and low dietary intake of folic acid. The anemia was completely reversed by oral supplementation of folic acid. It has already been recognized that additional nutritional deficiency is required to precipitate a frank megaloblastic anemia during therapy with antiepileptic drugs.

Administration, Oral↗
PubMed1985

Hepatic cirrhosis associated with long-term primidone therapy in a dog.

The anticonvulsant drug, primidone, was believed to be responsible for the development of hepatic cirrhosis in a 9-year-old German Shepherd Dog with idiopathic epilepsy. Marked increases in serum alanine aminotransferase, serum alkaline phosphatase, total bilirubin, and sulfobromophthalein retention, as well as decreases in albumin and BUN supported the diagnosis of hepatic failure. Biochemical abnormalities improved after primidone was discontinued. Previous reports indicated a poor prognosis for anticonvulsant-induced hepatic failure; however, this dog has remained stable for over a year after diagnosis and proper therapy.

Animals↗
PubMed1979

Improved determination of phenobarbital, primidone, and phenytoin by use of a preparative instrument for extraction, followed by gas chromatography.

A microprocessor-controlled automatic extractor, (PREMTM I) is described with which lipophilic components may be extracted from physiological fluids by means of a selective, solid-phase extraction cartridge, and the extracts presented in dry form for subsequent analysis. This instrument has been successfully evaluated for the extraction of phenobarbital, primidone, and phenytoin from human serum before chromatographic analysis. We describe a specific method for determination of these anticonvulsants, involving the PREP I and analysis, after flash-heater methylation, in a gas chromatograph equipped with a nitrogen-sensitive detector. Absolute recoveries ranged from 90 to 102%. Within-day and day-to-day precision (CV) ranged from 4 to 7% for all three drugs in therapeutic concentrations. Comparison of this method with results obtained with a liquid--liquid micro-scale extraction and a similar gas-chromatographic method resulted in correlation coefficients of 0.988 (phenobarbital), 0.978 (primidone), and 0.982 (phenytoin). These drugs in therapeutic concentrations can be simultaneously extracted and measured with confidence.

Autoanalysis↗
PubMed1980

[A gas-chromatographic method for the determination of carbamazepine, phenobarbital, phenytoin and primidone in the same extract of serum (author's transl)].

A gas-chromatographic method for the determination of the antiepileptic drugs carbamazepine, phenobarbital, phenytoin and primidone in the same extract of serum is presented. Saturated ammonium sulfate solution is added to 1 ml serum, followed by extraction with chloroform. The organic phase is separated and evaporated. The residue is dissolved in 100 microliter ethylacetate/acetic acid (100 ml + 1 ml) for gas-chromatography. The gas-chromatographic determination is carried out under isothermal conditions without derivatisation, using SP 2250 DA as stationary phase for the determination of phenobarbital and phenytoin, and Dexsil 300 for the determination of carbamazepine and primidone. The coefficient of variation for the precision from day to day ranges from 4.3 to 7.5%, the recovery from 93.5 to 111%. The specificity was proven by comparison with the relative retention times of about 100 drugs. The method is compared with the corresponding EMIT-tests.

Anticonvulsants↗
PubMed1982

High performance liquid chromatographic determination of primidone in tablets.

A high performance liquid chromatographic (HPLC) method is described for the quantitative determination of primidone in tablets. A ground tablet sample is diluted directly in the mobile phase, at a concentration of about 1 mg/mL of primidone, mixed and deaerated, and filtered. The resulting solution is then quantitated by HPLC. The average spike recoveries for the 50 mg and 250 mg tablets were 101.2% and 99.0%, respectively. The average recovery for an authentic mixture formulated at the 250 mg level was 100.1% with a relative standard deviation of 0.45%.

Chromatography, High Pressure Liquid↗
PubMed1983

Gas chromatographic alkylation studies of phenytoin, mephenytoin and primidone: investigation of butylated derivatives.

The alkylation of phenytoin, mephenytoin and primidone with n-alkyl iodides in N,N-dimethylacetamide with tetramethylammonium hydroxide was investigated by gas chromatography. With methyl iodide phenytoin and mephenytoin were each converted into a single derivative; the use of other alkyl iodides yielded more than one product. Primidone was converted with methyl iodide and butyl iodide into a major derivative (> 90%) and a minor one. Butylation of the compounds by this method was compared with butylation in an acetone-butyl iodide mixture with potassium carbonate, caesium carbonate or silver oxide added, and with on-column butylation. All these methods resulted in the production of more than one derivative. The derivatives were identified by mass spectrometry and by 1H NMR and 13C NMR. With the acetone-butyl iodide-silver oxide method the main derivatives were O-butylated compounds. The other methods yielded predominantly N-butylated derivatives.

Journal Article↗
PubMed1994

Simultaneous determination of primidone and its active metabolites in rat plasma by high-performance liquid chromatography using a solid-phase extraction technique.

Primidone (PRM) and its active metabolites, phenylethylmalonamide (PEMA) and phenobarbital (PB), in rat plasma were simultaneously determined using a solid-phase extraction technique followed by high-performance liquid chromatography (HPLC). Twenty microliters of plasma was applied to a Bond-Elut C-18 cartridge column with 0.1 microgram of acetanilide (internal standard, IS). After the column was washed, PRM, PEMA, PB, and IS were eluted with methanol and injected into the HPLC system. Calibrations for these substances were linear in the range of 0-20 micrograms/mL. The coefficients of variation were 1.5-7.9% and 3.4-9.1% in the within-day and between-day assays, respectively. The recovery rates were 96.8-101.8%. The pharmacokinetics of these substances were examined after oral administration of PRM (50 mg/kg) to rats. The Tmax values for PRM, PEMA, and PB were 1.4, 5.7, and 6.6 h, respectively, and the Cmax values were 18.2, 8.1, and 9.6 micrograms/mL, respectively. This method is useful for pharmacokinetic studies of PRM and its active metabolites.

Administration, Oral↗
PubMed1985

Goldenhar syndrome, anterior encephalocele, and aqueductal stenosis following fetal primidone exposure.

Fetal exposure to primidone was associated with Goldenhar syndrome, hemifacial microsomia, tetralogy of Fallot, aqueductal stenosis, and anterior encephalocele in this male infant. No similar cases in anticonvulsant-exposed pregnancies were found on literature review, despite the increased incidence of other anomalies following such exposure. Goldenhar syndrome, especially related to rare central nervous system anomalies, is reviewed. Experimental production of hemifacial microsomia by a folic acid antagonist, triaxene, is mediated via hemorrhage in the fetus. Intraventricular hemorrhage was noted in this infant as were dilated lateral and third ventricles. The hemorrhagic diathesis and/or the folic acid depletion of newborns following fetal anticonvulsant exposure may have been the underlying mechanism.

Adult↗
PubMed1979

Primidone metabolism in renal insufficiency and acute intoxication.

Primidone (PRIM) is metabolized into phenobarbital (PB) and phenylethylmalonamide (PEMA). During anticonvulsant therapy with PRIM under normal conditions PB represents by fat the largest portion of the total concentration of all three components (PRIM + PB + PEMA). In combined therapy with diphenylhydantoin (DPH), and during chronic PRIM overdosage, the relative concentration of PB is even higher. A case of renal insufficiency while on PRIM therapy and a case of acute PRIM intoxication are presented. In both cases PRIM and PEMA are elevated while PB is relatively low. The mechanisms involved in this phenomenon are discussed. Excluding young children with chronic PRIM overdosage, and the endogenous and exogenous intoxication described here, a relative PB concentration below 40% indicates a lack of patient compliance if a steady treatment schedule has been maintained for at least 3 weeks.

Acute Disease↗
PubMed1984

Single-dose kinetics of primidone in acute viral hepatitis.

The pharmacokinetics of primidone (PRM) after oral administration of a single 500 mg dose was studied in 7 patients with acute viral hepatitis and 7 healthy control subjects. The elimination half-life and the apparent clearance of unchanged PRM in the patients were 18.0 +/- 3.1 h and 42 +/- 14 ml X h-1 X kg-1, respectively (mean +/- SD) and did not differ significantly from the values in the controls (half-life 17.0 +/- 2.4 h; clearance 35 +/- 8 ml X h-1 X kg-1). The metabolite phenylethylmalonamide (PEMA) was detected in the serum of all normal subjects within 2-24 h. By contrast, serum levels of this metabolite were undetectable (less than 2 mumol/1) in all but one of the patients. Serum levels of phenobarbital (PB) remained below the limit of detection (less than 2 mumol/1) in all subjects. The findings indicate that accumulation of PRM with its attendant toxicity is unlikely to occur in epileptic patients who develop acute viral hepatitis, despite evidence that the metabolism of the drug is affected by this condition. The possibility of impaired conversion to PB and its implications are discussed.

Acute Disease↗
PubMed1976

Improved method for measurement of serum levels of phenobarbital, carbamazepine, primidone and diphenylhydantoin by gas-liquid chromatography.

A gas-liquid chromatographic method for the simultaneous determination of phenobarbital, primidone, carbamazepine and diphenylhydantoin in human serum following therapeutic doses has been developed. After extraction with chloroform, the anticonvulsant drugs were methylated with phenyltrimethylammonium hydroxide in dimethylformamide at 85 degrees C for gas-liquid chromatography. Linear temperature programming of a 1% OV-17 column was used to achieve separation and quantitation. The procedure described in the present paper is relatively simple, highly specific and sufficiently sensitive for use in routine clinical assays.

Analysis of Variance↗
PubMed1977

Evaluation of a rapid gas-chromatographic method for the simultaneous quantitative determination of ethosuximide, phenyletheylmalonediamide, carbamazepine, phenobarbital, primidone and diphenylhydantoin in human serum.

A simple and rapid gas chromatographic method for the simultaneous estimation of the anticonvulsant drugs ethosuximide, carbamazepine, phenobarbital, primidone, diphenylhydantoin and the metabolite PEMA in serum is presented. The method is based on a simple ether extraction of 1 ml serum before and after precipitation of the proteins by ammonium sulfate and injection of the extract dissolved in methanol without derivative formation. Gas chromatographic separation is performed on a highly polar acidic phase (SP 1000, a terephthalic acid modified Carbowax 20 M), for detection the instrument is equipped with a nitrogen selective detector, quantitation is performed by automatic electronic integration of peak areas in relation to the internal standard Mesantoin. The optimal approach to the gas chromatographic analysis of "problem drugs" like carbamazepine and phenobarbital is discussed, various stationary phases and support materials are compared for effectiveness with this method. In the analysis of over 800 routine serum samples as well as internal and external quality control samples this method was found to be reliable and the results reproducible.

Anticonvulsants↗
PubMed1981

Enzyme immunoassay of phenobarbital, phenytoin, primidone, carbamazepine and theophylline with the Abbott VP Bichromatic Analyzer.

The enzyme multiplied immunoassay technique (EMIT) for the assay of phenobarbital, phenytoin, primidone, carbamazepine and theophylline was adapted to the Abbott VP Bichromatic Analyzer. Reagent consumption is reduced by the use of a stable working dilution of EMIT reagent B in EMIT buffer. Correlation with the standard EMIT method is excellent. This procedure greatly increases the maximum number of tests per kit. The method is an accurate and economical alternative to the standard EMIT method.

Carbamazepine↗
PubMed1984

Mutagenicity of antiepileptic drugs. II. Phenytoin, primidone and phenobarbital.

The antiepileptic drugs, phenytoin, primidone and phenobarbital, were tested in Chinese hamster ovary (CHO) cells for their ability to induce sister-chromatid exchanges (SCEs) and structural chromosomal aberrations (CAs), with and without metabolic activation. SCEs and CAs were analyzed in the same cell population. The results are negative.

Animals↗
PubMed1986

Effect of primidone in somatic and germ cells of mice.

Primidone, an anti-convulsant drug, was tested in mice for mutagenicity in somatic cells by the micronucleus test and in germ cells by the sperm-head abnormality assay. Mice were treated orally with the drug at doses of 4.37, 8.75 and 13.11 mg/mouse. The results indicate that the drug is capable of inducing mutations both in somatic and germ cells of mice.

Animals↗
PubMed1993

Simultaneous determination of carbamazepine, phenytoin, phenobarbital, primidone and their principal metabolites by high-performance liquid chromatography with photodiode-array detection.

We have established a precise and accurate high-performance liquid chromatographic method for the simultaneous assay of carbamazepine, phenytoin, phenobarbital, primidone and their principal metabolites. This method has been used for the analysis of these drugs and the metabolites in serum, saliva and urine samples. Acetonitrile is used for the deproteinization of serum and saliva samples while solid-phase extraction is utilized for urine sample pretreatment. Samples of 2 microliters are injected onto a 3-microns ODS-Hypersil column (250 mm x 2 mm I.D.) with a column temperature of 40 degrees C. The drugs and metabolites are eluted with a mobile phase containing potassium phosphate buffer-acetonitrile-methanol (110:50:30, v/v/v) at a flow-rate of 0.2 ml/min. Signals are monitored by a photodiode-array detector at a sample wavelength of 200 nm with a bandwidth of 10 nm. These four commonly used antiepileptic drugs and their six metabolites are well separated from one another within 15 min. Within-day coefficients of variation (C.V.) are within 5% in most cases and between-day C.V. are from 2.32 to 4.75%. The recovery rates range from 95.12 to 104.42%. This method has the necessary sensitivity and linearity for routine therapeutic monitoring of both total and free drug levels and may be employed for pharmacokinetics studies of drug interactions and metabolism as well.

Anticonvulsants↗