Kinetics of phenobarbital in normal subjects and epileptic patients

Wilensky, Alan J.; Friel, Patrick N.; Levy, René H.; Comfort, Cara; Kaluzny, Stephen P.

doi:10.1007/bf01061382

Cited by 68 publications

(32 citation statements)

References 17 publications

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“…However, tmax value of 1 h in healthy children sug gested a fairly rapid absorption, and this value approximates with the fig ures reported by other authors [11,12], In contrast to normal children, the malnourished group exhibited a tmax value of 5.6 ± 0.98 h which suggests a prolonged absorption process. However, the observation of an almost sim ilar maximum drug concentration in both the groups (healthy = 15.6 ± 1.3, PEM = 16.6 ± 0.94 pg/ml) is suggestive of complete absorption of the drug, though the process seems to be delayed in malnutrition.…”

Section: Discussionsupporting

confidence: 72%

Pharmacokinetics of Phenobarbitone in Protein Energy Malnutrition

Gb¹,

Db²,

Rk³

1986

Dev Pharmacol Ther

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Phenobarbitone kinetics was studied in malnourished and normal children after single oral dose of approximately 7.0 mg/kg. Estimation of serum phenobarbitone concentration was performed by spectrophotometric method. Elimination half-life was 58.9 ± 9.5 h and 30.15 ± 6.1 h for malnourished and healthy children, respectively. Compared to healthy children, t(max) was prolonged in malnutrition group suggesting slow absorption in the latter group. The systemic bioavailability was observed to be higher in protein energy malnutrition. Modifications of the usual dosage regimen in malnutrition arc recommended.

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Section: Discussionsupporting

confidence: 72%

Pharmacokinetics of Phenobarbitone in Protein Energy Malnutrition

Gb¹,

Db²,

Rk³

1986

Dev Pharmacol Ther

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“…132,133 Its pharmacokinetics is linear, and protein binding is 55%. 132,133 Its pharmacokinetics is linear, and protein binding is 55%.…”

Section: Pharmacokinetic Characteristicsmentioning

confidence: 99%

Therapeutic Drug Monitoring of Antiepileptic Drugs by Use of Saliva

Patsalos¹,

Berry²

2013

Therapeutic Drug Monitoring

169

126

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Blood (serum/plasma) antiepileptic drug (AED) therapeutic drug monitoring (TDM) has proven to be an invaluable surrogate marker for individualizing and optimizing the drug management of patients with epilepsy. Since 1989, there has been an exponential increase in AEDs with 23 currently licensed for clinical use, and recently, there has been renewed and extensive interest in the use of saliva as an alternative matrix for AED TDM. The advantages of saliva include the fact that for many AEDs it reflects the free (pharmacologically active) concentration in serum; it is readily sampled, can be sampled repetitively, and sampling is noninvasive; does not require the expertise of a phlebotomist; and is preferred by many patients, particularly children and the elderly. For each AED, this review summarizes the key pharmacokinetic characteristics relevant to the practice of TDM, discusses the use of other biological matrices with particular emphasis on saliva and the evidence that saliva concentration reflects those in serum. Also discussed are the indications for salivary AED TDM, the key factors to consider when saliva sampling is to be undertaken, and finally, a practical protocol is described so as to enable AED TDM to be applied optimally and effectively in the clinical setting. Overall, there is compelling evidence that salivary TDM can be usefully applied so as to optimize the treatment of epilepsy with carbamazepine, clobazam, ethosuximide, gabapentin, lacosamide, lamotrigine, levetiracetam, oxcarbazepine, phenobarbital, phenytoin, primidone, topiramate, and zonisamide. Salivary TDM of valproic acid is probably not helpful, whereas for clonazepam, eslicarbazepine acetate, felbamate, pregabalin, retigabine, rufinamide, stiripentol, tiagabine, and vigabatrin, the data are sparse or nonexistent.

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“…Its pharmacokinetics are linear and protein binding is 55%. The bioavailability of oral PB is more than 95% and the peak blood level of PB is 0.5–4 h. The t 1/2 of PB is 2–7 days [85]. Discontinuing PB should be done with caution because a case report showed an increase of seizure frequency in patients tapering the doses of PB while stabilized on another AED [86].…”

Section: Introductionmentioning

confidence: 99%

The Impact of Anti-Epileptic Drugs on Growth and Bone Metabolism

Fan

Lee

Chang

et al. 2016

IJMS

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Epilepsy is a common neurological disorder worldwide and anti-epileptic drugs (AEDs) are always the first choice for treatment. However, more than 50% of patients with epilepsy who take AEDs have reported bone abnormalities. Cytochrome P450 (CYP450) isoenzymes are induced by AEDs, especially the classical AEDs, such as benzodiazepines (BZDs), carbamazepine (CBZ), phenytoin (PT), phenobarbital (PB), and valproic acid (VPA). The induction of CYP450 isoenzymes may cause vitamin D deficiency, hypocalcemia, increased fracture risks, and altered bone turnover, leading to impaired bone mineral density (BMD). Newer AEDs, such as levetiracetam (LEV), oxcarbazepine (OXC), lamotrigine (LTG), topiramate (TPM), gabapentin (GP), and vigabatrin (VB) have broader spectra, and are safer and better tolerated than the classical AEDs. The effects of AEDs on bone health are controversial. This review focuses on the impact of AEDs on growth and bone metabolism and emphasizes the need for caution and timely withdrawal of these medications to avoid serious disabilities.

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Kinetics of phenobarbital in normal subjects and epileptic patients

Cited by 68 publications

References 17 publications

Pharmacokinetics of Phenobarbitone in Protein Energy Malnutrition

Pharmacokinetics of Phenobarbitone in Protein Energy Malnutrition

Therapeutic Drug Monitoring of Antiepileptic Drugs by Use of Saliva

The Impact of Anti-Epileptic Drugs on Growth and Bone Metabolism

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