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Anticonvulsant drugs pharmacokinetics

Little is known as yet about the pharmacokinetics of carbamazepine in humans although preliminary reports suggest slow absorption (M21) and marked variations in blood levels during a day in some subjects (M15). Blood levels varying from trace quantities to 12 /ig/ml have been found in patients taking 400-1000 mg daily (P3), but no relation between the level observed and the dose was apparent. In the studies so far published carbamazepine blood levels have not correlated with seizure control (P3), but all the subjects wore receiving additional anticonvulsant drugs. [Pg.77]

Gabapentin does not bind to plasma proteins, is not appreciably metabolized, nor induces hepatic enzyme activity (AHFS, 2000) Consequently, it does not appear to alter the pharmacokinetics of commonly used anticonvulsant drugs or oral contraceptives (Ketter et al.,... [Pg.321]

Wilbur K, Ensom MH. Pharmacokinetic drug interactions between oral contraceptives and second-generation anticonvulsants. Clin Pharmacokinet 2000 38(4) 355-65. [Pg.251]

Nonlinear pharmacokinetics. Nonlinear pharmacokinetics simply means that the relationship between dose and Cp is not directly proportional for all doses. In nonlinear pharmacokinetics, drug concentration does not scale in direct proportion to dose (also known as dose-dependent kinetics). One classic drug example of nonlinear pharmacokinetics is the anticonvulsant drug phenytoin.38 Clinicians have learned to dose pheny-toin carefully in amounts greater than 300 mg/day above this point, most individuals will have dramatically increased phenytoin plasma levels in response to small changes in the input dose. [Pg.9]

Unlike most classes of psychotropic drugs where there is no direct correlation between the blood concentration and the therapeutic effect, for most of the commonly used anticonvulsants there is a high degree of correlation between the blood and brain concentrations and the therapeutic effect. A knowledge of the pharmacokinetic properties of the anticonvulsant drugs is therefore essential if their therapeutic efficacy is to be maximized and side effects minimized. [Pg.306]

Many biochemistry laboratories no longer undertake routine measurement of the plasma concentration for most anticonvulsant drugs because plasma concentrations are insufficiently stable to serve as a useful guide to change of dose. The exception is phenytoin, where a small increase in dose may lead to a disproportionate rise in the plasma drug concentration (see zero-order pharmacokinetics, p. 99) and plasma monitoring is essential. With other drugs the dose is increased to the maximum tolerated level and, if seizures continue, it is replaced by another. [Pg.415]

Because of the long elimination half-hfe of phenobarbital, the blood concentration does not change rapidly. Therefore a serum specimen collected late in the dose interval (trough) is representative of the overall effect. Results from specimens collected 2 to 4 hours after the dose can be misleading, because they may be construed to be the peak concentration when in actuality they precede the peak. Table 33-1 summarizes pharmacokinetic data of the anticonvulsant drugs. [Pg.1252]

Perucca E. Is there a role of therapeutic drug monitoring of new anticonvulsants. Clin Pharmacokinet 2000 38 191-204. [Pg.1047]

The reactivators of ChE are ordinarily used with cholinolitics and anticonvulsant drugs like diazepam. We studied the pharmacokinetic of HI-6 administrated i.m. to rats alone, with Diazepam and Scopolamin and with them after soman intoxication [14],... [Pg.220]

The application of Equation 1.48 is most apparent in dosing anticonvulsant drugs, which for some patients show nonlinear pharmacokinetics over therapeutic concentrations. [Pg.27]

B. D. Potts, S. Gabriel, C. J. Parli, Metabolism, Disposion, and Pharmacokinetics of a Potent Anticonvulsant, 4-Amino-A-(2,6-dimethylphenyl)benzamide (LY201116), in Rats , Drug Metab. Dispos. 1989,17, 656-661. [Pg.175]

S. W. Martin, F. E. Bishop, B. M. Kerr, M. Moor, M. Moore, P. Sheffels, M. Rashed, J. G. Slatter, L. Berthon-Cedille, F. Lepage, J.-J. Descombe, M. Picard, T. A. Baillie, R. H. Levy, Pharmacokinetics and Metabolism of the Novel Anticonvulsant Agent N-(2,6-Dimethylphenyl)-5-methyl-3-isoxazolecarboxamide (D2624) in Rats and Humans , Drug Metab. Dispos. 1997, 25, 40-46. [Pg.175]

Carbamazepine (CBZ) and divalproex sodium (DVP) are the most common anticonvulsant agents prescribed for adult BD (Bowden et ah, 1994) Post et ah, 1998b) and pediatric epileptic disorders (Trimble, 1990 Dunn et al., 1998). As a consequence of their documented efficacy in these populations, their use has been extended to pediatric behavioral and mood disorders (Biederman et ah, 1998). We review here their mechanisms of action, pharmacokinetics, side effects, and pediatric uses. The multiple cytochrome P450 (CYB)-mediated potential drug interactions of CBZ and DVP are not covered in detail in this chapter. For a comprehensive review of this subjects the reader is referred to a recent publication by Flockhart and Oesterheld (2000). [Pg.312]

Because most antidepressants require oxidative metabolism as a necessary step in their elimination, they can be the target of a pharmacokinetic drug-drug interaction, as well as the cause. The CYP enzymes mediating the biotransformation of the various antidepressants are also shown in Table 7-30. CYP 1A2 and 3A3/4 are induced by anticonvulsants such as barbiturates and carbamazepine. As expected, coadministration of these anticonvulsants has been shown to lower plasma levels of TCAs and would be predicted to have the same effect on nefazodone, sertraline, and venlafaxine. [Pg.155]

It can be concluded that no significant differences exist between anticonvulsive and neurotoxic effects for this series of derivatives. The variation in the anticonvulsive effect seems to be determined by drug-membrane interactions and not by the pharmacokinetics of these compounds. [Pg.236]

The individual benzodiazepines show small differences in their relative anxiolytic, anticonvulsant, and sedative properties. However, the duration of action varies widely among this group, and pharmacokinetic considerations are often important in choice of drug. [Pg.101]

Pharmacokinetics. Carbamazepine is extensively metabolised one of the main products, an epoxide (a chemically reactive form), has anticonvulsant activity similar to that of the parent drug but may also cause some of its adverse effects. The t) of carbamazepine falls from 35 h to 20 h over the first few weeks of therapy due to induction of hepatic enzymes that metabolise it as well as other drugs, including corticosteroids (adrenal and contraceptive), theophylline and warfarin. Cimetidine and valproate inhibit its metabolism. There are complex interactions with other antiepilepsy drugs, which constitute a reason for monodrug therapy. [Pg.419]

Collins RJ, Garnett WR. Extended release formulations of anticonvulsant medications clinical pharmacokinetics and therapeutic advantages. CNS Drugs 2000 14 203-12. [Pg.300]

Chloroquine can cause seizures in patients with epilepsy. The mechanism is uncertain, but it may include reductions in inhibitory neurotransmitters and pharmacokinetic interactions that alter anticonvulsant concentrations. Tonic-clonic convulsions were reported in four patients in whom chloroquine was part of a prophylactic regimen. Antiepileptic treatment was required to control the seizures. None had further seizures after withdrawal of the antimalarial drugs (9). [Pg.723]

A critical pharmacokinetic parameter that directs safe and effective medication use is the therapeutic index. This parameter establishes a quantitative comparison between a drug s effective concentration and its toxic concentration. The closer these measurements are, the narrower the index, and therefore the more care that must be taken in prescribing. Lithium and anticonvulsants, for example, have narrow therapeutic indices. [Pg.197]

Martin, S.W. et al., Pharmacokinetics and metabolism of the novel anticonvulsant agent N-(2,6-dimethylphenyl)-5-methyl-3-isoxazolecarboxamide (D2624) in rats and humans, Drug Metab. Dispos., 25(1), 40, 1997. [Pg.199]


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See also in sourсe #XX -- [ Pg.583 , Pg.585 , Pg.586 ]

See also in sourсe #XX -- [ Pg.583 , Pg.585 , Pg.586 ]




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