Steady‐state plasma nortriptyline concentrations in epileptic patients [letter].

Braithwaite, R. A.; Flanagan, R.J.; Richens, A.

doi:10.1111/j.1365-2125.1975.tb00559.x

Cited by 34 publications

(6 citation statements)

References 16 publications

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“…Earlier studies on phenytoin interaction with tricyclic antidepressant drugs have not all been conclusive. h i p r a m i n e was reported to cause a substantial rise in phenytoin levels (Perruca & Richens 1977) but theclosely related amitriptyline and nortriptyline were without effect when coadministered with phenytoin (Braithwaite et al 1975;Pond et al 1975). Comparison of the plasma phenytoin concentration profiles Obtained following single and multiple doses of phenytoin showed a faster concentration decay pattern in multiple phenytoin dosing.…”

Section: Discussionmentioning

confidence: 95%

Phenytoin-bupropion interaction: effect on plasma phenytoin concentration in the rat

Tekle

Al-Khamis

1990

Journal of Pharmacy and Pharmacology

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The effect of coadministration of bupropion (50 mg kg-1, p.o.) on the disposition profile of phenytoin has been studied in the rat. Plasma phenytoin concentration was measured serially for 10 h by HPLC. Bupropion had little or no effect on the pharmacokinetic parameters of an acutely administered dose of phenytoin. Following multiple doses of phenytoin however (i.e. steady state) the coadministration of bupropion resulted in significant increases in the elimination half-life (t 1/2), the area under the plasma concentration-time curve (AUC) and the time to maximum plasma concentration (tmax). Allowing for the limitations of single dose studies, these results point to a possible pharmacokinetic interaction between bupropion and phenytoin--the clinical significance of which needs to be assessed.

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Section: Discussionmentioning

confidence: 95%

Phenytoin-bupropion interaction: effect on plasma phenytoin concentration in the rat

Tekle

Al-Khamis

1990

Journal of Pharmacy and Pharmacology

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“…Being potent inducers of hepatic drug‐metabolizing enzymes, particularly CYP3A4, CYP1A2, and CYP2C9, CBZ, phenytoin (PHT), and barbiturates stimulate the oxidative transformation of many concurrently prescribed antidepressants. In particular, these AEDs have been found to decrease the plasma concentration of tricyclic antidepressants such as amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, desmethylclomipramine, protriptyline, and doxepin (8–16). Because the demethylation of tricyclic antidepressants is catalyzed by multiple isozymes, including CYP1A2, CYP2C19, and CYP3A4, it is likely that induction of these isoforms is involved in at least some of the reported interactions.…”

Section: Interactions Between Aeds and Antidepressantsmentioning

confidence: 99%

Clinical Significance of Pharmacokinetic Interactions Between Antiepileptic and Psychotropic Drugs

2002

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Summary: As antiepileptic drugs (AEDs) and psychotropic agents are increasingly used in combination, the possibility of pharmacokinetic interactions between these compounds is relatively common. Most pharmacokinetic interactions between AEDs and psychoactive drugs occur at a metabolic level, and usually involve changes in the activity of the cytochrome P450 mixed‐function oxidases (CYP) involved in their biotransformation. As a consequence of CYP inhibition or induction, plasma concentrations of a given drug may reach toxic or subtherapeutic levels, and dosage adjustments may be required to avoid adverse effects or clinical failure. Enzyme‐inducing AEDs, such as carbamazepine (CBZ), phenytoin (PHT), and barbiturates, stimulate the oxidative biotransformation of many concurrently prescribed psychotropics. In particular, these AEDs may decrease the plasma concentrations of tricyclic antidepressants, many antipsychotics, including traditional compounds, i.e., haloperidol and chlorpromazine, and newer agents, i.e., clozapine, risperidone, olanzapine, quetiapine, and ziprasidone, and some benzodiazepines. Conversely, new AEDs appear to have a lower potential for interactions with all psychotropic drugs. While antipsychotics and anxiolytics do not significantly influence the pharmacokinetics of most AEDs, some newer antidepressants, such as viloxazine, fluoxetine, and fluvoxamine, may lead to higher serum levels of some AEDs, namely CBZ and PHT, through inhibition of CYP enzymes. No significant pharmacokinetic interactions have been documented between AEDs and lithium. Information about CYP enzymes responsible for the biotransformation of individual agents and about the effects of these compounds on the activity of specific CYP enzymes may help in predicting and avoiding clinically significant interactions. Apart from careful clinical observation, serum level monitoring of AEDs and psychotropic drugs can be useful in determining the need for dosage adjustments, especially if there is any change in seizure control, or possible toxicity.

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“…Not only is the metabolism of the inducing drug stimulated, but many other drugs and endogenous substances will be turned over much more rapidly (Richens, 1974). This can lead to a reduction in the anticoagulant effect of dicoumarol (Hansen, Siersbaek-Nielsen, Kristensen, Skovsted, and Christensen, 1971), the anti-asthmatic effect of corticosteroids (Brooks, Werk, Ackerman, Sullivan, and Thrasher, 1972), the contraceptive effect of the 'pill' (Laengner and Detering, 1974), the antidepressant effect of nortriptyline (Alexanderson, Evans, and Sjoqvist, 1969;Braithwaite, Flanagan, and Richens, 1975) and the antibiotic effect of doxycycline (Neuvonen and Penttila, 1974).…”

Section: Interactions At Site Of Metabolismmentioning

confidence: 99%

Drug interactions and lethal drug combinations

Richens¹

1975

J Clin Pathol

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Although the development of drugs of greater potency and efficacy confers on the physician increasing power to treat serious diseases, it also increases the number and seriousness of potential adverse effects and drug interactions which can occur. Most hospital patients receive more than one drug at a time, the average number often being greater than five (Smith, Seidl, and Cluff, 1966). The incidence of drug reactions rises with the number of drugs prescribed simultaneously. In patients prescribed one to five drugs the incidence of reactions is 18-6%, while in patients prescribed six or more it rises to 814 % (Hurwitz and Wade, 1969). 94 copyright.

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Steady‐state plasma nortriptyline concentrations in epileptic patients [letter].

Cited by 34 publications

References 16 publications

Phenytoin-bupropion interaction: effect on plasma phenytoin concentration in the rat

Phenytoin-bupropion interaction: effect on plasma phenytoin concentration in the rat

Clinical Significance of Pharmacokinetic Interactions Between Antiepileptic and Psychotropic Drugs

Drug interactions and lethal drug combinations

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