Evidence map›Paper›PMID 16487217›Full record

ReviewBritish journal of clinical pharmacology2006

Clinically relevant drug interactions with antiepileptic drugs.

Emilio Perucca

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of clinical pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 8 pooled it
24.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

164 citing papers in PubMed, 8 syntheses or guidelines pooled it, 587 citations in OpenAlex.

  1. Pooled it
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  7. A systematic review of population pharmacokinetics of valproic acid.British journal of clinical pharmacology · 2018
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  14. Peripheral metabolism of (R)-[11C]verapamil in epilepsy patients.European journal of nuclear medicine and molecular imaging · 2008
    Trial
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  16. Review
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104 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 2 countries.

Emilio PeruccaInstitute of Neurology IRCCS C. Mondino Foundation, Pavia, and Clinical Pharmacology Unit, Department of Internal Medicine and Therapeutics, University of Pavia, Pavia, Italy. perucca@unipv.it
Urology Foundation · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Some patients with difficult-to-treat epilepsy benefit from combination therapy with two or more antiepileptic drugs (AEDs). Additionally, virtually all epilepsy patients will receive, at some time in their lives, other medications for the management of associated conditions. In these situations, clinically important drug interactions may occur. Carbamazepine, phenytoin, phenobarbital and primidone induce many cytochrome P450 (CYP) and glucuronyl transferase (GT) enzymes, and can reduce drastically the serum concentration of associated drugs which are substrates of the same enzymes. Examples of agents whose serum levels are decreased markedly by enzyme-inducing AEDs, include lamotrigine, tiagabine, several steroidal drugs, cyclosporin A, oral anticoagulants and many cardiovascular, antineoplastic and psychotropic drugs. Valproic acid is not enzyme inducer, but it may cause clinically relevant drug interactions by inhibiting the metabolism of selected substrates, most notably phenobarbital and lamotrigine. Compared with older generation agents, most of the recently developed AEDs are less likely to induce or inhibit the activity of CYP or GT enzymes. However, they may be a target for metabolically mediated drug interactions, and oxcarbazepine, lamotrigine, felbamate and, at high dosages, topiramate may stimulate the metabolism of oral contraceptive steroids. Levetiracetam, gabapentin and pregabalin have not been reported to cause or be a target for clinically relevant pharmacokinetic drug interactions. Pharmacodynamic interactions involving AEDs have not been well characterized, but their understanding is important for a more rational approach to combination therapy. In particular, neurotoxic effects appear to be more likely with coprescription of AEDs sharing the same primary mechanism of action.

Indexed as

AbsorptionAnticoagulantsAnticonvulsantsContraceptives, OralCytochrome P-450 Enzyme SystemDrug InteractionsDrug Therapy, CombinationEnzyme InductionEnzyme InhibitorsEpilepsyGastrointestinal TractGlucuronosyltransferaseHumansAnticoagulantsAnticonvulsantsContraceptives, OralCytochrome P-450 Enzyme SystemEnzyme InhibitorsGlucuronosyltransferase

Identifiers

PMID16487217
PMCPMC1885026
OpenAlexW2069987842

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.