Evidence map›Paper›PMID 24122696›Full record

ReviewClinical pharmacokinetics2014

Pharmacokinetic of antiepileptic drugs in patients with hepatic or renal impairment.

Gail D Anderson, Shahin Hakimian

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical pharmacokinetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  8. Review
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  13. Observational
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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

2 authors.

Gail D Anderson
Shahin Hakimian

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many factors influence choice of antiepileptic drugs (AEDs), including efficacy of the drug for the indication (epilepsy, neuropathic pain, affective disorder, migraine), tolerability, and toxicity. The first-generation AEDs and some newer AEDs are predominately eliminated by hepatic metabolism. Other recent AEDs are eliminated by renal excretion of unchanged drug or a combination of hepatic metabolism and renal excretion. The effect of renal and hepatic disease on the dosing will depend on the fraction of the AED eliminated by hepatic and/or renal excretion, the metabolic isozymes involved, as well as the extent of protein binding, if therapeutic drug monitoring is used. For drugs that are eliminated by renal excretion, methods of estimating creatinine clearance can be used to determine dose adjustments. For drugs eliminated by hepatic metabolism, there are no specific markers of liver function that can be used to provide guidance in dosage adjustments. Based on studies with probe drugs, the hepatic metabolic enzymes are differentially affected depending on the cause and severity of hepatic disease, which can aid in predicting dose adjustment when clinical data are not available. Several AEDs are also associated with laboratory markers of mild hepatic dysfunction and, rarely, more severe hepatic injury. In contrast, the risk of renal injury from AEDs is generally low. In general, co-morbid hepatic or renal diseases influence the decision for the selection of an AED. For some patients dosing changes to their existing AEDs may be appropriate. For others, a change to another AED may be a better option.

Indexed as

AnticonvulsantsChemical and Drug Induced Liver InjuryHumansKidney DiseasesLiver DiseasesAnticonvulsants

Identifiers

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.