Evidence map›Paper›PMID 23894496›Full record

ArticlePloS one2013

Nonlinear mixed-effects modelling of in vitro drug susceptibility and molecular correlates of multidrug resistant Plasmodium falciparum.

Julie A Simpson, Kris M Jamsen, Tim J C Anderson, Sophie Zaloumis, Shalini Nair, Charles Woodrow, Nicholas J White, Francois Nosten, Ric N Price

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
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

9 authors.

Julie A SimpsonCentre for Molecular, Environmental, Genetic & Analytic Epidemiology, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Australia. julieas@unimelb.edu.au
Kris M Jamsen
Tim J C Anderson
Sophie Zaloumis
Shalini Nair
Charles Woodrow
Nicholas J White
Francois Nosten
Ric N Price

Funding

MAPPING DRUG RESISTANCE GENES IN PLASMODIUM FALCIPARUMR01AI048071 · NIAID · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI Tim J Anderson · 2000 to 2026
$8.4M
Mapping Drug Resistance Genes in Plasmodium falciparumR37AI048071 · NIAID · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI ANDERSON, TIM J · 2012 to 2021
$7.9M
MOLECULAR AND BIOCHEMICAL GENETICS LABORATORY RENOVATIONC06RR013556 · NCRR · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI SHADE, ROBERT E · 1998 to 1998
–
NCRR NIH HHS C06 RR013556NIAID NIH HHS R01 AI048071NIAID NIH HHS R01 AI48071NIAID NIH HHS R37 AI048071Wellcome Trust 089275Wellcome Trust 091625Wellcome Trust 093956
6 · The paper itself

Abstract

The analysis of in vitro anti-malarial drug susceptibility testing is vulnerable to the effects of different statistical approaches and selection biases. These confounding factors were assessed with respect to pfmdr1 gene mutation and amplification in 490 clinical isolates. Two statistical approaches for estimating the drug concentration associated with 50% effect (EC50 ) were compared: the commonly used standard two-stage (STS) method, and nonlinear mixed-effects modelling. The in vitro concentration-effect relationships for, chloroquine, mefloquine, lumefantrine and artesunate, were derived from clinical isolates obtained from patients on the western border of Thailand. All isolates were genotyped for polymorphisms in the pfmdr1 gene. The EC50 estimates were similar for the two statistical approaches but 15-28% of isolates in the STS method had a high coefficient of variation (>15%) for individual estimates of EC50 and these isolates had EC50 values that were 32 to 66% higher than isolates derived with more precision. In total 41% (202/490) of isolates had amplification of pfmdr1 and single nucleotide polymorphisms were found in 50 (10%). Pfmdr1 amplification was associated with an increase in EC50 for mefloquine (139% relative increase in EC50 for 2 copies, 188% for 3+ copies), lumefantrine (82% and 75% for 2 and 3+ copies respectively) and artesunate (63% and 127% for 2 and 3+ copies respectively). In contrast pfmdr1 mutation at codons 86 or 1042 were associated with an increase in chloroquine EC50 (44-48%). Sample size calculations showed that to demonstrate an EC50 shift of 50% or more with 80% power if the prevalence was 10% would require 430 isolates and 245 isolates if the prevalence was 20%. In conclusion, although nonlinear mixed-effects modelling did not demonstrate any major advantage for determining estimates of anti-malarial drug susceptibility, the method includes all isolates, thereby, potentially improving confirmation of candidate molecular markers of anti-malarial drug susceptibility.

Indexed as

AntimalarialsArtemisininsArtesunateATP-Binding Cassette, Sub-Family C ProteinsChloroquineEthanolaminesFluorenesLumefantrineMefloquineModels, StatisticalPlasmodium falciparumPolymorphism, GeneticPolymorphism, Single NucleotideProtozoan ProteinsAntimalarialsArtemisininsArtesunateATP-Binding Cassette, Sub-Family C ProteinsChloroquineEthanolaminesFluorenesLumefantrineMdr1 protein, Plasmodium falciparumMefloquineProtozoan Proteins

Identifiers

PMID23894496
PMCPMC3722116

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.