Evidence map›Paper›PMID 21920347›Full record

ArticleActa tropica2011

In vitro amodiaquine resistance and its association with mutations in pfcrt and pfmdr1 genes of Plasmodium falciparum isolates from Nigeria.

O A Folarin, C Bustamante, G O Gbotosho, A Sowunmi, M G Zalis, A M J Oduola, C T Happi

Abstract read
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In one paragraph

Article in Acta tropica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
4.1field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. bioRxiv : the preprint server for biology · 2026
    Article
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  12. Review
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  14. Review
  15. Article
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  17. Polymorphism Analysis ofDiseases (Basel, Switzerland) · 2021
    Article
  18. Article
  19. Ex vivo Sensitivity Profile ofInfection and drug resistance · 2021
    Article
  20. 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

7 authors at 3 institutions in 2 countries.

O A FolarinMalaria Research Laboratories, IMRAT, College of Medicine, University of Ibadan, Ibadan, Nigeria.
C Bustamante
G O Gbotosho
A Sowunmi
M G Zalis
A M J Oduola
C T Happi
University of Ibadan · NGHospital Universitário Clementino Fraga Filho · BRSpecial Programme for Research and Training in Tropical Diseases

Funding

Molecular determinants of P. falciparum resistance to ACTs in Nigeria.R03TW007757 · FIC · COLLEGE OF MEDICINE, UNIVERSITY OF IBADAN · PI HAPPI, CHRISTIAN T. · 2008 to 2010
$112k
FIC NIH HHS R03 TW007757FIC NIH HHS R03TW007757-03
6 · The paper itself

Abstract

Amodiaquine (AQ) is currently being used as a partner drug in combination with artesunate for treatment of uncomplicated malaria in most endemic countries of Africa. In the absence of molecular markers of artemisinin resistance, molecular markers of resistance to AQ may be useful for monitoring the development and spread of parasites resistance to Artesunate-Amodiaquine combination. This study was designed to assess the potential role of polymorphisms on pfcrt and pfmdr1 genes and parasite in vitro susceptibility for epidemiological surveillance of amodiaquine resistance in Plasmodium falciparum. The modified schizont inhibition assay was used to determine in vitro susceptibility profiles of 98 patients' isolates of P. falciparum to amodiaquine. Polymorphisms on parasites pfcrt and pfmdr1 genes were determined with nested PCR followed by sequencing. The geometric mean (GM) of AQ 50% inhibitory concentration (IC-50) in the 97 P. falciparum isolates was 20.48 nM (95% CI 16.53-25.36 nM). Based on the cut-off value for AQ in vitro susceptibility, 87% (84) of the P. falciparum isolates were sensitive to AQ (GM IC-50=16.32 nM; 95%CI 13.3-20.04 nM) while 13% were resistant to AQ in vitro (GM IC-50=88.73nM; 95%CI 69.67-113.0nM). Molecular analysis showed presence of mutant CVIET pfcrt haplotype, mutant pfmdr1Tyr86 allele and the double mutant CVIET pfcrt haplotype+pfmdr1Tyr86 in 72%, 49% and 35%, respectively. The GM IC-50 of isolates harboring the wild-type pfcrt CVMNK haplotype+pfmdr1Asn86 allele (3.93nM; 95%CI 1.82-8.46 nM) was significantly lower (p=0.001) than those isolates harboring the double mutant pfcrt CVIET haplotype+pfmdr1Tyr86 allele (50.40 nM; 95%CI 40.17-63.24 nM). Results from this study suggest that polymorphisms in pfcrt and pfmdr1 genes are important for AQ resistance and therefore may be useful for epidemiological surveillance of P. falciparum resistance to AQ.

Indexed as

Mutation, MissenseAllelesAmodiaquineAntimalarialsATP-Binding Cassette, Sub-Family C ProteinsChildChild, PreschoolDNA, ProtozoanFemaleHaplotypesHumansInfantMaleMembrane Transport ProteinsNigeriaParasitic Sensitivity TestsAmodiaquineAntimalarialsATP-Binding Cassette, Sub-Family C ProteinsDNA, ProtozoanMdr1 protein, Plasmodium falciparumMembrane Transport ProteinsPfCRT protein, Plasmodium falciparumProtozoan Proteins

Identifiers

PMID21920347
PMCPMC3214618
OpenAlexW2090693309

What OpenQuestion holds

Textmetadata
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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.