Evidence map›Paper›PMID 22168261›Full record

ArticleMalaria journal2011

Association of ADAMTS13 polymorphism with cerebral malaria.

Sirima Kraisin, Izumi Naka, Jintana Patarapotikul, Duangdao Nantakomol, Pornlada Nuchnoi, Hathairad Hananantachai, Naoyuki Tsuchiya, Jun Ohashi

Open access · goldAbstract read
In one paragraph

Article in Malaria journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The von Willebrand factor - ADAMTS-13 axis in malaria.Research and practice in thrombosis and haemostasis · 2022
    Article
  5. Article
  6. Review
  7. ADAMTS13 and von Willebrand factor interactions.Current opinion in hematology · 2015
    Article
  8. Review
  9. Article
  10. Structure-function and regulation of ADAMTS-13 protease.Journal of thrombosis and haemostasis : JTH · 2013
    Review
  11. ADAMTS13, TTP and Beyond.Hereditary genetics : current research · 2013
    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

8 authors at 4 institutions in 2 countries.

Sirima KraisinDoctoral Program in Biomedical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, Japan.
Izumi Naka
Jintana Patarapotikul
Duangdao Nantakomol
Pornlada Nuchnoi
Hathairad Hananantachai
Naoyuki Tsuchiya
Jun Ohashi
University of Tsukuba · JPMahidol University · THChulalongkorn University · THMahidol Oxford Tropical Medicine Research Unit · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebral malaria is one of the most severe manifestations of Plasmodium falciparum malaria. The sequestration of parasitized red blood cells (PRBCs) to brain microvascular endothelium has been shown to contribute to the pathophysiology of cerebral malaria. Recent studies reported increased levels of von Willebrand factor (VWF) and reduced activity of VWF-cleaving protease, ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13), in patients with cerebral malaria.

methodsAssociation of six single nucleotide polymorphisms (SNPs) of the ADAMTS13 gene with cerebral malaria was examined in 708 Thai patients with P. falciparum malaria.

resultsAmong six SNPs, the derived allele of a SNP located in intron 28, rs4962153-A, was significantly associated with protection against cerebral malaria when 115 cerebral malaria patients were compared with 367 mild malaria patients (Fisher's exact P-value = 0.0057; OR = 0.27; 95% CI = 0.096-0.76). Significant association was also detected between 115 cerebral malaria and 593 non-cerebral malaria (226 non-cerebral severe malaria and 367 mild malaria) patients (Fisher's exact P-value = 0.012; OR = 0.30; 95% CI = 0.11-0.83).

conclusionsExcessive adhesion of PRBCs to the platelet-decorated ultra-large VWF (ULVWF) appears to enhance the sequestration of PRBCs to cerebral microvascular endothelium. The genetic association observed in the present study implies that the regulation of platelet-decorated ULVWF strings by ADAMTS13 may play a role in the development of cerebral malaria.

Indexed as

Genetic Predisposition to DiseaseADAM ProteinsADAMTS13 ProteinAdolescentAdultDisease ResistanceGene FrequencyGenetic Association StudiesHumansMalaria, CerebralMalaria, FalciparumPlasmodium falciparumPolymorphism, Single NucleotideThailandYoung AdultADAM ProteinsADAMTS13 ProteinADAMTS13 protein, human

Identifiers

PMID22168261
PMCPMC3261218
OpenAlexW2170325640

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Registered trials

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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.