Evidence map›Paper›PMID 18598365›Full record

ArticleBMC medical genetics2008

Analytical approaches to detect maternal/fetal genotype incompatibilities that increase risk of pre-eclampsia.

Neeta Parimi, Gerard Tromp, Helena Kuivaniemi, Jyh Kae Nien, Ricardo Gomez, Roberto Romero, Katrina Ab Goddard

Abstract read
In one paragraph

Article in BMC medical genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

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

  1. Pooled it
  2. Preeclampsia and eclampsia: the conceptual evolution of a syndrome.American journal of obstetrics and gynecology · 2022
    Review
  3. Joint Associations of Maternal-Fetal APOL1 Genotypes and Maternal Country of Origin With Preeclampsia Risk.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2021
    Article
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  13. A NovelMolecular genetics & genomic medicine · 2013
    Article
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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

7 authors.

Neeta ParimiDepartment of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, OH, USA. NParimi@sfcc-cpmc.net
Gerard Tromp
Helena Kuivaniemi
Jyh Kae Nien
Ricardo Gomez
Roberto Romero
Katrina Ab Goddard

Funding

The Role Of Subclinical Infection And Cytokines In Preterm ParturitionZIAHD002400 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI ROMERO, ROBERTO · 2009 to 2025
$254.4M
X-LINKED EXTENSION OF THE REVISED HASEMAN-ELSTON ALGORITHM FOR LINKAGE ANALYSISP41RR003655 · NCRR · LOUISIANA STATE UNIV HSC NEW ORLEANS · PI ELSTON, ROBERT C. · 1987 to 2011
$11.5M
THE ROLE OF SUBCLINICAL INFECTION AND CYTOKINES IN PRETERM PARTURITIONZ01HD002400 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI ROMERO, ROBERTO · 1992 to 2008
$8.2M
NCRR NIH HHS P41 RR003655NCRR NIH HHS RR03655
6 · The paper itself

Abstract

backgroundIn utero interactions between incompatible maternal and fetal genotypes are a potential mechanism for the onset or progression of pregnancy related diseases such as pre-eclampsia (PE). However, the optimal analytical approach and study design for evaluating incompatible maternal/offspring genotype combinations is unclear.

methodsUsing simulation, we estimated the type I error and power of incompatible maternal/offspring genotype models for two analytical approaches: logistic regression used with case-control mother/offspring pairs and the log-linear regression used with case-parent triads. We evaluated a real dataset consisting of maternal/offspring pairs with and without PE for incompatibility effects using the optimal analysis based on the results of the simulation study.

resultsWe identified a single coding scheme for the incompatibility effect that was equally or more powerful than all of the alternative analysis models evaluated, regardless of the true underlying model for the incompatibility effect. In addition, the log-linear regression was more powerful than the logistic regression when the heritability was low, and more robust to adjustment for maternal or fetal effects. For the PE data, this analysis revealed three genes, lymphotoxin alpha (LTA), von Willebrand factor (VWF), and alpha 2 chain of type IV collagen (COL4A2) with possible incompatibility effects.

conclusionThe incompatibility model should be evaluated for complications of pregnancy, such as PE, where the genotypes of two individuals may contribute to the presence of disease.

Indexed as

FetusGenotypeComputer SimulationFemaleGenetic MarkersGenetic Predisposition to DiseaseHumansLogistic ModelsMaternal-Fetal ExchangeModels, GeneticPolymorphism, Single NucleotidePre-EclampsiaPregnancyRisk FactorsGenetic Markers

Identifiers

PMID18598365
PMCPMC2474585

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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.