Evidence map›Paper›PMID 31519994›Full record

ReviewNature reviews. Cardiology2020

Genetics of rheumatic fever and rheumatic heart disease.

Babu Muhamed, Tom Parks, Karen Sliwa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
7.1field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Predictors of rheumatic fever in sore throat patients: a systematic review and meta-analysis.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2022
    Pooled it
  3. Review
  4. The global burden of rheumatic heart disease: 1990-2021.Clinical medicine (London, England) · 2026
    Article
  5. Article
  6. Valve biology and rheumatic heart disease pathogenesis.Nature cardiovascular research · 2026
    Review
  7. Acute rheumatic fever and rheumatic heart disease.Nature reviews. Disease primers · 2026
    Review
  8. Article
  9. Review
  10. Article
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  14. Review
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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

3 authors at 2 institutions in 2 countries.

Babu MuhamedHatter Institute for Cardiovascular Diseases Research in Africa, Department of Medicine, University of Cape Town, Cape Town, South Africa.ORCID http://orcid.org/0000-0003-4832-0671
Tom ParksFaculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, UK.ORCID http://orcid.org/0000-0002-1163-8654
Karen SliwaHatter Institute for Cardiovascular Diseases Research in Africa, Department of Medicine, University of Cape Town, Cape Town, South Africa. karen.sliwa-hahnle@uct.ac.za.
University of Cape Town · ZACentre for Human Genetics · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatic heart disease (RHD) is a complication of group A streptococcal infection that results from a complex interaction between the genetic make-up of the host, the infection itself and several other environmental factors, largely reflecting poverty. RHD is estimated to affect 33.4 million people and results in 10.5 million disability-adjusted life-years lost globally. The disease has long been considered heritable but still little is known about the host genetic factors that increase or reduce the risk of developing RHD. In the 1980s and 1990s, several reports linked the disease to the human leukocyte antigen (HLA) locus on chromosome 6, followed in the 2000s by reports implicating additional candidate regions elsewhere in the genome. Subsequently, the search for susceptibility loci has been reinvigorated by the use of genome-wide association studies (GWAS) through which millions of variants can be tested for association in thousands of individuals. Early findings implicate not only HLA, particularly the HLA-DQA1 to HLA-DQB1 region, but also the immunoglobulin heavy chain locus, including the IGHV4-61 gene segment, on chromosome 14. In this Review, we assess the emerging role of GWAS in assessing RHD, outlining both the advantages and disadvantages of this approach. We also highlight the potential use of large-scale, publicly available data and the value of international collaboration to facilitate comprehensive studies that produce findings that have implications for clinical practice.

Indexed as

Genetic LociAnimalsGenes, Immunoglobulin Heavy ChainGenetic Predisposition to DiseaseGenome-Wide Association StudyHLA-DQ alpha-ChainsHLA-DQ beta-ChainsHumansPhenotypeRheumatic FeverRheumatic Heart DiseaseRisk AssessmentRisk FactorsHLA-DQA1 antigenHLA-DQ alpha-ChainsHLA-DQB1 antigenHLA-DQ beta-Chains

Identifiers

PMID31519994
OpenAlexW2973126319

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.