Evidence map›Paper›PMID 23730990›Full record

ArticleJournal of clinical hypertension (Greenwich, Conn.)2013

Association of B2 receptor polymorphisms and ACE activity with ACE inhibitor-induced angioedema in black and mixed-race South Africans.

Retsilisitsoe R Moholisa, Brian R Rayner, E Patricia Owen, Sylva L U Schwager, Joalice S Stark, Motassim Badri, Clint L Cupido, Edward D Sturrock

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical hypertension (Greenwich, Conn.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Frontiers in genetics · 2025
    Article
  7. Review
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  11. Review
  12. Review
  13. Article
  14. Review
  15. Pharmacogenomics of off-target adverse drug reactions.British journal of clinical pharmacology · 2017
    Review
  16. "Nuts and Bolts" of Laboratory Evaluation of Angioedema.Clinical reviews in allergy & immunology · 2016
    Review
  17. Genetics of Hereditary Angioedema Revisited.Clinical reviews in allergy & immunology · 2016
    Review
  18. 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 2 institutions in 1 country.

Retsilisitsoe R MoholisaDivision of Medical Biochemistry, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
Brian R Rayner
E Patricia Owen
Sylva L U Schwager
Joalice S Stark
Motassim Badri
Clint L Cupido
Edward D Sturrock
University of Cape Town · ZAVictoria Hospital · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin-converting enzyme (ACE) inhibitors are first-line therapy for the treatment of hypertension, congestive heart failure, and diabetic nephropathy. ACE inhibitors are associated with adverse side effects such as persistent dry cough (ACE-cough) and, rarely, life-threatening angioedema (ACE-AE). The authors investigated the influence of ACE I/D polymorphism in combination with serum ACE activity, B₂ receptor -9/+9 polymorphism, and B₂ receptor C-58T single nucleotide polymorphism (SNP) on the development of ACE-AE and ACE-cough. The frequencies of ACE I/D as well as B₂ receptor +9/-9 and C-58T polymorphisms were compared in patients with ACE-AE, ACE-cough, and ACE inhibitor-exposed controls, and serum ACE activity was measured. There were 52 cases of ACE-AE, 36 cases of ACE-cough, and 77 controls. The genotyping revealed a significant association between the B₂ -9 allele and ACE inhibitor-induced AE (62% vs 38%, P=.008), and ACE inhibitor-induced cough (61% vs 38%, P=.02) when compared with controls. There was no significant association between ACE I/D polymorphism as well as the B₂ C-58T SNP with both ACE-induced AE and cough. ACE activity was significantly higher in controls compared with patients with ACE-AE (34.5 ± 1.14 mU/mL vs 17.8 ± 0.86 mU/mL, P=.0001) and ACE-cough (34.5 ± 1.14 mU/mL vs 23.3 ± 1.88 mU/mL, P=.0001). Thus, our data suggest that the B₂ -9 allele and reduced ACE activity are associated with both ACE-AE and ACE-cough.

Indexed as

Polymorphism, GeneticAgedAngioedemaAngiotensin-Converting Enzyme InhibitorsBlack PeopleComorbidityCoughFemaleGenotypeHumansHypertensionMaleMiddle AgedPeptidyl-Dipeptidase APolymerase Chain ReactionReceptor, Bradykinin B2Angiotensin-Converting Enzyme InhibitorsPeptidyl-Dipeptidase AReceptor, Bradykinin B2

Identifiers

PMID23730990
PMCPMC8033847
OpenAlexW1974061702

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.