Evidence map›Paper›PMID 21541267›Full record

SynthesisMolecular vision2011

Complement factor B polymorphism 32W protects against age-related macular degeneration.

Anne E Hughes, Gemma M Mullan, Declan T Bradley

Open access · greenAbstract readMeta-Analysis
In one paragraph

Synthesis in Molecular vision, 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
2.2field-weighted citation impact, top 14% 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, 16 citations in OpenAlex.

  1. Article
  2. Immunogenetic and Environmental Factors in Age-Related Macular Disease.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Functional Evaluation of AMD-Associated Risk Variants of Complement Factor B.Investigative ophthalmology & visual science · 2020
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
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 1 institution in 1 country.

Anne E HughesCentre for Public Health, Queen's University Belfast, UK. a.hughes@qub.ac.uk
Gemma M Mullan
Declan T Bradley
Queen's University Belfast · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe 32Q (rs641153; A) and 32W (rs12614; T) variants of complement factor B (CFB) cause less efficient complement activation in vitro than the common 32R variant. This is thought to be the reason that the 32Q variant is associated with decreased risk of age-related macular degeneration (AMD). We investigated whether the 32W variant was also associated with decreased risk of AMD.

methodsWe genotyped 367 cases with neovascular AMD and 251 disease-free controls. Association with the disease phenotype was assessed by logistic regression for polymorphisms of CFB alone and in combination with smoking status and genetic risk markers of complement factor H (CFH) and HtrA serine peptidase 1 (HTRA1). We performed meta-analysis of all previously published reports of 32W allele frequency in AMD cases and controls.

resultsThe CFB variant 32W was associated with protection against neovascular AMD, compared to the common 32R variant (odds ratio 0.64, p<0.05, in logistic regression with CFB variants; odds ratio 0.53, p<0.05, in logistic regression with CFB variants, CFH haplotypes, HTRA1 rs10490924 genotype, and smoking status). Meta-analysis (n=1,795) including this study and two others of neovascular AMD showed a combined odds ratio of 0.75 (p<0.05) for 32W, compared to 32R. Meta-analysis (n=2,600) of all reported studies of all types of AMD showed a combined odds ratio of 0.79 (p<0.01).

conclusionsOur study shows that the 32W variant of CFB is associated with protection against AMD, in keeping with evidence of its functional effect on the complement system. The protective effect is less strong than that associated with 32Q.

Indexed as

AgedAged, 80 and overArginineCase-Control StudiesComplement ActivationComplement Factor BComplement Factor HFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeGlutamineHaplotypesHigh-Temperature Requirement A Serine Peptidase 1HumansLinkage DisequilibriumArginineComplement Factor BComplement Factor HGlutamineHigh-Temperature Requirement A Serine Peptidase 1HTRA1 protein, humanSerine EndopeptidasesTryptophan

Identifiers

PMID21541267
PMCPMC3084221
OpenAlexW181826786

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.