Evidence map›Paper›PMID 29050534›Full record

ArticleLupus2018

Low copy numbers of complement C4 and homozygous deficiency of C4A may predispose to severe disease and earlier disease onset in patients with systemic lupus erythematosus.

M Jüptner, F Flachsbart, A Caliebe, W Lieb, S Schreiber, R Zeuner, A Franke, J O Schröder

Open access · bronzeAbstract read
In one paragraph

Article in Lupus, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Full resolution HLA and KIR genes annotation for human genome assemblies.bioRxiv : the preprint server for biology · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

M Jüptner1 First Clinic of Internal Medicine, University Hospital of Kiel, Kiel, Germany.
F Flachsbart2 Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany.
A Caliebe3 Institute of Medical Informatics and Statistics, Christian-Albrechts-University of Kiel, Kiel, Germany.
W Lieb4 Institute of Epidemiology, Christian-Albrechts-University of Kiel, Kiel, Germany.
S Schreiber1 First Clinic of Internal Medicine, University Hospital of Kiel, Kiel, Germany.
R Zeuner1 First Clinic of Internal Medicine, University Hospital of Kiel, Kiel, Germany.
A Franke2 Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany.
J O Schröder1 First Clinic of Internal Medicine, University Hospital of Kiel, Kiel, Germany.
Kiel University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives Low copy numbers and deletion of complement C4 genes are potent risk factors for systemic lupus erythematosus (SLE). However, it is not known whether this genetic association affects the clinical outcome. We investigated C4 copy number variation and its relationship to clinical and serological features in a Northern European lupus cohort. Methods We genotyped the C4 gene locus using polymerase chain reaction (PCR)-based TaqMan assays in 169 patients with SLE classified according to the 1997 revised American College of Rheumatology (ACR) criteria and in 520 matched controls. In the patient group the mean C4 serum protein concentrations nephelometrically measured during a 12-month period prior to genetic analysis were compared to C4 gene copy numbers. Severity of disease was classified according to the intensity of the immunosuppressive regimens applied and compared to C4 gene copy numbers, too. In addition, we performed a TaqMan based analysis of three lupus-associated single-nucleotide polymorphisms (SNPs) located inside the major histocompatibility complex (MHC) to investigate the independence of complement C4 in association with SLE. Results Homozygous deficiency of the C4A isotype was identified as the strongest risk factor for SLE (odds ratio (OR) = 5.329; p = 7.7 × 10

Indexed as

DNA Copy Number VariationsGene DeletionGene DosageHomozygoteAdultAgedCase-Control StudiesChi-Square DistributionComplement C4aDrug Therapy, CombinationFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseGermanyHLA-DRB1 ChainsComplement C4aHLA-DRB1*03:01 antigenHLA-DRB1 ChainsImmunosuppressive Agentscomplement C4copy number variationHLASystemic lupus erythematosus

Identifiers

PMID29050534
PMCPMC5871021
OpenAlexW2766393665

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.