Evidence map›Paper›PMID 30374748›Full record

ArticleClinical rheumatology2019

The association of CD40 polymorphism (rs1883832C/T) and soluble CD40 with the risk of systemic lupus erythematosus among Egyptian patients.

Taghreed G Mousa, Hanan H Omar, Rasha Emad, Mona I Salama, Waleed Omar, Mohamed Fawzy, Howayda M Hassoba

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Article in Clinical rheumatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Regulation of Toll-like receptor-mediated inflammatory response by microRNA-152-3p-mediated demethylation of MyD88 in systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Taghreed G MousaClinical Pathology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Hanan H OmarClinical Pathology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Rasha EmadClinical Pathology Department, Faculty of Medicine, Port Said University, Port Said, Egypt.
Mona I SalamaClinical Pathology Department, Faculty of Medicine, Port Said University, Port Said, Egypt.
Waleed OmarInternal Medicine Department, Nephrology Unit, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Mohamed FawzyInternal Medicine Department, Nephrology Unit, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Howayda M HassobaClinical Pathology Department, Faculty of Medicine, Suez Canal University, Ismailia, Egypt. hhassoba@yahoo.com.
Suez Canal University · EGPort Said University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus (SLE) is a complex autoimmune disorder of unknown etiology. Considerable evidence supports a genetic basis for susceptibility to SLE. Genetic and functional data suggested the CD40 receptor (CD40) and CD40 ligand (CD40L) as strong candidate genes for SLE.

aimTo investigate whether CD40 gene rs1883832 C/T single-nucleotide polymorphism (SNP) and/or soluble CD40 (sCD40) are associated with SLE in the Egyptian population. SUBJECTS AND

methodsThe study included a hundred SLE patients, and a fifty age- and gender-matched healthy control subjects. CD40 gene rs1883832 C/T genotyping was carried out using restriction fragment length polymorphism (RFLP), while sCD40 levels were measured by ELISA.

resultsCD40 rs1883832C/T genotypes (CC, TT, and CT) as well as CD40 alleles (C and T) did not differ between SLE patients and normal control (p = 0.63, 0.37, and 0.31 respectively). Though did not reach statistical significance, carriers of genotype CT had 1.5 times more chance to develop SLE compared to wild homozygous CC genotype carriers (OR 1.44), while carriers of genotype TT had ~ 2 times more chance to have SLE than CC carries (OR 1.96). Accordingly, the carriers of the T allele had ¬ 1.5 times more chance to get SLE compared to the carriers of the C allele (OR 1.4). The serum sCD40 level was significantly higher in SLE patients compared to healthy control (3.4 vs. 0.8 ng/mL, p < 0.001). In SLE patients, using CC as the reference genotype, serum sCD40 level was significantly higher in the carriers of the homozygous genotype TT (3.8 ± 1.3 vs. 2.9 ± 1.9, p = 0.0001), and T allele (3.6 ± 1.4 vs. 3.0 ± 1.5, p = 0.003). Moreover, sCD40 could discriminate SLE patients from normal subjects at a cutoff value of 0.885 ng/mL with 98% sensitivity and 96% specificity (AUC = 0.999, p < 0.001).

conclusionsThe study did not prove CD40 gene (rs1883832 C/T) polymorphism as a clear risk factor of SLE in this cohort of Egyptian patients, though it was highly likely associated with the carriers of T allele. In the same context, significant high sCD40 levels were observed in the T allele carriers.

Indexed as

AdultAllelesCase-Control StudiesCD40 AntigensEgyptEnzyme-Linked Immunosorbent AssayFemaleGenetic Predisposition to DiseaseGenotypeHumansLupus Erythematosus, SystemicMalePolymorphism, Restriction Fragment LengthPolymorphism, Single NucleotideCD40 AntigensCD40 genotypesEgyptRFLP

Identifiers

PMID30374748
OpenAlexW2899014029

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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.