Evidence map›Paper›PMID 30508004›Full record

ArticleGenetics and molecular biology

CTLA-4 gene polymorphisms are associated with obesity in Turner Syndrome.

Luana Oliveira Dos Santos, Adriana Valéria Sales Bispo, Juliana Vieira de Barros, Raysa Samanta Moraes Laranjeira, Rafaella do Nascimento Pinto, Jaqueline de Azevêdo Silva, Andréa de Rezende Duarte, Jacqueline Araújo, Paula Sandrin-Garcia, Sergio Crovella and 4 more

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In one paragraph

Article in Genetics and molecular biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.1field-weighted citation impact, top 52% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Guideline
  2. 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

14 authors at 4 institutions in 1 country.

Luana Oliveira Dos SantosDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Adriana Valéria Sales BispoInstituto Federal de Educação, Ciência e Tecnologia do Sertão Pernambucano, Campus Serra Talhada, Serra Talhada, PE, Brazil.
Juliana Vieira de BarrosDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Raysa Samanta Moraes LaranjeiraDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Rafaella do Nascimento PintoDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Jaqueline de Azevêdo SilvaDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Andréa de Rezende DuarteServiço de Genética Medica, Instituto de Medicina Integral Professor Fernando Figueira, Recife, PE, Brazil.
Jacqueline AraújoServiço de Endocrinlogia Pediátrica do Hospital das Clínicas, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Paula Sandrin-GarciaDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Sergio CrovellaDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.ORCID 0000-0001-8493-1168
Marcos André Cavalcanti BezerraDepartmento de Biofísica e Radiobiologia, Universidade Federal de Pernambuco, Recife, PE, Brazil.
Taciana Furtado de Mendonça BelmontInstituto de Biociências, Universidade de Pernambuco, Recife, PE, Brazil.
Maria do Socorro CavalcantiInstituto de Biociências, Universidade de Pernambuco, Recife, PE, Brazil.
Neide SantosDepartmento de Genética, Universidade Federal de Pernambuco, Recife, PE, Brazil.ORCID 0000-0002-6343-7707
Universidade Federal de Pernambuco · BRUniversidade de Pernambuco · BRInstituto de Medicina Integral Professor Fernando Figueira · BRInstituto Federal do Sertão Pernambucano · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Turner syndrome (TS) is characterized by a set of clinical conditions, including autoimmune/inflammatory diseases and infectious conditions, that can compromise a patient's quality of life. Here we assessed polymorphisms in CTLA-4 +49A/G (rs231775), PTPN22 +1858G/A (rs2476601), and MBL2 -550 (H/L) (rs11003125), -221(X/Y) (rs7096206) and exon 1 (A/O) in women from northeastern Brazil to determine whether polymorphisms within these key immune response genes confer differential susceptibility to clinical conditions in TS. A case-control genetic association study was performed, including 86 female TS patients and 179 healthy women. An association was observed for the A/G genotype of CTLA-4 +49A/G in TS patients (p=0.043, odds ratio [OR]=0.54). In addition, an association between the CTLA-4 G/G genotype and obesity was detected in TS patients (p=0.02, OR=6.04). Regarding, the -550(H/L) polymorphism in the MBL2 promoter, the frequency of the H/L genotype was significantly higher in the TS group than healthy controls (p=0.01, OR=1.96). The H/H genotype indicated a protective effect in TS patients (p=0.01, OR=0.23). No differences were observed in the distribution of -221(X/Y), MBL2 exon 1 variants, and PTPN22 +1858G/A in any assessed groups. CTLA-4 variants are potentially involved in obesity in this cohort of TS patients from northeastern Brazil.

Identifiers

PMID30508004
PMCPMC6415610
OpenAlexW2902942887

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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.