Evidence map›Paper›PMID 26902538›Full record

ArticleThe pharmacogenomics journal2017

Role of the C1858T polymorphism of protein tyrosine phosphatase non-receptor type 22 (PTPN22) in children and adolescents with type 1 diabetes.

A Blasetti, C Di Giulio, S Tumini, M Provenzano, D Rapino, L Comegna, G Prezioso, R Chiuri, S Franchini, F Chiarelli and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in The pharmacogenomics journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

4 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

11 authors at 1 institution in 1 country.

A BlasettiDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
C Di GiulioDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
S TuminiDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
M ProvenzanoLaboratory of Molecular Genetics, DISPUTer (Department of Psychological Sciences, Health and Territory), School of Medicine and Health Sciences, 'G. d'Annunzio' University, Chieti, Italy.
D RapinoDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
L ComegnaDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
G PreziosoDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
R ChiuriDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
S FranchiniDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
F ChiarelliDepartment of Pediatrics, 'G. d'Annunzio' University, Chieti, Italy.
L StuppiaLaboratory of Molecular Genetics, DISPUTer (Department of Psychological Sciences, Health and Territory), School of Medicine and Health Sciences, 'G. d'Annunzio' University, Chieti, Italy.
University of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, increasing interest has been devoted to the susceptibility gene polymorphisms in type 1 diabetes (T1D) as well as in other autoimmune diseases. Among these, a nucleotide polymorphism of the gene encoding for the protein tyrosine phosphatase non-receptor type 22 (PTPN22) has been associated with T1D in several studies. The aim of this study is to define the frequency of the C1858T polymorphism in the PTPN22 gene in a cohort of 113 Caucasian patients (58 males and 55 females) with T1D, and to assess a possible correlation with a group of clinically relevant variables: age at onset, gender, diabetes-related autoantibodies, residual β-cell function and daily insulin requirement (IR) 6 months after diagnosis. Using a PCR-RFLP approach, we evidenced a 17.7% frequency of the PTPN22 C1858T polymorphism in diabetic patients, higher than the frequency showed in the general population. A statistically significant correlation between this polymorphism and higher levels of C-peptide at diagnosis and lower IR at 6 months from diagnosis was observed (P=0.001 and P=0.04). Moreover, 1858T variant carriers were more frequently positive for glutamic acid decarboxylase (GAD) autoantibodies at diagnosis than wild-type subjects (P=0.19). On the other hand, no significant difference regarding age at onset, gender distribution, insulinoma-associated 2 molecule (IA2) and islet cell antibodies (ICA) positivity was found. These findings, if adequately confirmed in the future and extended to larger samples, may characterize a subset of T1D patients with a defined genetic pattern, who may be eligible for trials aimed to preserve residual β-cell function in the coming years.

Indexed as

Pharmacogenomic VariantsPolymorphism, Single NucleotideAdolescentAge FactorsAutoantibodiesBiomarkersBlood GlucoseChildChild, PreschoolC-PeptideDiabetes Mellitus, Type 1FemaleGene FrequencyGenetic Predisposition to DiseaseGlutamate DecarboxylaseGlycated HemoglobinAutoantibodiesBiomarkersBlood GlucoseC-PeptideGlutamate DecarboxylaseGlycated Hemoglobinhemoglobin A1c protein, humanHypoglycemic AgentsInsulinProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, human

Identifiers

PMID26902538
OpenAlexW2415154667

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.