Evidence map›Paper›PMID 29776388›Full record

ArticleBMC gastroenterology2018

Contributions of HLA haplotypes, IL8 level and Toxoplasma gondii infection in defining celiac disease's phenotypes.

Mohammad Rostami-Nejad, Seyed Hossein Hejazi, Amado Salvador Peña, Hamid Asadzadeh-Aghdaei, Kamran Rostami, Umberto Volta, Mohammad Reza Zali

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. ChronicProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  3. Genetic and Environmental Contributors for Celiac Disease.Current allergy and asthma reports · 2019
    Review
  4. Article
  5. 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

7 authors at 5 institutions in 4 countries.

Mohammad Rostami-NejadCeliac Disease Department, Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Seyed Hossein HejaziSkin Diseases and Leishmaniasis Research Center, Isfahan University of Medical sciences, Isfahan, Iran.
Amado Salvador PeñaLaboratory of Immunogenetics, Department of Medical Microbiology and Infection Control, Vrije Universiteit Medical Center (VUmc), Amsterdam, the Netherlands.
Hamid Asadzadeh-AghdaeiBasic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Kamran RostamiDepartment of Gastroenterology, Milton Keynes University Hospital, Milton Keynes, UK. krostami@hotmail.com.
Umberto VoltaDepartment of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
Mohammad Reza ZaliCeliac Disease Department, Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Shahid Beheshti University of Medical Sciences · IRAmsterdam UMC Location VUmc · NLIsfahan University of Medical Sciences · IRMilton Keynes Hospital · GBUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is not clear why some patients with coeliac disease (CD) present with severe symptoms and small intestinal mucosal damages while others present with milder symptoms and no frank enteropathy. There is no study to assess the associated factors with mild/severe symptoms and enteropathy. The terminologies like latent, silent and potential are difficult to use and are unrepresentative. In the present study we describe coeliac disease's phenotypes based on HLA haplotypes, IL8 production and past infection with Toxoplasma gondii (T. gondii) infection.

methodsIn this case-control study, sera originating from 150 healthy subjects and 150 patients diagnosed with CD during the years 2013-14 were analyzed for the presence of antibodies specific T. gondii of the IgG and IgM subclasses. The level of IL8 were measured and HLA-DQ2 and HLA-DQ8 alleles were genotyped. The correlation between these parameters and the damages in intestinal mucosal were assessed using an accepted histopathological classification.

resultsHigh levels of IgG antibodies against T. gondii were found in the sera of control group compared to the CD group (52.6% vs. 39.4%, P = 0.02). Mean serum levels of IL8 was significantly higher in CD patients compared with control (P ≤ 0.05). By comparing the level of anti- T. gondii IgG and mucosal damage in celiac disease, we found a significant relationship between the severity of mucosal damages and anti- T. gondii IgG level (P = 0.02). No correlation was detected between Toxoplasma gondii infection and types of HLA (P > 0.05). However, patients with severely abnormal histology carried HLA-DQ2 risk alleles (92 patients (61%)) more often than the controls and those with mild histological abnormalities.

conclusionsCD patients with severe histological changes had more often Toxoplasma gondii infection than those affected with mild histological features. This suggests that CD's phenotypes are correlated to additional factors like infections and to particular HLA DQ2 alleles that may need additional investigations and potentially will require additional treatment.

Indexed as

HaplotypesAllelesCase-Control StudiesCeliac DiseaseHLA-DQ AntigensHumansImmunoglobulin GInterleukin-8Intestinal MucosaToxoplasmaToxoplasmosisHLA-DQ2 antigenHLA-DQ8 antigenHLA-DQ AntigensImmunoglobulin GInterleukin-8AntibodiesCeliac diseaseGlutenHistological featuresHLA allelesToxoplasmosis

Identifiers

PMID29776388
PMCPMC5960085
OpenAlexW2805309404

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Registered trials

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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.