Evidence map›Paper›PMID 38284726›Full record

Trial reportEndocrine, metabolic & immune disorders drug targets2024

Alterations in CD4

Reza Chahardoli, Behrouz Robat-Jazi, Fereidoun Azizi, Atieh Amouzegar, Davood Khalili, Azita Zadeh-Vakili, Fatemeh Mansouri, Ali Akbar Saboor-Yaraghi

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Endocrine, metabolic & immune disorders drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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.

Reza ChahardoliSchool of Advanced Technologies in Medicine, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-7053-3676
Behrouz Robat-JaziDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.ORCID 0000-0001-7366-0972
Fereidoun AziziResearch Institute for Endocrine Science, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-6470-2517
Atieh AmouzegarResearch Institute for Endocrine Science, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0003-1046-0003
Davood KhaliliResearch Institute for Endocrine Science, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0003-4956-1039
Azita Zadeh-VakiliResearch Institute for Endocrine Science, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0001-6775-5537
Fatemeh MansouriDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.ORCID 0000-0003-3252-0708
Ali Akbar Saboor-YaraghiDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.ORCID 0000-0001-8612-4773

Funding

Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical SciencesTehran University of Medical Sciences and Health Services grant number 95-01-27-30905
6 · The paper itself

Abstract

backgroundHashimoto's thyroiditis (HT) is an autoimmune disease characterized by the destruction of thyroid cells through immune processes involving T helper (Th)1 cytokines. This clinical trial investigates the impact of vitamin D supplementation on serum cytokine levels and gene expression in CD4+ T cells from HT patients, aiming to understand its effects on Th-1, Th-2, Th-17, and regulatory T (Treg) cell-associated factors.

methodsFemale patients were randomly assigned in a double-blind design to either a vitamin D-supplemented group, which received cholecalciferol (1, 25(OH)

resultsSerum 25-hydroxyvitamin D and levels exhibited a significant increase following vitamin D supplementation, in comparison to the placebo group. Additionally, the vitamin D supplementation resulted in a significant elevation of serum calcium (Ca) levels compared to baseline. In the vitamin D group, there was a significant decrease in both serum levels and expression of the interleukin (IL)-17 gene when compared to baseline, although no statistical difference was observed between the placebo and vitamin D groups. The gene expression of transforming growth factor-beta (TGFβ) was significantly increased in the vitamin D group compared to baseline, with no significant difference between the two study groups. Vitamin D treatment had no effect on serum levels of interferon-gamma (IFNϒ) and IL-4. While the gene expression of IL-4 in the vitamin D group did not exhibit a statistically significant increase, the level of GATA3 transcription factor increased significantly when compared to the placebo group. The expression of IFNϒ and transcription factors, T-bet, RORc, and forkhead box protein 3 (FOXP3) in genes did not show significant changes following vitamin D supplementation.

conclusionThe findings suggest that vitamin D supplementation may hold potential benefits for autoimmune diseases, such as HT. However, further longitudinal clinical trials are necessary to gain a more comprehensive understanding of the specific effects of vitamin D on HT.

Indexed as

CytokinesDietary SupplementsHashimoto DiseaseVitamin DAdultCD4-Positive T-LymphocytesCholecalciferolDouble-Blind MethodFemaleHumansMiddle AgedTreatment Outcome25-hydroxyvitamin DCholecalciferolCytokinesVitamin DHashimoto’s thyroiditisIFNγrandomized clinical trial studyTGFβthyroid gland.vitamin D

Identifiers

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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.