Evidence map›Paper›PMID 40536711›Full record

Observational studyPharmacological reports : PR2025

Iodothyronine deiodinases in patients with stable chronic obstructive pulmonary disease - preliminary results.

Elżbieta Małujło-Balcerska, Anna Kumor-Kisielewska, Maria Gałecka, Tadeusz Pietras

Abstract readObservational Study
In one paragraph

Observational study in Pharmacological reports : PR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Elżbieta Małujło-BalcerskaDepartment of Pneumonology, Medical University of Łódź, Łódź, Poland. elzbieta.malujlo-balcerska@umed.lodz.pl.
Anna Kumor-KisielewskaDepartment of Pneumonology, Medical University of Łódź, Łódź, Poland.
Maria GałeckaMedical University of Łódź, Łódź, Poland.
Tadeusz PietrasDepartment of Clinical Pharmacology, Medical University of Łódź, Łódź, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDifferent immune/inflammatory molecules play key roles in the development of inflammatory diseases, including chronic obstructive pulmonary disease (COPD). Thyroid hormones (THs) participate in immune/inflammatory reactions and may play a role in COPD. The main TH metabolism reactions are dependent on iodothyronine deiodinase (DIO). Accumulating evidence also supports the role of cytokines in TH metabolism-related factors. This cross-sectional, observational study investigated the levels of DIO and proinflammatory cytokines and their correlations with stable COPD.

methodsA total of 55 participants, comprising 25 patients diagnosed with stable COPD and 30 control patients, were enrolled in this study. Cytokine and DIO levels were measured using commercially available human enzyme-linked immunosorbent assay (ELISA) kits from R&D Systems and My BioSource.

resultsIncreased levels of DIO1-3 and interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-ɑ, and interferon (IFN)-ɣ were found. Correlation analysis revealed several significant correlations, including interdependence between DIO and cytokine levels, with strong correlations between DIO2 and IFN-ɣ levels and an association between the above protein levels and clinical data. The levels of DIO 1-3 and cytokines (IL-6, TNF-α, and IFN-γ) all showed a positive relationship with COPD relative risk, suggesting that higher levels of DIO and cytokines may influence COPD biology.

conclusionsFindings from our novel study indicate that DIO and proinflammatory cytokines are possibly involved in the mechanisms underlying processes related to COPD, including immune-endocrine interaction. These can be discussed for further evaluation in COPD-related studies with more precise diagnostic and therapeutic monitoring of all confounding factors and a larger cohort.

Indexed as

CytokinesIodide PeroxidasePulmonary Disease, Chronic ObstructiveAgedCross-Sectional StudiesFemaleHumansMaleMiddle AgedThyroid HormonesCytokinesIodide PeroxidaseThyroid HormonesCOPDCytokinesInflammationIodothyronine deiodinaseThyroid hormone

Identifiers

PMID40536711
PMCPMC12241153

What Socratic holds

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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 Socratic graph.