Evidence map›Paper›PMID 42368891›Full record

ArticleInternational journal of endocrinology2026

Causal Association Between Thyroid Function and Myeloproliferative Disease: A Two-Sample Mendelian Randomization Study.

Jingjing Xiang, Jun Yan, Jianping Shen, Mengke Mao, Zhiyin Zheng, Shu Deng

Abstract read
In one paragraph

Article in International journal of endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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. 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

6 authors.

Jingjing XiangDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China, zjhtcm.com.ORCID https://orcid.org/0000-0001-9386-4016
Jun YanLaboratory of Chemistry and Physics, Hangzhou Center for Disease Control and Prevention (Hangzhou Health Supervision Institution), Hangzhou, Zhejiang, China.ORCID https://orcid.org/0009-0003-9957-6578
Jianping ShenDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China, zjhtcm.com.ORCID https://orcid.org/0000-0002-7027-7369
Mengke MaoDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China, zjhtcm.com.ORCID https://orcid.org/0009-0008-6522-9232
Zhiyin ZhengDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China, zjhtcm.com.ORCID https://orcid.org/0009-0005-8419-7115
Shu DengDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China, zjhtcm.com.ORCID https://orcid.org/0000-0001-8353-6705

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Thyroid dysfunction has been linked to hematologic abnormalities, but whether thyroid function has a causal role in myeloproliferative diseases (MDs), including chronic myeloproliferative disease (CMD), remains unclear. We used Mendelian randomization (MR) to assess the potential causal effects of thyroid-related traits on MD risk. Methods: A two-sample MR analysis was performed using genome-wide association study (GWAS) summary statistics. Outcome data for CMD and MD, excluding chronic myelogenous leukemia (CML), were obtained from the Finnish R12 cohort (European ancestry). Genetic instruments for thyroid traits-including thyrotropin (TSH), free thyroxine (FT4), free/total triiodothyronine (FT3/TT3), FT3/FT4 and TT3/FT4 ratios, high/low TSH, and genetic liability to hyperthyroidism and hypothyroidism-were selected at genome-wide significance ( Results: Most thyroid function measures (TSH, FT4, FT3, TT3, hormone ratios, and hypothyroidism) showed no evidence of a causal association with CMD or MD excluding CML (IVW Conclusions: In this MR study, we found no robust evidence for a causal association between most genetically predicted thyroid function traits and MD after multiple-testing correction. The nominal signals observed for hyperthyroidism were phenotype-dependent and statistically unstable, particularly for self-reported CMD. These results emphasize that previously observed associations may be driven by nongenetic factors or clinical confounding.Jingjing Xiang and Jun Yan were co-first authors.

Indexed as

chronic myeloproliferative diseasehyperthyroidismMendelian randomizationmyeloproliferative diseasethyroid function

Identifiers

PMID42368891
PMCPMC13309939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.