Evidence map›Paper›PMID 40384886›Full record

ArticleJCEM case reports2025

Marked Increase in Thyrotropin Receptor Antibodies With the Development of Pretibial Myxedema After Total Thyroidectomy.

Yoshinari Obata, Yukari Fujita, Ayaka Korechika, Rieko Nakatani, Junji Kozawa, Iichiro Shimomura

Abstract readCase Reports
In one paragraph

Article in JCEM case reports, 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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0cells of the map it votes in
0citing 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

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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

6 authors.

Yoshinari ObataDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.ORCID https://orcid.org/0000-0002-3443-3635
Yukari FujitaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.ORCID https://orcid.org/0000-0002-8847-5654
Ayaka KorechikaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.
Rieko NakataniDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.ORCID https://orcid.org/0000-0002-7684-466X
Junji KozawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.ORCID https://orcid.org/0000-0001-9665-8947
Iichiro ShimomuraDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.ORCID https://orcid.org/0000-0002-0851-9603

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A recent study revealed that the complex of thyrotropin receptors (TSHRs) and human leukocyte antigen (HLA) class II molecules within the thyroid gland, rather than TSHR alone, induces anti-TSHR autoantibody production by disrupting self-tolerance in Graves disease (GD). However, this complex has not yet been identified outside the thyroid gland. Complete removal of the thyroid gland typically reduces autoantibody titers by eliminating the antigen source. We present the case of a 51-year-old woman with GD and Graves ophthalmopathy who exhibited a marked increase in anti-TSHR autoantibodies concurrent with the development of pretibial myxedema (PTM) despite having undergone a total thyroidectomy. Immunohistological analysis of PTM tissues revealed the coexpression of TSHR and HLA class II molecules, forming a complex similar to that previously identified in the thyroid gland. These findings suggest that TSHR complexed with HLA class II molecules in PTM tissues may contribute to autoantibody production in this patient after total thyroidectomy, although the involvement of potential residual thyroid tissue cannot be entirely excluded. This case suggests that autoantibodies can be induced outside the thyroid gland and provides novel insights into the pathogenesis and progression of GD and related disorders.

Indexed as

autoantibodyGraves diseaseGraves ophthalmopathyhuman leukocyte antigen class II moleculespretibial myxedemathyrotropin receptor

Identifiers

PMID40384886
PMCPMC12079030

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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.