Evidence map›Paper›PMID 40660280›Full record

ArticleThyroid research2025

Challenges in subtyping disease entities of thyroid dysfunction following combined immune checkpoint inhibitor therapy: a case report.

Marco Juul Thomsen, Stine Linding Andersen, Nanna Maria Uldall Torp, Stig Andersen, Allan Carlé

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Article in Thyroid research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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3 citing papers in PubMed.

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5 · Who and what money

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5 authors.

Marco Juul ThomsenDepartment of Clinical Biochemistry, Aalborg University Hospital, Hobrovej 18-22, Aalborg, 9000, Denmark.
Stine Linding AndersenDepartment of Clinical Biochemistry, Aalborg University Hospital, Hobrovej 18-22, Aalborg, 9000, Denmark. stine.a@rn.dk.ORCID http://orcid.org/0000-0001-6336-1936
Nanna Maria Uldall TorpDepartment of Clinical Biochemistry, Aalborg University Hospital, Hobrovej 18-22, Aalborg, 9000, Denmark.
Stig AndersenDepartment of Clinical Medicine, Aalborg University, Aalborg, 9000, Denmark.
Allan CarléDepartment of Clinical Medicine, Aalborg University, Aalborg, 9000, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmune checkpoint inhibitor (ICI) therapy is used in the management of advanced malignancies. Thyroid function abnormalities have been reported, but more evidence is needed to substantiate the subtypes and course of thyroid disease associated with this treatment. CASE PRESENTATION: A 51-year-old woman with metastatic pancreatic cancer and no previous history of autoimmune disease was referred to the Endocrine Department six days after the initiation of combined treatment with ipilimumab (anti-CTLA-4) and nivolumab (anti-PD-1). At the initial endocrinologic assessment, the patient had biochemical overt thyrotoxicosis with suppressed thyroid stimulating hormone < 0.01 mIU/L (reference range (RR), 0.3-4.5 mIU/L), elevated total thyroxine (TT4) > 309 nmol/L (> 24.0 µg/dL) (RR, 60-140 nmol/L; 4.7-10.9 µg/dL), and total triiodothyronine (TT3) 7.0 nmol/L (454.5 ng/dL) (RR, 1.1-2.5 nmol/L; 71.4-162.3 ng/dL). Despite marked biochemical thyrotoxicosis, the patient presented with few symptoms. TSH-receptor antibodies (TRAb) were negative, as were thyroid peroxidase antibodies, whereas elevated levels of thyroglobulin antibodies were found. Thyroid ultrasound revealed an enlarged, heterogeneous hypoechoic gland with increased vascularity. High-dose antithyroid drug (ATD) therapy were followed by a decline in thyroid hormone levels (after one week of treatment: TT4: >309 nmol/L (> 24.0 µg/dL); TT3: 1.8 nmol/L (116.9 ng/dL); after two weeks: TT4: 164 nmol/L (12.7 µg/dL); TT3: 0.9 nmol/L (58.4 ng/dL)). After five weeks, the patient developed biochemical hypothyroidism. Thus, ATD therapy was discontinued, and levothyroxine was initiated.

conclusionThis case report illustrates with a short time frame from the initiation of ICI therapy the onset of thyrotoxicosis, followed by the development of thyroid insufficiency. This case highlights the challenges associated with subtyping the cause of thyroid dysfunction in patients treated with ICIs. Further, this case highlights the importance of clinical awareness and close monitoring of thyroid function in patients receiving immunotherapy.

Indexed as

CTLA-4HyperthyroidismHypothyroidismImmune-related adverse eventsPD-1

Identifiers

PMID40660280
PMCPMC12261766

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