Evidence map›Paper›PMID 31111437›Full record

ArticleEndocrine pathology2019

Pembrolizumab-Induced Thyroiditis.

Brittney A Imblum, Zubair W Baloch, Douglas Fraker, Virginia A LiVolsi

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in Endocrine pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 10% of its field
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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  15. Endocrine immune-related adverse events: a double-edged sword?Translational lung cancer research · 2021
    Article
  16. Review
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  18. First line Immunotherapy for Non-Small Cell Lung Cancer.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Brittney A ImblumDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Six Founders Pavilion, Philadelphia, PA, 19104-4283, USA. Brittney.imblum@uphs.upenn.edu.
Zubair W BalochDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Six Founders Pavilion, Philadelphia, PA, 19104-4283, USA.
Douglas FrakerDepartment of Surgery and Division of Endocrine & Oncologic Surgery, Hospital of the University of Pennsylvania, 3400 Spruce Street, Four Silverstein, Philadelphia, PA, 19104-4283, USA.
Virginia A LiVolsiDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Six Founders Pavilion, Philadelphia, PA, 19104-4283, USA.
Hospital of the University of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint inhibitors act to restore T cell-mediated antitumor immunity. By this nature, these cancer immunotherapy drugs are associated with various immune-related adverse events such as thyroid dysfunction. We describe a case of thyrotoxicosis secondary to a programmed cell death 1 (PD-1) immune checkpoint inhibitor, pembrolizumab. A 30-year-old female was started on pembrolizumab immunotherapy for stage III small cell carcinoma of the ovary, hypercalcemic type. Thirteen days after her second cycle of therapy, she presented with symptoms consistent with thyrotoxicosis. A thyroiditis was diagnosed by thyroid function tests and ultrasonography. She was originally treated with prednisone and metoprolol for possible Grave's disease. Pertechnetate thyroid scan was more consistent with thyroiditis secondary to pembrolizumab. She underwent a total thyroidectomy 10 days after initial presentation for refractory thyrotoxicosis despite maximal medical therapy. Her symptoms resolved and thyroid function tests significantly improved. Pathology was consistent with severe thyroiditis. Immune microenvironment may play a role in the expression of programmed cell death protein 1 ligand 1 (PD-L1). Chronic inflammation surrounding tumor upregulates PD-L1 expression on tumor cells by the release of cytokines, which acts to inhibit tumor destruction. We suggest that our patient had an undetected chronic inflammation of the thyroid, specifically Hashimoto's thyroidits, which predisposed her to thyroid destruction when taking pembrolizumab. Understanding that an inflammatory environment impacts thyroid toxicity to PD-1 inhibitor therapy is novel and should be further studied.

Indexed as

AdultAntibodies, Monoclonal, HumanizedAntithyroid AgentsCarcinoma, Small CellFemaleGraves DiseaseHumansMethimazoleOvarian NeoplasmsThyroidectomyThyroid GlandThyroiditisAntibodies, Monoclonal, HumanizedAntithyroid AgentsMethimazolepembrolizumabPD-1 inhibitorPDL-1 inhibitorPembrolizumabSmall cell carcinoma of ovaryThyroidThyroiditisThyrotoxicosis

Identifiers

PMID31111437
OpenAlexW2946263357

What OpenQuestion holds

Textmetadata
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.