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Cited by 161Cancer Immunotherapy and BiomarkersThyroid Disorders and TreatmentsAutoimmune Neurological Disorders and Treatments

The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.

Characterization of Thyroid Disorders in Patients Receiving Immune Checkpoint Inhibition Therapy

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Lee, Hyunju, Hodi, F. Stephen, Giobbie-Hurder, Anita, Ott, Patrick A., Buchbinder, Elizabeth I., Haq, Rizwan, Tolaney, Sara, Barroso-Sousa, Romualdo, Zhang, Kevin, Donahue, Hilary, Davis, Meredith, Gargano, Maria E., Kelley, Kristina M., Carroll, Rona S., Kaiser, Ursula B., Min, Le·2017·Cancer Immunology Research
DOI 10.1158/2326-6066.cir-17-0208PMC PMC5748517
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Abstract

Thyroid disorders have emerged as one of the most common immune-related adverse events associated with anti–PD-1 monotherapy or combination anti–PD-1 and anti–CTLA-4 therapy. This study characterizes and compares the evolution of monotherapy and combination therapy-related thyroid disorders. We analyzed the dynamic evolution of thyroid disorders in 45 patients who developed thyroid disorders following treatment with either anti–PD-1 monotherapy or anti–PD-1 and anti–CTLA-4 combination therapy. The patients presented with thyrotoxicosis or hypothyroidism as the initial presentation of their thyroid disorder. Thyrotoxicosis as the initial presentation occurred in the majority of patients (93% and 56% of the patients receiving combination therapy and monotherapy, respectively). The onset pattern of the thyroid disorder was significantly different between the two groups (P = 0.01). Subsequently, 76% and 90% of the patients with thyrotoxicosis evolved to develop hypothyroidism in the combination and monotherapy groups, respectively. In the combination therapy and monotherapy groups, the median times to onset of thyrotoxicosis and hypothyroidism after first treatment were 21 and 63 days, and 31 and 68 days, respectively. The median time for transition from thyrotoxicosis to hypothyroidism was 42 days in both groups. Our study demonstrates that most thyroid disorders induced by either anti–PD-1 or combination anti–PD-1 and anti–CTLA-4 therapy are thyroiditis. The time to onset of thyrotoxicosis after treatment initiation and evolution of thyrotoxicosis to hypothyroidism was short, emphasizing the importance of close monitoring of thyroid function in these patients. Cancer Immunol Res; 5(12); 1133–40. ©2017 AACR.

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  • ICPi-induced thyrotoxicosis is generally due to destructive thyroiditis, with a first stage of hyperthyroidism which then resolves or evolves into secondary hypothyroidism in 50-80% of cases.

    “ICPi-induced thyrotoxicosis is generally due to destructive thyroiditis, with a first stage of hyperthyroidism which then resolves or evolves into secondary hypothyroidism (50–80%) [17,18,19].”

    From Graves’ Disease during Immune Checkpoint Inhibitor Therapy (A Case Series and Literature Review) (2021) · cites this paper as [17]

    The Results section, “Conversion of thyrotoxicosis to hypothyroidism” (page unavailable), reports that 80% (28/35) of patients initially presenting with thyrotoxicosis subsequently developed hypothyroidism. The Discussion says most checkpoint-inhibitor-related thyroid disorders are likely thyroiditis, but does not establish a destructive mechanism. The Methods explicitly uses “thyrotoxicosis” rather than “hyperthyroidism,” because the latter means thyroid-hormone overproduction. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • In the only published histologic examination of pancreatic tissue from a patient with immune checkpoint inhibitor-associated diabetes mellitus, Yoneda et al. found increased peri-islet infiltration of CD8+ T lymphocytes.

    “Yoneda et al noted increased peri-islet infiltration of CD8+ T lymphocytes74”

    From Endocrine toxicities of immune checkpoint inhibitors (2021) · cites this paper as [74]

  • Yoneda et al. also found an almost complete absence of insulin-positive cells.

    “they also noted an almost complete absence of insulin-positive cells”

    From Endocrine toxicities of immune checkpoint inhibitors (2021) · cites this paper as [74]

  • Immune checkpoint inhibitor-associated diabetes mellitus may involve more severe and rapid destruction of pancreatic beta cells than type 1 diabetes.

    “suggesting that ICI-DM may be characterized by a more severe and rapid destruction of pancreatic beta cells than T1D”

    From Endocrine toxicities of immune checkpoint inhibitors (2021) · cites this paper as [74]

  • Immune checkpoint inhibitor-associated diabetes mellitus is presumably caused by immune destruction of pancreatic beta cells, as in classic type 1 diabetes.

    “Similar to classic type 1 diabetes (T1D), ICI-DM is presumably caused by immune destruction of pancreatic beta cells.”

    From Endocrine toxicities of immune checkpoint inhibitors (2021) · cites this paper as [74]

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Metadata

Authors
Lee, H., Hodi, F. S., Giobbie-Hurder, A., Ott, P. A., Buchbinder, E. I., Haq, R., Tolaney, S., Barroso-Sousa, R., Zhang, K., Donahue, H., Davis, M., Gargano, M. E., Kelley, K. M., Carroll, R. S., Kaiser, U. B., & Min, L.
Affiliations
  • Brigham and Women's Hospital (US)
  • Dana-Farber Cancer Institute (US)
  • 4Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
  • 3Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Corresponding author
Min, Le
ORCID
Venue
Cancer Immunology Research
Publisher
American Association for Cancer Research (AACR)
Published
2017-11-30
Volume
5
Issue
12
Pages
1133-1140
ISSN
  • 2326-6066 (ISSN-L)
  • 2326-6074
DOI
10.1158/2326-6066.cir-17-0208
PMC
PMC5748517
OpenAlex
W2766268302
Cited by
161
References
25
Citations by year
2026: 9 · 2025: 14 · 2024: 13 · 2023: 25 · 2022: 21 · 2021: 24 · 2020: 23 · 2019: 24 · 2018: 7 · 2017: 1
FWCI
6.63
Type
journal article
Language
en
Open access
Locations
  • Cancer Immunology Research (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • NICHD NIH (K08 HD070957)
  • NIH (R01 HD019938 and HD082314)
Topics
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Clinical Neurology › Autoimmune Neurological Disorders and Treatments
Keywords
thyroid dysfunction, immune checkpoint inhibitors, anti-PD-1 monotherapy, immune-related adverse events, thyrotoxicosis, hypothyroidism, thyroiditis, time to onset, thyroid function monitoring
MeSH terms
Antineoplastic Agents, Immunological, Adult, Aged, Antineoplastic Combined Chemotherapy Protocols, Female, Humans, Hypothyroidism, Male, Middle Aged, Neoplasms, Thyroid Diseases, Thyrotoxicosis, Biomarkers, Cell Line, Tumor, Immunomodulation, Molecular Targeted Therapy

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