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Tremelimumab-Induced Graves Hyperthyroidism.

Earn H Gan1, Anna L Mitchell1, Ruth Plummer1

  • 1Institute of Genetic Medicine, International Centre for Life, Newcastle upon Tyne, United Kingdom.

European Thyroid Journal
|August 9, 2017
PubMed
Summary
This summary is machine-generated.

Tremelimumab immunotherapy can cause delayed Graves hyperthyroidism, a thyroid disorder, years after treatment. Early monitoring and antithyroid drug therapy are crucial for managing this immune-related adverse event alongside cancer treatment.

Keywords:
Graves diseaseHyperthyroidismTremelimumab

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Area of Science:

  • Immunology
  • Endocrinology
  • Oncology

Background:

  • Monoclonal antibodies like tremelimumab and ipilimumab target cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) for cancer immunotherapy.
  • Anti-CTLA-4 therapies are effective against cancers such as metastatic melanoma but can cause immune-related adverse events, including thyroid disorders.
  • These adverse events typically emerge within the first year of treatment, though delayed occurrences are possible.

Purpose of the Study:

  • To report a rare case of Graves hyperthyroidism induced by tremelimumab therapy.
  • To highlight the potential for delayed endocrine-related adverse events from anti-CTLA-4 therapy.
  • To discuss the management and implications of anti-CTLA-4-induced thyroid dysfunction.

Main Methods:

  • A case report of a 55-year-old male patient with metastatic melanoma treated with tremelimumab.
  • Clinical and biochemical evaluation of thyroid function, including serum free thyroid hormones, thyroid-stimulating hormone, and thyrotropin receptor antibodies.
  • Management involved temporary discontinuation of tremelimumab, antithyroid drug therapy (carbimazole), and subsequent recommencement of immunotherapy.

Main Results:

  • The patient developed Graves hyperthyroidism eight years after initiating tremelimumab therapy, with no prior history of thyroid or autoimmune disease.
  • Biochemical tests confirmed Graves disease; treatment with carbimazole was successful and well-tolerated.
  • Tremelimumab was safely restarted after achieving biochemical euthyroidism, and no relapse of hyperthyroidism occurred after discontinuing block and replace therapy.

Conclusions:

  • Anti-CTLA-4 therapy, including tremelimumab, can induce late-onset Graves hyperthyroidism.
  • The long-term endocrine safety profile and mechanisms of anti-CTLA-4-induced thyroid dysfunction require further investigation.
  • Continuous monitoring of thyroid function is essential in patients receiving anti-CTLA-4 therapies due to potential delayed or prolonged endocrine effects.