Meet the Professor

Updates to Endocrine Case Management: Meet the Professor (MTP)

UPDATE FOR 2024 Endocrine Case Management: Meet the Professor

Thyroid
Layal Chaker, MD, PhD and Robin Peeters, MD, PhD
Page: 354
Updated: 23 April 2025

Clinical Case Vignette – Case 3, Answer (Page 354)

Original Text: 

Which 2 of the following explanations could be a likely cause of this patient’s current biochemical thyrotoxicosis?

  • A. Iodine-induced hyperthyroidism
  • B. Graves disease induced by immune checkpoint inhibitor therapy
  • C. Thyroiditis induced by immune checkpoint inhibitor therapy
  • D. Assay interference
  • E. Toxic multinodular goiter

Answer: A and C) Iodine-induced hyperthyroidism and Graves disease induced by immune checkpoint inhibitor therapy

There are several possible explanations for thyrotoxicosis in this patient. Her pretherapy TSH value was relatively low, and in combination with her free T4 value, she could be classified as having subclinical hyperthyroidism. At her age, multinodular goiter (Answer E) is a common cause of subclinical hyperthyroidism, and this may be aggravated by iodine-containing contrast media (Answer A) that is used for CT. Immune checkpoint inhibitor–induced thyroiditis (Answer C) is common, especially with anti-PD1/PDL-1 therapy, and it can occur in up to 10% of patients with anti-PD1/PDL-1 and CTLA4 combination therapy (eg, nivolumab/ipilimumab). Although Graves disease after initiation of immune checkpoint inhibitors (Answer B) has been described, it is far less likely, especially because the TRAb is negative. Assay interference (Answer D) has not been described, and it is unlikely in a patient only using vitamin D supplementation in addition to her anticancer therapy.

Updated Text: 

Which 2 of the following explanations could be a likely cause of this patient’s current biochemical thyrotoxicosis?

  • A. Iodine-induced hyperthyroidism
  • B. Graves disease induced by immune checkpoint inhibitor therapy
  • C. Thyroiditis induced by immune checkpoint inhibitor therapy
  • D. Assay interference
  • E. Toxic multinodular goiter

Answer: A and C) Iodine-induced hyperthyroidism and Thyroiditis induced by immune checkpoint inhibitor therapy

There are several possible explanations for thyrotoxicosis in this patient. Her pretherapy TSH value was relatively low, and in combination with her free T4 value, she could be classified as having subclinical hyperthyroidism. At her age, multinodular goiter (Answer E) is a common cause of subclinical hyperthyroidism, and this may be aggravated by iodine-containing contrast media (Answer A) that is used for CT. Immune checkpoint inhibitor–induced thyroiditis (Answer C) is common, especially with anti-PD1/PDL-1 therapy, and it can occur in up to 10% of patients with anti-PD1/PDL-1 and CTLA4 combination therapy (eg, nivolumab/ipilimumab). Although Graves disease after initiation of immune checkpoint inhibitors (Answer B) has been described, it is far less likely, especially because the TRAb is negative. Assay interference (Answer D) has not been described, and it is unlikely in a patient only using vitamin D supplementation in addition to her anticancer therapy.

 

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