Thyroid dysfunction induced by alectinib in a patient with a non-small cell lung cancer

Background: Hypothyroidism is a well-known side effect associated with tyrosine kinase inhibitors (TKIs) therapy. We describe a case of a patient with a history of postsurgical hypothyroidism who presented TSH elevation ranging from 1.68 to 17.09 IU/ml with normal free thyroxine (T4) after starting...

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Bibliographic Details
Main Authors: Henriquez, F. (Author), Plaza-Enriquez, L. (Author), Sanchez-Valenzuela, M. (Author)
Format: Article
Language:English
Published: Elsevier Inc. 2022
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Online Access:View Fulltext in Publisher
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Summary:Background: Hypothyroidism is a well-known side effect associated with tyrosine kinase inhibitors (TKIs) therapy. We describe a case of a patient with a history of postsurgical hypothyroidism who presented TSH elevation ranging from 1.68 to 17.09 IU/ml with normal free thyroxine (T4) after starting treatment with alectinib for non-small cell lung cancer (NSCLC). Case presentation: A 78-year-old female, with past medical history of Graves’ disease with subsequent total thyroidectomy and residual postsurgical hypothyroidism, was diagnosed with non-small cell lung cancer (NSCLC) and presented with TSH elevation with normal free T4 after starting therapy with alectinib. Conclusion: The most likely etiology for TSH elevation during her therapy with alectinib is an increased requirement of thyroid hormone secondary to increase activity of type 3 deiodinase and/or inhibition of monocarboxylate transporter 8 (MCT8) with consequent lower tissue availability of active T3. Further studies of thyroid dysfunction after alectinib administration are lacking. © 2022 The Authors
ISBN:22146245 (ISSN)
DOI:10.1016/j.jecr.2022.100113