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 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.