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TKI Thyroid Toxicity — SCE Medical Oncology MCQ

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HardImmunotherapy & Targeted TherapyTKI Thyroid ToxicitySCE Medical Oncology

A 60-year-old man on sunitinib for GIST develops hypothyroidism and is started on levothyroxine. Six months later, he switches to regorafenib for progressive disease. His thyroid function deteriorates further. What is the mechanism of multi-kinase inhibitor thyroid dysfunction?

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Correct answer: B — VEGFR inhibition causing thyroid capillary regression and follicular injury

VEGFR blockade can regress thyroid capillaries and injure follicles, producing or worsening primary hypothyroidism across multikinase inhibitors. VEGFR inhibition causing pituitary TSH suppression and secondary hypothyroidism: the recognised process is thyroid-gland vascular regression rather than central TSH suppression. RET inhibition causing thyroid capillary regression and follicular injury: the cross-agent class effect tracks VEGF-pathway inhibition more than RET specificity. KIT inhibition causing thyroid-peroxidase blockade and dyshormonogenesis: direct thyroid-peroxidase blockade is not the established multikinase mechanism. PDGFR inhibition causing thyroxine-binding-globulin loss and low total thyroxine: binding-protein change does not explain worsening primary thyroid function.

Reference: Sunitinib-induced hypothyroidism through thyroid capillary regression (Published June 2010): https://pubmed.ncbi.nlm.nih.gov/20187785/; SUTENT UK summary of product characteristics (Current UK SmPC, accessed July 2026): https://www.medicines.org.uk/emc/product/7968/smpc