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The clinical implications of sunitinib-induced hypothyroidism: a prospective evaluation
P Wolter1, C Stefan, B Decallonne
1Department of General Medical Oncology, University Hospital Gasthuisberg, Catholic University Leuven, Leuven Cancer Institute, Herestraat 49, Leuven B-3000, Belgium. Pascal.Wolter@uz.kuleuven.be
Abstract:
Sunitinib is approved for the treatment of metastatic renal cell carcinoma (RCC) and imatinib-resistant or -intolerant gastrointestinal stromal tumours (GIST). Several studies have identified unexpected rates of thyroid dysfunction with sunitinib treatment. We performed a prospective observational study with the aim of more accurately defining the incidence and severity of hypothyroidism in RCC or GIST patients receiving sunitinib. Thyroid function was assessed at baseline and on days 1 and 28 of each treatment cycle. Thyroid antibodies were assessed at baseline and during follow-up if abnormal thyroid function tests were recorded. Sixteen patients (27%) developed sub- or clinical hypothyroidism and required hormone replacement and 20 patients (34%) showed at least one elevated thyroid-stimulating hormone not requiring therapeutic intervention. Twenty patients (34%) did not develop any biochemical thyroid abnormality. Thus, sunitinib can induce (sub-) clinical hypothyroidism, warranting close monitoring of thyroid function. We propose a new algorithm for managing this side effect in clinical practise.
Insights
Sunitinib treatment for renal cell carcinoma and gastrointestinal stromal tumors can cause hypothyroidism. Close thyroid function monitoring is essential for patients receiving sunitinib therapy.
Area of Science:
- Oncology
- Endocrinology
- Pharmacology
Background:
- Sunitinib is a targeted therapy used for metastatic renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumors (GIST).
- Previous research indicates a notable incidence of thyroid dysfunction associated with sunitinib treatment.
Purpose of the Study:
- To prospectively evaluate the incidence and severity of hypothyroidism in patients with RCC or GIST undergoing sunitinib therapy.
- To define the clinical impact of sunitinib on thyroid function and establish monitoring guidelines.
Main Methods:
- A prospective observational study was conducted.
- Thyroid function tests (thyroid-stimulating hormone) were performed at baseline and during each treatment cycle (days 1 and 28).
- Thyroid antibodies were assessed at baseline and during follow-up for patients with abnormal thyroid function.
Main Results:
- 27% of patients developed subclinical or overt hypothyroidism requiring hormone replacement.
- 34% exhibited elevated thyroid-stimulating hormone levels not necessitating intervention.
- 34% of patients did not experience any biochemical thyroid abnormalities.
Conclusions:
- Sunitinib therapy is associated with the induction of (sub)clinical hypothyroidism in a significant proportion of patients.
- Regular monitoring of thyroid function is crucial for patients receiving sunitinib.
- An algorithm for managing sunitinib-induced hypothyroidism in clinical practice is proposed.
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