Hypothyroidism related to tyrosine kinase inhibitors
Posted: Mon Oct 20, 2008 8:53 pm
The clinical implications of sunitinib-induced hypothyroidism: a prospective evaluation
http://www.ncbi.nlm.nih.gov/pubmed/18665181
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.
http://www.ncbi.nlm.nih.gov/pubmed/18665181
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.