[Thyroid dysfunction in patients with advanced renal cell carcinoma treated with sunitinib: a multifactorial issue]

Several studies have reported the substantial prevalence of sunitinib-induced thyroid dysfunction. However, the underlying mechanism and the benefit of thyroid hormone replacement therapy remain to be determined. To evaluate the effect of sunitinib on thyroid function, we carried out a descriptive study in patients with advanced renal cell carcinoma.

A total of 24 patients treated by sunitinib between 2006 and 2008 at Hospital Clínico San Carlos were included. The data were collected retrospectively and analyzed with SPSS 15.0.

Treatment duration was 30 weeks (18-42) [median (IQR)]. Five patients (20.8%) developed subclinical hypothyroidism and three (12.5%) developed overt hypothyroidism. The number of weeks needed to observe an increase in thyroid-stimulating hormone (TSH) values in these patients was 15 (6-20) [median (IQR)]. TSH levels were below the normal range in five patients (20.8%) before or during the treatment period, but the diagnosis of subclinical hyperthyroidism could not be established because of concomitant factors. Fourteen patients (58.3%) showed sunitinib adverse events, but these were not related to the development of hypothyroidism (p=0.388).

Because of the high prevalence of sunitinib-induced hypothyroidism, thyroid function should be systematically monitored in patients with renal cell carcinoma treated with this drug. However, several pathophysiological and pharmacological factors may interfere with monitoring. Consequently, it might be useful to determine not only TSH and free T4 but also free T3 and, ideally, reverse T3. Evidence-based recommendations to manage hypothyroidism in oncology patients are not available at present.