Abstract
Tyrosine kinase inhibitors (TKIs) are currently used by most oncologists. Among their side effects, thyroid dysfunctions are nowadays clearly observed. Whereas changes in thyroid function tests have been originally described with sunitinib, we now know that many TKIs can induce hypothyroidism and hyperthyroidism. In this study, the various molecules implicated in thyroid dysfunctions are analysed and the latest data on physiopathological mechanisms are approached in order to propose a strategy of thyroid monitoring of patients on TKI therapy.
http://m.eje-online.org/content/171/3/R91.full
ENDOCRINE SIDE-EFFECTS OF ANTI-CANCER DRUGS: Thyroid effects of tyrosine kinase inhibitors
Re: ENDOCRINE SIDE-EFFECTS OF ANTI-CANCER DRUGS: Thyroid effects of tyrosine kinase inhibitors
Introduction( released 2014)
For the last 10 years tyrosine kinase inhibitors (TKIs) have been largely used as first- or second-line therapy of various solid tumours or haemopathies. They inhibit the transfer of phosphate from ATP to tyrosine residues in the catalytic domain of growth factor receptors. Their targets are involved in the survival, proliferation, invasiveness and angiogenesis of the tumours (1). The safety and tolerability are different and depend on the molecules, but thyroid effects of sunitinib were rapidly observed (2, 3). Since 2006, changes in thyroid function tests (TFTs) have been reported with different TKIs in subjects with thyroid in situ and in thyroidectomised subjects (3, 4). In the first part of this review, we discuss the effects of TKI on TFT. In the second part, we focus on the mechanisms that are currently proposed to explain the changes on TFT. Finally, we endeavour to propose a strategy to monitor the TFT before, during and after the withdrawal of the TKI.
For the last 10 years tyrosine kinase inhibitors (TKIs) have been largely used as first- or second-line therapy of various solid tumours or haemopathies. They inhibit the transfer of phosphate from ATP to tyrosine residues in the catalytic domain of growth factor receptors. Their targets are involved in the survival, proliferation, invasiveness and angiogenesis of the tumours (1). The safety and tolerability are different and depend on the molecules, but thyroid effects of sunitinib were rapidly observed (2, 3). Since 2006, changes in thyroid function tests (TFTs) have been reported with different TKIs in subjects with thyroid in situ and in thyroidectomised subjects (3, 4). In the first part of this review, we discuss the effects of TKI on TFT. In the second part, we focus on the mechanisms that are currently proposed to explain the changes on TFT. Finally, we endeavour to propose a strategy to monitor the TFT before, during and after the withdrawal of the TKI.
Debbie