Inappropriate Elevation of Serum Thyrotropin Levels in Patients Treated with Axitinib

Ohba, Kenji; Takayama, Tatsuya; Matsunaga, Hideyuki; Matsushita, Akio; Sasaki, Shigekazu; Osuga, Yutaka; Ozono, Seiichiro; Nakamura, Hirotoshi

doi:10.1089/thy.2012.0378

Cited by 28 publications

(13 citation statements)

References 21 publications

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“…Thyroid dysfunction in TKI treatment is a commonly recognized AE. Axitinib, pazopanib, sorafenib, sunitinib, and lenvatinib have been reported to cause thyroid-related AEs [5,6,[13][14][15]. Lenvatinib has been used for thyroid cancer and thyroidectomy; however, reports of AEs of thyroid dysfunction are limited.…”

Section: Discussionmentioning

confidence: 99%

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

et al. 2019

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Lenvatinib has anti-tumor activity against advanced hepatocellular carcinoma (HCC). Hypothyroidism is also a frequent complication in patients treated with lenvatinib. However, studies on lenvatinib-induced thyroid toxicity and destructive thyroiditis are limited. Therefore, this study aimed to clarify the frequency and timing of thyroid abnormalities in lenvatinib for unresectable HCC. This retrospective study enrolled 50 patients with advanced HCC treated with lenvatinib. Patients were classified to have euthyroid, subclinical hypothyroidism, overt hypothyroidism, and thyrotoxicosis. The timing of thyroid dysfunction was assessed, and risk factors for incident hypothyroidism or thyrotoxicosis were evaluated using multivariate models. Subclinical hypothyroidism, overt hypothyroidism, and thyrotoxicosis occurred in 7 (14.0%), 26 (52.0%), and 5 (10.0%) patients, respectively. In the 33 patients with hypothyroidism, 27 (84.4%) developed the condition within 2 weeks of starting lenvatinib treatment. Of the 5 patients with thyrotoxicosis, 3 developed the condition within 8 weeks of starting lenvatinib administration. One patient developed thyrotoxicosis in only 1 week of the initiation of treatment. No correlation between the presence of antibodies and the incidence and severity of thyroid dysfunction due to the autoimmune mechanism was observed. The progression-free survival was significantly better in the hypothyroidism group. Lenvatinib treatment for unresectable HCC not only causes hypothyroidism, but also thyrotoxicosis. Moreover, these thyroid conditions develop within the early period of treatment at a higher prevalence. Patients with thyroid dysfunction had better prognosis. Based on these results, in patients administered with lenvatinib, there is need for careful assessment for the possibility of thyroid dysfunction from the onset of treatment.

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Section: Discussionmentioning

confidence: 99%

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

et al. 2019

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“…Further evidence suggests an impairment in deiodases activity in TKIinduced hypothyroidism. Indeed, in this condition, TSH levels are often inappropriately high for the concomitant serum free T3 and free T4 levels (194,207). This might be related to a far more reduced activity of DIO2 (expressed in the pituitary gland) than of deiodinase-1 (expressed mainly in the liver and kidney), leading to an intracellular depletion of T3 in the thyrotrophs and an inappropriately high TSH level (194).…”

Section: Tyrosine Kinase Inhibitorsmentioning

confidence: 99%

Thyroid Dysfunction as an Unintended Side Effect of Anticancer Drugs

Torino

Barnabei²,

Paragliola

et al. 2013

Thyroid

103

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“…From an oncological viewpoint, the fact that Graves’ disease occurred after two different TKIs suggests that it could be a rare but important class effect. As several studies have also demonstrated impaired thyroid function with sunitinib [10–14], axitinib [15, 16] and motesanib [17], our case report emphasizes the need for thyroid follow-up during any treatment with a TKI in order to screen for both hypothyroidism and hyperthyroidism. Systematically measuring anti-TSH receptor antibodies before TKI initiation is not realistic due to the low frequency of hyperthyroidism, unlike with hypothyroidism.…”

Section: Resultsmentioning

confidence: 68%

Auto-immune thyroid dysfunction induced by tyrosine kinase inhibitors in a patient with recurrent chordoma

et al. 2016

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BackgroundWhile hypothyroidism has frequently been reported with the use of TKIs, the thyroid-stimulating hormone (TSH) suppressing effect of TKIs is rare, except for thyroiditis. We describe a case with progressive recurrent chordoma who initially became hyperthyroid in a context of autoimmunity under sorafenib treatment and later under imatinib treatment.Case presentationA 57-year-old man with lumbar chordoma began daily treatment of 800 mg sorafenib. He did not have any other medication or recent iodinated-contrast exposure and his family history was negative for thyroid and autoimmune disease. There was no history of neck pain, irradiation or trauma, recent fever or viral illness. Pre-treatment TSH was normal. After 18 weeks of treatment, the patient presented hyperthyroidism with positive anti-TSH receptor antibodies. More surprisingly, Graves’ disease recurred during treatment with imatinib.ConclusionThe fact that Graves’ disease occurred after two different TKIs suggests that it could be a rare but important class effect. Anti-TSH receptor antibodies should be systematically measured when TSH decreases in order to avoid the erroneous diagnosis of transient hyperthyroidism due to thyroiditis.

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Inappropriate Elevation of Serum Thyrotropin Levels in Patients Treated with Axitinib

Abstract: This is the first study to report an inappropriate elevation of serum TSH levels in patients treated with axitinib.

Cited by 28 publications

References 21 publications

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

Thyroid Dysfunction as an Unintended Side Effect of Anticancer Drugs

Auto-immune thyroid dysfunction induced by tyrosine kinase inhibitors in a patient with recurrent chordoma

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