Shrinkage of Thyroid Volume in Sunitinib-Treated Patients with Renal-Cell Carcinoma: A Potential Marker of Irreversible Thyroid Dysfunction?

Rogiers, Aljosja; Wolter, Pascal; Beeck, Ken Op de; Thijs, Marleen; Decallonne, Brigitte; Schöffski, Patrick

doi:10.1089/thy.2009.0125

Cited by 46 publications

(37 citation statements)

References 32 publications

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“…As described above, Rogiers et al (2010) reported two cancer patients with a pre-existing nodular thyroid gland who developed hypothyroidism and showed marked shrinkage of the thyroid during treatment with sunitinib, necessitating permanent thyroid hormone replacement therapy even after discontinuation of sunitinib. They suggested the possibility that shrinkage of thyroid volume in sunitinib-treated patients could be a potential marker of irreversible organ damage.…”

Section: Discussionmentioning

confidence: 81%

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Sunitinib-Induced Thyrotoxicosis Followed by Persistent Hypothyroidism with Shrinkage of Thyroid Volume

Sakurai

Fukazawa

Arihara

et al. 2010

Tohoku J. Exp. Med.

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Sunitinib, a tyrosine kinase inhibitor, has been approved for the treatment of cancers, such as advanced renal cell carcinoma (RCC). On the other hand, sunitinib treatment is known to induce thyroid dysfunction in a substantial proportion of patients treated for advanced RCC; in fact, hypothyroidism is a frequent complication. However, little is known about sunitinib-induced thyrotoxicosis and destructive thyroiditis. Here, we report a patient with RCC who developed transient overt thyrotoxicosis followed by hypothyroidism due to sunitinib treatment. A 58-year-old woman, who had been treated with chronic thyroiditis, was diagnosed as having left RCC with bone metastasis to the rib. The patient underwent resection of the left kidney and the bone metastasis lesion. However, 3 months later, bone metastasis to the rib recurred, and sunitinib treatment was started. At 6 weeks of sunitinib therapy, the patient developed transient thyrotoxicosis, followed by persistent hypothyroidism. In the thyrotoxic phase, the patient was diagnosed as having destructive thyroiditis based on an increased thyroglobulin level, a low radioactive iodine uptake, increased free thyroxine level, and suppressed thyroid-stimulating hormone level. The thyroid volume in the hypothyroid phase was 68% of that in the thyrotoxic phase. In conclusion, the present report suggests that sunitinib-induced persistent hypothyroidism may be a consequence of preceding destructive thyroiditis with transient thyrotoxicosis. The decreased volume of the thyroid during the hypothyroid phase indicates irreversible organ damage in the present patient, thereby resulting in persistent hypothyroidism. Thus, periodic surveillance of thyroid function is mandatory during sunitinib therapy.

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Section: Discussionmentioning

confidence: 81%

“…In a recent report, sunitinib-induced shrinkage of the thyroid gland appears to have been a potential marker of irreversible organ damage, resulting in persistent hypothyroidism (Rogiers et al 2010). …”

mentioning

confidence: 99%

Sunitinib-Induced Thyrotoxicosis Followed by Persistent Hypothyroidism with Shrinkage of Thyroid Volume

Sakurai

Fukazawa

Arihara

et al. 2010

Tohoku J. Exp. Med.

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show abstract

“…However, the mechanisms involved in sunitinib-induced hypothyroidism are still unclear. The reduction in capillary blood flow caused by VEGFR inhibition may explain the marked decrease in thyroid size [13][14][15]. Another mechanism involved in thyroid dysfunction may be the inhibition of thyroid peroxidase leading to reduced synthesis of thyroid hormone [4].…”

Section: ※3mentioning

confidence: 99%

Clinical characteristics of thyroid abnormalities induced by sunitinib treatment in Japanese patients with renal cell carcinoma

et al. 2010

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“…Supporting evidence for this theory include findings that thyroid cells express VEGF and VEGFR mRNA, and preclinical studies in mouse models have shown glandular capillary regression with TKI exposure [115]. In humans, case reports demonstrated reduced thyroid volume and reduced vascularity by Doppler ultrasound [116,117], with rapid increase in the size of the thyroid with cessation of sunitinib. This reduced thyroid volume secondary to reduced blood flow, may also explain the impaired radioactive iodine uptake in vivo, but not in vitro [118].…”

Section: Tyrosine Kinase Inhibitorsmentioning

confidence: 96%

Thyroid Function Abnormalities in Patients Receiving Anticancer Agents

Torino¹,

Barnabei²,

Baldelli³

et al. 2012

Thyroid Hormone

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Shrinkage of Thyroid Volume in Sunitinib-Treated Patients with Renal-Cell Carcinoma: A Potential Marker of Irreversible Thyroid Dysfunction?

Abstract: Morphological changes of the thyroid gland can be associated with the well-described adverse biochemical effects of treatment with sunitinib and can be a potential marker of the irreversible organ damage.

Cited by 46 publications

References 32 publications

Sunitinib-Induced Thyrotoxicosis Followed by Persistent Hypothyroidism with Shrinkage of Thyroid Volume

Sunitinib-Induced Thyrotoxicosis Followed by Persistent Hypothyroidism with Shrinkage of Thyroid Volume

Clinical characteristics of thyroid abnormalities induced by sunitinib treatment in Japanese patients with renal cell carcinoma

Thyroid Function Abnormalities in Patients Receiving Anticancer Agents

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