Sunitinib-Associated Lymphocytic Thyroiditis without Circulating Antithyroid Antibodies

Alexandrescu, Doru T; Popoveniuc, Geanina; Farzanmehr, Haleh; Dasanu, Constantin A; Dawson, Nancy A.; Wartofsky, Léonard

doi:10.1089/thy.2007.0349

Cited by 30 publications

(24 citation statements)

References 14 publications

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“…There have been several clinical reports about sunitinib-induced thyrotoxicosis (Faris et al 2007;Alexandrescu et al 2008;Grossmann et al 2008). Desai et al (2006) published a prospective study of 42 patients treated with sunitinib for GIST and found that 15 (36%) developed primary hypothyroidism, and 7 (17%) had transient, mild TSH Sunitinib treatment was started at 0 weeks.…”

Section: Discussionmentioning

confidence: 99%

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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: 99%

“…In RCC patients, hypothyroidism has been reported at rates of up to 85% (Desai et al 2006;Rini et al 2007;Wolter et al 2007). However, little is known about sunitinib-induced thyrotoxicosis and destructive thyroiditis (Faris et al 2007;Alexandrescu et al 2008;Grossmann et al 2008). …”

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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“…A presumable autoimmunological damage on thyroid gland by sunitinib comes from the observation of cases of lymphocytic thyroiditis among patients receiving the drug (Alexandrescu et al 2008, Wolter et al 2008, but different studies (Mannavola et al 2007, Rini et al 2007 have excluded autoimmunological background.…”

Section: Autoimmunological Processmentioning

confidence: 99%

Thyroid dysfunction and tyrosine kinase inhibitors in renal cell carcinoma

Bianchi¹,

Rossi²,

Tomao³

et al. 2013

Endocrine-Related Cancer

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The most recent World Health Organization classification of renal neoplasms encompassed nearly 50 distinctive renal neoplasms. Different histological subtypes have different clinical outcomes and show different responses to therapy. Overall, the incidence of kidney cancer has increased worldwide in the last years. Although the most common type of kidney cancer is localized renal cell carcinoma (RCC), with a 5-year survival rate of 85%, about one third of patients present advanced or metastatic disease at diagnosis, with a 5-year survival rate of only 10%. Multi-targeted receptor tyrosine kinase inhibitors (TKIs, sunitinib and sorafenib), the anti-VEGF MAB bevacizumab in association with interferon-a, and the mTOR inhibitors are now approved for the treatment of mRCC. Recently, the novel agents pazopanib and axitinib have also demonstrated efficacy in mRCC patients. Several recent retrospective and prospective trials have suggested that some of their adverse events, such as hypertension, hypothyroidism, and hand foot syndrome (HFS) may act as potential biomarkers of response and efficacy of treatment. In this review, we analyzed the studies that have suggested a relationship between hypothyroidism onset and a better outcome of mRCC patients treated with TKIs. The biological mechanisms suggesting and explaining this correlation are not well known and different speculative theories have been considered in order to investigate the clinical link between hypothyroidism occurrence and the prolonged therapy with TKIs in solid tumors. Furthermore, the management of this unexplained side effect is very important to maximize the efficacy of therapy in mRCC patients because there is a clear and consistent relationship between drug dose and efficacy of treatment. Certainly, other studies are needed to clarify whether a better outcome is associated with hypothyroidism induced to TKIs in patients with mRCC.

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“…The mechanism of SUN-associated hypothyroidism is unclear and the course of the disease is not fully understood [22,24]. Several underlying Introduction mechanisms might be involved: reduced synthesis of thyroid hormones through inhibition of thyroid peroxidase (TPO) activity and progressive depletion of the thyroid reserve (19); inhibition of iodine thyroidal uptake [21]; glandular atrophy induced by TKIs through the inhibition of vascularisation (direct action on VEGFR and/or PDGFR) [29,30]; possible autoimmune damage that causes lymphocytic thyroiditis in patients receiving SUN [22,31]. As regards thyroid ultrasound assessment, the majority of literature demonstrated a progressive reduction in thyroid size, mainly after three months of SUN treatment, regardless of the SUN phase (ON/OFF).…”

Section: Sunitinib and Thyroid Dysfunctionmentioning

confidence: 99%

Role of Sunitinib-Induced Hypothyroidism in Oncological Patients

Baldelli¹

2017

EMIJ

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Sunitinb (SUN) belongs to a new class of multi targeted tyrosine kinase inhibitors (TKIs) used in treatment of metastatic renal cell carcinoma, gastrointestinal stromal tumors and pancreatic neuroendocrine tumors. Although generally well tolerated with favourable safety profile, SUN has distinct side effects that differ from the standard chemotherapy and require monitoring and management. Hypothyroidism is one of the most important adverse events induced by SUN. It is usually subclinical and rarely severe, with variable incidence. . The potential mechanisms involved in thyroid dysfunction are not fully understood. Generally, SUN-induced hypothyroidism does not require discontinuation of cancer therapy but only needs the thyroid replacement therapy. The occurrence of SUNinduced hypothyroidism appears with successful treatment in term of survival of oncological patients but more clinical investigations are necessary to validate this correlation.

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Sunitinib-Associated Lymphocytic Thyroiditis without Circulating Antithyroid Antibodies

Cited by 30 publications

References 14 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

Thyroid dysfunction and tyrosine kinase inhibitors in renal cell carcinoma

Role of Sunitinib-Induced Hypothyroidism in Oncological Patients

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