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Hypothyroidism after sunitinib treatment for patients with gastrointestinal stromal tumors
Jayesh Desai1, Leila Yassa, Ellen Marqusee
1Brigham and Women's Hospital, Dana Farber Cancer Institute, and Harvard Medical School, Boston, Massachusetts 02115, USA.
Background:
Sunitinib malate is an oral tyrosine kinase inhibitor recently approved for the treatment of gastrointestinal stromal tumors and renal cell carcinoma. Because the ret proto-oncogene is also inhibited by this agent, clinical evaluation of thyroid function was performed.
Objective:
To describe the prevalence and clinical presentation of thyroid dysfunction related to sunitinib therapy.
Design:
Prospective, observational cohort study.
Setting:
Tertiary care hospital.
Patients:
42 patients treated for a median of 37 weeks (range, 10 to 167 weeks).
Measurements:
Following analysis of serial thyroid-stimulating hormone (TSH) measurements collected prospectively during a clinical trial of sunitinib, the authors determined the proportion of patients with thyroid dysfunction.
Results:
Abnormal serum TSH concentrations were documented in 26 of 42 patients (62%): 15 (36%) developed persistent, primary hypothyroidism; 4 (10%) developed isolated TSH suppression; and 7 (17%) experienced transient, mild TSH elevations. The risk for hypothyroidism increased with the duration of sunitinib therapy. Six of 15 (40%) hypothyroid patients had suppressed TSH concentrations before developing hypothyroidism, suggesting thyroiditis. Two hypothyroid patients evaluated with thyroid ultrasonography had no visualized thyroid tissue despite normal baseline thyroid function.
Limitations:
The exploratory nature of this study precluded more frequent biochemical and sonographic analysis that may better define the mechanism of sunitinib-associated thyroid dysfunction.
Conclusion:
Hypothyroidism is a frequent complication of sunitinib therapy. Regular surveillance of thyroid function is warranted in patients receiving the drug. Although the mechanism by which this complication occurs is unknown, the observations of preceding TSH suppression and subsequent absence of visualized thyroid tissue in some patients suggest that sunitinib may induce a destructive thyroiditis through follicular cell apoptosis. This provides a rationale for further investigation of sunitinib treatment in patients with advanced thyroid cancer.
Insights
Sunitinib therapy frequently causes thyroid dysfunction, with 62% of patients developing abnormal thyroid-stimulating hormone (TSH) levels, primarily hypothyroidism. Regular thyroid function monitoring is recommended for patients on sunitinib.
Area of Science:
- Endocrinology
- Oncology
- Pharmacology
Background:
- Sunitinib malate is an oral tyrosine kinase inhibitor used for gastrointestinal stromal tumors and renal cell carcinoma.
- Its inhibition of the ret proto-oncogene prompted an evaluation of its effects on thyroid function.
Observation:
- A prospective, observational study monitored thyroid function in 42 patients treated with sunitinib for a median of 37 weeks.
- Serial thyroid-stimulating hormone (TSH) levels were analyzed to determine the prevalence of thyroid dysfunction.
Findings:
- Thyroid dysfunction occurred in 62% of patients (26 of 42).
- Persistent primary hypothyroidism developed in 36%, isolated TSH suppression in 10%, and transient TSH elevations in 17%.
- Hypothyroidism risk increased with treatment duration, and some cases suggested sunitinib-induced thyroiditis.
Implications:
- Hypothyroidism is a significant complication of sunitinib therapy, necessitating regular thyroid function surveillance.
- The findings suggest sunitinib may induce destructive thyroiditis, warranting further investigation for potential applications in advanced thyroid cancer treatment.
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