Implication of plat elet-derived growth factor in sunitinib-induced hypothyroidism

• Autores: Rocío Jiménez Galán, Beatriz Bernárdez Ferrán, M.ª Jesús Lamas Díaz, C. Carrascosa Rodríguez, Patricia Monje Agudo
• Localización: European journal of clinical pharmacy: atención farmacéutica, ISSN 2385-409X, Vol. 16, Nº. 6, 2014, págs. 11-11
• Idioma: inglés
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• Resumen

  • Sunitinib belongs to the group of «tyrosine kinase inhibitors» (TKI). This drug is capable to inhibit those members from the family of receptor tyrosine kinases, including vascular endothelial growth factor receptors (VEGFR) and platelet-derived growth factor receptors (PDGFR). Fatigue and hypothyroidism are the most common toxicities among patients with renal cell carcinoma (RCC) treated with sunitinib.

    We present the case of a 46-year old female patient with significant past Medical history of a papillary thyroid cancer that required a total thyroidectomy. Following that, she started on hormonal replacement therapy with levothyroxine. Six years later, she was diagnosed of a metastatic renal cell carcinoma. The patient began first line treatment with sunitinib. Prior to starting sunitinib, basal thyrotropin (TSH) serum levels were below the normal limits, however five months after starting sunitinib, TSH serum levels increased to values of 30.95 mU/L. The patient required an increase of the dose of levothyroxine.

    The relationship between the platelet-derived growth factor and the development of hypothyroidism could be the theory that may justify this case. Some autors have found that T3 (Triiodothyronine) activates the PDGF-Akt signalling pathway, which is essential for T3 induced sprouting angiogenesis.

    In conclusion, this case allows us to discard those theories that explain that sunitinib’s induced hypothyroidism is due to a single effect on the thyroid and the blocking of PDGFR is the most robust mechanism that could explain this adverse event