Onset of Male Gynaecomastia in a Patient Treated with Sunitinib for Metastatic Renal Cell Carcinoma
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CASE REPORT
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Onset of Male Gynaecomastia in a Patient Treated with Sunitinib for Metastatic Renal Cell Carcinoma Pierluigi Ballardini,1 Guido Margutti,1 Camillo Aliberti2 and Roberto Manfredini1 1 Department of Internal Medicine, Hospital of the Delta, Lagosanto (FE), Azienda USL di Ferrara, Italy 2 Department of Radiology, Hospital of the Delta, Lagosanto (FE), Azienda USL di Ferrara, Italy
Abstract
Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor that has demonstrated substantial antitumour activity in patients with metastatic renal cell carcinoma. The more common grade 3 or 4 adverse effects of sunitinib include hypertension, fatigue, hand-foot syndrome, elevated lipase and lymphopenia. We report the case of a 69-year-old patient with metastatic renal clear-cell carcinoma, treated with nephrectomy and three lines of therapy (interleukin-2 plus interferon-a2a, vinorelbine plus gemcitabine, and capecitabine), who started a fourth-line therapy with oral sunitinib because of disease progression. At the end of his fifth cycle of sunitinib therapy, the patient complained of the development of abnormally large mammary glands associated with pain and peri-areolar erythema. After 2 weeks’ off therapy, a partial reduction in mammary gland enlargement, local pain and erythema was observed. However, re-initiation of sunitinib treatment was followed by bilateral breast enlargement again. The mechanism by which sunitinib induces gynaecomastia is thought to be associated with an unknown direct action on breast hormonal receptors. To the best of our knowledge, this is the first report of an association between sunitinib and gynaecomastia.
Sunitinib (Sutent, Pfizer Inc., New York, USA) is an orally administered multitargeted tyrosine-kinase inhibitor recently authorized for the treatment of metastatic renal clear-cell carcinoma (mRCC). It is a small molecule inhibitor with high binding affinity for specific tyrosinekinase receptors, e.g. vascular endothelial growth factor receptor (VEGFR) types 1 and 2, plateletderived growth factor receptors (PDGFRa and PDGFRb), FMS-like receptor tyrosine kinase (FLT3), stem cell factor receptor (c-kit) and glial cell line-derived neurotrophic factor (rearranged during transfection [RET]).[1-3] The antitumoral
action of sunitinib could derive from its inhibitory activity on tumoral angiogenesis mediated by inhibition of the intracellular signalling arising from VEGFR when it is activated by its ligand. Sunitinib has been shown to be effective in the treatment of mRCC either as a first- or secondline therapy,[2,4] and, together with other targeted therapies recently adopted into clinical practice (sorafenib, temsirolimus and bevacizumab in combination with interferon-a2a), has dramatically improved the outcome of patients affected with this disease. Presently sunitinib is recommended as one of the two standard-of-care first-line treatments
Ballardini et al.
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for mRCC with favourable or intermediate risk
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