title: The incidence and mechanism of sunitinib-induced thyroid atrophy in patients with metastatic renal cell carcinoma.
abstract: BACKGROUND
  To elucidate the incidence and mechanisms of sunitinib-induced thyroid atrophy, we investigated serial volumetric and functional changes, and evaluated histological changes of the thyroid gland in metastatic renal cell carcinoma patients who received sunitinib.
  
  
  METHODS
  Thyroid volume (by computed tomography volumetry) and thyroid function were measured at baseline, during the treatment, and at post-treatment periods. Histological evaluation of the thyroid gland was performed in four autopsied patients.
  
  
  RESULTS
  The median reduction rate in thyroid volume at last evaluation during sunitinib treatment was 30% in all 17 patients. The incidence of hypothyroidism during sunitinib treatment was significantly higher in the high reduction rate group (n=8; more than 50% reduction in volume) than in the low reduction rate group (n=9; less than 50% reduction in volume). Half of the patients in the high reduction rate group exhibited a transient thyroid-stimulating hormone suppression, suggesting thyrotoxicosis during sunitinib treatment. Histological evaluation demonstrated atrophy of thyroid follicles and degeneration of follicular epithelial cells without critical diminution of vascular volume in the thyroid gland.
  
  
  CONCLUSIONS
  Thyroid atrophy is frequently observed following sunitinib treatment and may be brought about by sunitinib-induced thyrotoxicosis or the direct effects of sunitinib that lead to degeneration of thyroid follicular cells.
authors.affiliation: Department of Renal and Genitourinary Surgery, Hokkaido University Graduate School of Medicine, North-15, West-7, Kitaku, Sapporo 060-8638, Japan. nobuo-s@med.hokudai.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Shinohara
authors.forename: M
authors.initials: M
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Kamishima
authors.forename: H
authors.initials: H
authors.lastname: Ikushima
authors.forename: N
authors.initials: N
authors.lastname: Otsuka
authors.forename: A
authors.initials: A
authors.lastname: Ishizu
authors.forename: C
authors.initials: C
authors.lastname: Shimizu
authors.forename: H
authors.initials: H
authors.lastname: Kanayama
authors.forename: K
authors.initials: K
authors.lastname: Nonomura
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D002292:Carcinoma, Renal Cell / Q000188:drug therapy* / Q000473:pathology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007211:Indoles / Q000009:adverse effects* / Q000627:therapeutic use; D007680:Kidney Neoplasms / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D009362:Neoplasm Metastasis; D011758:Pyrroles / Q000009:adverse effects* / Q000627:therapeutic use; D000077210:Sunitinib; D013960:Thyroid Function Tests; D013961:Thyroid Gland / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D014057:Tomography, X-Ray Computed
chemical_list: D000970:Antineoplastic Agents; D007211:Indoles; D011758:Pyrroles; D000077210:Sunitinib