Bowel perforation associated sunitinib therapy for recurred gastric gastrointestinal stromal tumor.
10.4174/astr.2014.86.4.220
- Author:
Hyo Sin KIM
1
;
Sung Soo KIM
;
Sang Gon PARK
Author Information
1. Department of Surgery, Chosun University Hospital, Gwangju, Korea.
- Publication Type:Case Report
- Keywords:
Gastrointestinal stromal tumors;
Sunitinib;
Intestinal perforation
- MeSH:
Endothelial Growth Factors;
Gastrointestinal Stromal Tumors*;
Gastrointestinal Tract;
Humans;
Intestinal Perforation;
Neoplasm Metastasis;
Phosphotransferases;
Protein-Tyrosine Kinases;
Imatinib Mesylate
- From:Annals of Surgical Treatment and Research
2014;86(4):220-225
- CountryRepublic of Korea
- Language:English
-
Abstract:
Gastrointestinal stromal tumor (GIST) is the most common mesenchymal neoplasm of the gastrointestinal tract. Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib. Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST. Sunitinib is generally well tolerated and has an acceptable toxicity profile; an adverse event such as bowel perforation is rare. We present a patient with imatinib-refractory GIST who was successfully treated using sunitinib, but developed bowel perforation. The mechanism involved in bowel perforation associated with sunitinib is unknown. However, we presume that in our patient, the dramatic reduction in disseminated peritoneal metastases and bowel invasion of recurrent GIST during sunitinib treatment might have resulted in the bowel perforation.
