Abstract
BackgroundPleomorphic leiomyosarcomas (PLMSs) are extremely rare tumors. We present the first case of hepatic primary PLMS after surgery for gastric gastrointestinal stromal tumor (GIST).Case presentationThe patient was a 62-year-old man who was referred to our hospital for resection of a hepatic tumor arising after gastric GIST surgery that was resistant to imatinib and sunitinib. A 40-mm tumor in the left lobe of the liver and three small nodules in the right lobe were detected. We performed hepatic left lobectomy and partial resections for three lesions. According to the histopathological and immunohistochemical findings and c-kit gene mutations analysis, the main tumor was diagnosed as a PLMS.ConclusionIt is necessary to consider the possibility that imatinib-resistant GIST recurrence lesions are a different kind of soft-tissue sarcoma. Accurate diagnosis is required to not miss the opportunity for radical excision of PLMS.
Highlights
Pleomorphic leiomyosarcomas (PLMSs) are extremely rare tumors
We present a case of hepatic resection for primary hepatic PLMS 2 years after surgery for gastric gastrointestinal stromal tumor (GIST)
It is necessary to consider that recurring imatinib-resistant GIST lesions may be different tumors
Summary
Pleomorphic leiomyosarcomas (PLMSs) account for 10% of leiomyosarcomas [1]. PLMSs often arise from skeletal muscle or retroperitoneal tissue in older people, have very poor prognosis, and are highly aggressiveness [1, 2]. PLMSs are diagnosed by histopathological and immunohistochemical analyses, a differential diagnosis is difficult for patients with complicated backgrounds. We present a case of hepatic resection for primary hepatic PLMS 2 years after surgery for gastric gastrointestinal stromal tumor (GIST). Case presentation The patient was a 62-year-old man who underwent gastric partial resection for GIST 2 years previously. Because it was thought that tumor was metastasis of In contrast with these findings, the gastric GIST specimen resected 2 years previously showed that c-kit was positive and CD34 was weakly positive, the desmin, αSMA, and S-100 protein were negative. C-kit gene mutations were not detected in the hepatic tumor. According to these findings, we diagnosed the patient with primary hepatic PLMS. The S3+4 tumor verge represented high FDG accumulation (SUVmax=12.13)
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