摘要:目的:總結十二指腸間質瘤的診斷及外科手術體會。方法:回顧分析1999年~2008年收治的25例十二指腸間質瘤患者的臨床資料。結果:臨床表現最多見為黑便(14/25)，其次為右上腹不適(11/25)，腹塊被(2/25)，無明顯癥狀者(2/25)。術前診斷采用上消化道鋇餐造影、CT、B超、胃鏡或十二指腸鏡、超聲內鏡檢查。25例均手術治療,其中胰十二指腸切除6例,局部切除18例,組織活檢術+胃腸吻合1例。術后隨訪5~96個月,1、3、5年生存率為95.4%、85.5%和67.3%。結論:綜合CT、胃腸道鋇餐造影、消化內鏡可使大部分十二指腸間質瘤術前得到確診。手術方式依據腫瘤部位、大小而定,局部切除應選擇正確重建方式。Abstract: Objective: To investigate the diagnosis and surgery treatment of duodenal gastrointestinal stromal tumors(GIST).Methods: The clinical data of 25 patients with GIST from 1999 to 2008 were analyzed retrospectively.Results: The most common symptoms of duodenal GIST were melena(14/25), as well as abdominal pain(11/25),abdominal mass, absence of symptoms(2/25). We performed the diagnosis by upper gastrointestinal radiography, gastroscopy, endoscopic ultrasonography and CT scan. All the 25 patients underwent surgical resection, of which 6 with pancreaticoduodenectomy, 18 with local resection, 1 with tissue biopsy and stomach intestinal anastomosis. With 5 to 96 months followup after operation, 1, 3 and 5year survival rates were 95.4%, 85.5% and 67.3%. Conclusion: Preoperative diagnosis of most of GIST was dependent on CT scan, upper gastrointestinal radiography and gastroscopy. The choices of surgical procedures are mainly determined by the location and size of the tumors, local excision should choose the correct way to rebulid alimentary tract.
Objective To detective KRAS and BRAF mutations in gastrointestinal stromal tumors (GISTs) and explore its significance in resistance of imatinib treatment. Methods Three hundred and eighty-one c-kit/PDGFRA mutation samples, 119 c-kit/PDGFRA wild type samples, and 19 pairs of samples before and after imatinib resistance from 519 patients with GIST were enrolled in this study. Polymerase chain reaction was used to detect KRAS exon 2 and BRAF exon 15 mutations. The survival data were evaluated in patients with KRAS or BRAF mutation. Results KRAS mutation was found in 2 cases (1.7%) of c-kit /PDGFRA wild type GISTs, the type of KRAS mutation was G12D and G12C, respectively. BRAFV600E mutation was found in 2 cases (1.7%) of wild type GISTs. No KRAS and BRAF mutations were found in the patients with the c-kit/PDGFRA mutation GISTs and pairs of GISTs before and after imatinib resistance. Two patients with KRAS mutation showed shorter progression free survivals for imatinib treatment. Two patients with BRAF mutation had longer recurrence free survivals. Conclusions Low frequency of KRAS or BRAF mutation only happens in wild type GISTs. KRAS mutation might be related to imatinib primary resistance, but not to secondary resistance.