目的 探讨转移性肝癌的手术治疗效果。方法 回顾性分析1996～2003年四川大学华西医院对116例转移性肝癌施行手术切除的情况，比较施行同期手术组与非同期手术组的治疗效果。结果 全组无手术死亡。1、3、5年生存率分别为74.1%、39.7%、23.3%，其中同期手术组1、3、5年生存率分别为73.3%、41.7%、21.7%。非同期手术组分别为75.0%、37.5%、25.0%，两组1、3、5年生存率比较差异无显著性（P>0.05）。结论 手术切除是转移性肝癌有效的治疗方法。

目的 探讨原发性腹腔内恶性淋巴瘤的病因、诊治方法。方法 对我院收治的原发性腹腔内恶性淋巴瘤185例的临床资料进行回顾性分析。结果 185例原发性腹腔内恶性淋巴瘤，其中原发于胃的恶性淋巴瘤56例，误诊27例，手术切除38例；原发于肠的恶性淋巴瘤79例，误诊39例，手术切除63例。原发于脾脏的恶性淋巴瘤30例、肝脏6例，均误诊。原发于腹膜后间隙的肾上腺恶性淋巴瘤9例、腹主动脉旁深部淋巴结5例。结论 腹腔内恶性淋巴瘤误诊率高，综合治疗效果较单一治疗好。

目的 探讨冷冻手术对无法切除的胰腺癌的治疗效果。方法 对近7年44例无法切除的胰腺癌进行冷冻治疗。胰腺癌冷冻手术附加内引流术（胆囊或胆管空肠吻合+胃空肠吻合术）共28例，同时联合区域性灌注化疗20例，联合腹腔神经丛无水乙醇区域性注射镇痛20例。大多数病人（77.4%，314/44）常规行空肠造瘘术，用作术后肠内营养通道。术后常规观察，定期检查血CA19-9、CT、血淀粉酶等。结果 全组无手术死亡。术后腹、背疼痛缓解率89.47%（34/38），多数肿瘤有不同程度缩小，血CA19-9下降，血淀粉酶1周内轻度升高，但无胰腺炎表现。主要并发症为胃排空障碍（40.90%，18/44）。34例获得随访，中位生存期14个月，1年生存率为57.5%。许多存活者还在继续随随护中。结论 冷冻手术对无法切除的胰腺癌病人是安全、简便、有效、可供选择的一种新的治疗手段。

目的 了解胰十二指肠切除术中良性病例所占比例，分析其病变类型，探讨术前、术中诊断及其它治疗方式的可行性。方法 回顾性分析我院1996～2001年期间206例术前诊断为胰头或壶腹周围恶性肿瘤而作胰十二指肠切除术病例中，术后病理诊断为良性病变者23例的临床、病理资料。结果 术后病理检查发现慢性胰腺炎14例，胰头囊腺瘤2例，十二指肠乳头异位胰腺l例，十二指肠乳头良性腺瘤4例，胆总管下段炎性狭窄2例。良性病变占整个胰十二指肠切除术病例的11.2%。结论 在作胰十二指肠切除术的良性病变巾慢性胰腺炎占大多数。术中取活检作冰冻切片病理检查是鉴别良、恶性病变的最有效方法。对这些良性病变可选择保守治疗或行较小的局部切除术。

AIM: To explore the etlology, pathogenesis, diagnosis, and treatment of postsurgical gastroparesis syndrome (PGS) after pancreatic cancer cryotherapy (PCC) or pancreatico-duodenccomy (PD), and to analyze the correlation between the multiple factors and PGS caused by the operations. METHODS: Clinical data of 210 patients undergoing PD and 46 undergoing PCC were analyzed retrospectively. RESULTS: There were 31 (67%, 31/46) patients suffering PGS in PCC group, including 29 with pancreatic head and uncinate tumors and 2 with pancreatic body and tall tumors. Ten patients (4.8%, 10/210) developed PGS In PD group, which had a significantly lower Incldence of PGS than PCC group (χ=145, P<0.001). In PCC group, 9 patients with PGS were managed with non-operative treatment (drugs, dlet, nasogastric sucion, etc.), and one received reoperation at the 16th day, but the symptoms were not relieved. In PD group, all the patients with PGS were managed with non-operative treatment. The PGS in patients undergoing PCC had close assoclation with PCC, tumor location, but not with age, gender, obstructive jaundice, dypoproteinemia, preoperative gastric outlet obstruction and the type and number of gastric biliary tract operations. The mechanisms of PGS caused by PD were similar to those of PGS following gastrectomy. The damage to interstitial cells of Cajal might play a role in the pathogenesis of PGS after PCC, for which multiple factors were posslbly responsible, including ischemic and neural injury to the antropyloric muscle and the duodenum after freezing of the panctaatico-duodenal regions or reduced circulating levels of motilin. CONCLUSION: PGS after PCC or PD is induced by multiple factors and the exact mechanisms, which might differ between these two operations, remain unknown. Radiography of the upper gastrointestinal tract and gastroscopy are main diagnostic for PGS, and reoperation should be avolded in patients whith PGS caused by PCC.