肝癌门静脉癌栓的介入治疗

肝癌合并门静脉癌栓(PVTT)的治疗仍是医学难题,既往一直被视为手术禁忌,近年随着介入医学的进步,发展了多种微创治疗方法,取得了可喜的疗效,使肝癌并PVTT由不可治变为部分可治,展现了介入方法治疗肝癌并PVTT的乐观前景.本文就当前针对门静脉癌栓的介入治疗方法,技术要点及各种介入治疗方法的初步疗效进行了综述.为进一步的临床规范化综合治疗肝癌并门静脉癌栓提供参考.     

Extrahepatic portal vein thrombosis

Noncirrhotic, nontumoral portal vein thrombosis (PVT) is the second most-frequent cause of portal hypertension in the world. General thrombophilic factors can be identified in approximately 60% of patients. PVT may manifest as an acute process. However, the acute episode more frequently is asymptomatic or paucisymptomatic and portal vein thrombosis is misdiagnosed until the development of complications secondary to portal hypertension, such as variceal bleeding or portal biliopathy. Although no randomized controlled trials have been performed, after the diagnosis of acute PVT early initiation of anticoagulation (within 30 days of the onset of symptoms) is recommended to achieve recanalization. In patients with portal cavernoma, anticoagulation is aimed to prevent the progression and recurrence of thrombosis. Because of the lack of data in this specific population, variceal bleeding is managed as in cirrhotic patients. Ursodeoxycholic acid has been proposed empirically for the treatment of patients with symptomatic portal biliopathy. Choledocholithiasis might be present, complicating a bile duct stenosis. Accordingly, an endoscopic retrograde cholangiopancreatography with sphincterotomy, extraction with balloon catheter, and stent placement is indicated. Mortality among patients with PVT is low (5-year mortality rate of 5 to 10%) and is mainly related to associated diseases rather than to complications of portal hypertension.     

门静脉血栓的研究进展

近年来,随着诊断技术的进步,门静脉血栓检出率明显提高,而且在门静脉血栓的危险因素、对门脉系统的影响、临床表现、诊断方法及治疗等方面均有了新的认识,本文就以上几方面的研究进展做一综述。     

Post-hepatectomy survival in advanced hepatocellular carcinoma with portal vein tumor thrombosis

AIM: To analyze hepatocellular carcinoma(HCC) patients with portal vein tumor thrombosis(PVTT) using the tumor-node-metastasis(TNM) staging system.METHODS: We retrospectively analyzed 372 patients with HCC who underwent hepatectomy between 1980 and 2009.We studied the outcomes of HCC patients with PVTT to evaluate the American Joint Committee on Cancer TNM staging system(7th edition) for stratifying and predicting the prognosis of a large cohort of HCC patients after hepatectomy in a single-center.Portal vein invasion(vp) 1 was defined as an invasion or tumor thrombus distal to the second branch of the portal vein,vp2 as an invasion or tumor thrombus in the second branch of the portal vein,vp3 as an invasion or tumor thrombus in the first branch of the portal vein,and vp4 as an invasion or tumor thrombus in the portal trunk or extending to a branch on the contralateral side.RESULTS: The cumulative 5-year overall survival(5yr OS) and 5-year disease-free survival(5yr DFS) rates of the 372 patients were 58.3% and 31.3%,respectively.The 5yr DFS and 5yr OS of vp3-4 patients(n = 10) were 20.0%,and 30.0%,respectively,which was comparable with the corresponding survival rates of vp1-2 patients(P = 0.466 and 0.586,respectively).In the subgroup analysis of patients with macroscopic PVTT(vp2-4),the OS of the patients who underwent preoperative transarterial chemoembolization was comparable to that of patients who did not(P = 0.747).There was a significant difference in the DFS between patients with stage Ⅰ HCC and those with stage Ⅱ HCC(5yr DFS 39.2% vs 23.1%,P 0.001); however,theDFS for stage Ⅱ was similar to that for stage Ⅲ(5yrD FS 23.1% vs 13.8%,P = 0.330).In the subgroup analysis of stage Ⅱ-Ⅲ HCC(n = 148),only alpha-fetoprotein(AFP) 100 mg/dL was independently associated with DFS.CONCLUSION: Hepatectomy for vp3-4 HCC results in a survival rate similar to hepatectomy for vp1-2.AFP stratified the stage Ⅱ-Ⅲ HCC patients according to prognosis.     

A case of portal vein thrombosis in patient with ulcerative colitis

Portal vein thrombosis is a rare and serious complication in ulcerative colitis (UC). We report a patient with UC who developed portal vein thrombosis with persistent ascites which was successfully managed with total colectomy. A 46-year-old man was admitted complaining of bloody stool. UC had been diagnosed 11 years previously. He required subtotal colectomy because his colitis did not respond to conservative therapy and worsened with suspected peritonitis. Although the portal vein thrombosis was diagnosed after surgery and the systemic anti-coagulant therapy was started, this was stopped after 2 days because of massive rectal bleeding. Fortunately, sufficient hydration with intravenous infusion and re-infusion of concentrated ascites led to portal vein thrombolysis successfully after 28 postoperative days. This case suggests that colectomy and sufficient hydration may have a favorable effect on treatment of portal vein thrombosis in patients with UC.     

Development of portal vein thrombosis complicating idiopathic portal hypertension. A case report

A 58-yr-old woman with biopsy-proven idiopathic portal hypertension presented with ascites and pretibial pitting edema. On admission, ultrasonic Doppler flowmetry demonstrated hepatopetal flow of a markedly reduced velocity in the portal vein, hepatofugal flow in the splenic vein, and a large spontaneous splenorenal shunt. The patient spontaneously developed hepatic encephalopathy 1 mo later. Percutaneous transhepatic portography demonstrated mural thrombi at the porta hepatis after the catheter had penetrated the mural thrombi without resistance; there was also a long retention of contrast medium in the portal vein. 99mTc-Macroaggregated albumin instilled into the superior mesenteric vein was caught in the lungs, and no activity entered the liver. Measurements of ammonia and immunoreactive insulin clearly indicated that superior mesenteric venous blood was shunted through the splenic vein and the splenorenal shunt. Subsequent ultrasonic examination with Doppler flowmetry suggested further growth of the thrombi and lack of blood flow in the portal vein. Although the procedure of percutaneous transhepatic catheterization could have contributed to the growth of thrombi, it is more likely that the thrombosis in the portal vein was a sequela to idiopathic portal hypertension, and was growing at the time of catheterization. This case may be of significance in the understanding of the relationship between idiopathic portal hypertension and extrahepatic portal obstruction.     

急性广泛门静脉系统血栓合并肺栓塞1例报告

门静脉血栓形成（portal vein thrombosis,PVT）是由于门静脉血管腔内血栓形成造成门静脉内血流部分或完全受阻的病理生理过程,人群中发病率为0.6%～1%[1],分为急性和慢性血栓[2]。急性门静脉血栓形成是一种临床表现复杂且少见的急腹症,占肠道血管性疾病的5%～15%[3]。而急性广泛门静脉系统血栓形成是指门静脉、脾静脉、肠系膜上静脉、肠系膜下静脉中有2条或2条以上血管急性血栓形成,     

肝细胞癌伴门静脉左支癌栓形成多学科综合治疗1例报告

肝细胞癌(简称肝癌)是一类常见的消化系统恶性肿瘤,在我国的恶性肿瘤中肝癌发病率和死亡率分别位居第4位和第2位,目前针对肝癌的主要治疗方式仍然是外科手术切除。但肝癌起病隐匿,早期缺乏典型临床表现,导致患者就诊时已经失去最佳手术时机,并且由于肝功能异常、并发症以及患者意愿,能够行使手术切除或者肝移植的患者仅占20%[1]。单一诊疗方法存在疗效差、患者生存期短、生活质量低等缺点,随着综合治疗的理念逐步兴起,使得肝癌治疗的效果得到明显提高。本院收治了1例肝癌Ⅲa期的患者,经多学科综合治疗(multi-disciplinary team,MDT)讨论后,采取了以手术为主,介入治疗及靶向药物为辅的综合治疗,现将其诊疗经过进行总结。     

肝细胞癌伴门静脉癌栓的介入综合治疗

伴门静脉癌栓(PVTT)的肝细胞癌(HCC)常见于进展期肝癌,PVTT可引起肿瘤播散、肝功能衰竭和门静脉高压,从而导致顽固性腹水、静脉曲张破裂和肝性脑病,严重影响肝癌患者预后。根据巴塞罗那临床肝癌分期(BCLC),伴PVTT的进展期HCC,索拉非尼被推荐为一线治疗方案,但由于其疗效有限且价格昂贵限制了它在国内的应用。而介入治疗以其微创、可重复性等优点在临床得到广泛应用,并取得一定的疗效。目前主要应用的介入治疗方法包括:经肝动脉灌注化疗术(HAIC)、经肝动脉化疗栓塞术(TACE)、TACE联合索拉非尼、TACE联合消融术、TACE联合适形放疗、TACE联合门静脉支架、门静脉粒子条置放术、经颈静脉肝内门体分流术(TIPS)等。最后指出多种方法综合治疗有望取得较好疗效。     

Nonmalignant portal vein thrombosis in adults

Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT. Acute PVT usually presents as abdominal pain. When the thrombus extends to the mesenteric venous arches, intestinal infarction can occur. Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy. Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease. Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively. A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT. For patients with either form of PVT, permanent anticoagulation therapy should be considered if they have a permanent risk factor. In patients with large varices, beta-adrenergic blockade or endoscopic therapy seems to prevent bleeding as a result of portal hypertension, even in patients on anticoagulation therapy. In patients with jaundice or recurrent biliary symptoms caused by cholangiopathy, insertion of a biliary endoprosthesis is the first treatment option. Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.     

Hepatic arterial infusion chemotherapy in hepatocellular carcinoma with portal vein tumor thrombosis

AIM: To evaluate the prognostic factors and efficacy of hepatic arterial infusion chemotherapy in hepatocellular carcinoma with portal vein tumor thrombosis. METHODS: Fifty hepatocellular carcinoma (HCC) patients with portal vein tumor thrombosis (PVTT) were treated using hepatic arterial infusion chemotherapy (HAIC) via a subcutaneously implanted port. The epirubicin-cisplatin-5-fluorouracil (ECF) chemotherapeutic regimen consisted of 35 mg/m 2 epirubicin on day 1, 60 mg/m 2 cisplatin for 2 h on day 2, and 500 mg/m 2 5-fluorouracil for 5 h on days 1-3. The treatments were repeated every 3 or 4 wk. RESULTS: Three (6%) of the 50 patients achieved a complete response (CR), 13 (26%) showed partial responses (PR), and 22 (44%) had stable disease (SD).The median survival and time to progression were 7 and 2 mo, respectively. After 2 cycles of HAIC, CR was achieved in 1 patient (2%), PR in 10 patients (20%) and SD in 26 patients (52%). Significant pre-treatment prognostic factors were a tumor volume of < 400 cm 3 (P = 0.01) and normal levels of protein induced by vitamin K absence or antagonist (PIVKA)-Ⅱ (P = 0.022). After 2 cycles of treatment, disease control (CR + PR + SD) (P = 0.001), PVTT response (P = 0.003) and α-fetoprotein reduction of over 50% (P = 0.02) were independent factors for survival. Objective response (CR + PR), disease control, PVTT response, and combination therapy during the HAIC were also significant prognostic factors. Adverse events were tolerable and successfully managed. CONCLUSION: HAIC may be an effective treatment modality for advanced HCC with PVTT in patients with tumors < 400 cm 3 and good prognostic factors.     

Changing perspectives in portal vein thrombosis

The aetiology of portal vein thrombosis (PVT) is heterogeneous. Important primary risk factors for PVT are cirrhosis, hepatobiliary malignancies and pancreatitis. Newly discovered thrombotic risk factors, such as latent myeloproliferative disorders and prothrombotic genetic defects, have also been identified as major risk factors for PVT. At least one-third of PVT patients demonstrate a combination of thrombotic risk factors. PVT, which does not have a detrimental effect on liver function, usually becomes manifest as a variceal haemorrhage in the oesophagus months to years after the development of thrombosis. Owing to intact coagulation variceal bleeding has a better prognosis among patients with PVT than cirrhotics. Endoscopic sclerotherapy or band ligation is the primary therapeutic option for variceal bleeding in patients with PVT. It is questionable whether anticoagulant therapy should be started, since it has not proven beneficial for most PVT patients. Therapy with anticoagulants is only recommended for those with acute PVT (especially in association with mesenteric vein thrombosis), those who recently underwent a portosystemic shunt procedure, and those with other thrombotic manifestations, particularly in case of proven hypercoagulability. Mortality of patients with PVT may be associated with concomitant medical conditions which lead to the PVT or with manifestations of portal hypertension, such as variceal haemorrhage. Multivariate analysis of a large Dutch PVT population has shown that age, malignancy, ascites and the presence of mesenteric vein thrombosis are independently related to survival. Death due to a variceal haemorrhage is rare. Poor outcome of PVT thus appears to be associated primarily with concomitant diseases which lead to PVT, and not the complications of portal hypertension. It is therefore uncertain whether surgical portosystemic shunting affects survival favourably.