Balloon dilatation for treatment of hepatic venous outflow obstruction following pediatric liver transplantation

AIM To assess the efficacy and safety of balloon dilatation for the treatment of hepatic venous outflow obstruction(HVOO) following pediatric liver transplantation.METHODS A total of 246 pediatric patients underwent liver transplantation at our hospital between June 2013 and September 2016. Among these patients, five were ultimately diagnosed with HVOO. Seven procedures(two patients underwent two balloon dilatation procedures) were included in this analysis. The demographic data,types of donor and liver transplant, interventional examination and therapeutic outcomes of these five children were analyzed. The median interval time between pediatric liver transplantation and balloon dilatation procedures was 9.8 mo(range: 1-32).RESULTS Five children with HVOO were successfully treated by balloon angioplasty without stent placement, with seven procedures performed for six stenotic lesions. All children underwent successful percutaneous intervention. Among these five patients, four were treated by single balloon angioplasty, and these patients did not develop recurrent stenosis. In seven episodes of balloon angioplasty across the stenosis, the pressure gradient was 12.0 ± 8.8 mm Hg before balloon dilatation and 1.1 ± 1.5 mm Hg after the procedures, which revealed a statistically significant reduction(P < 0.05). The overall technical success rate among these seven procedures was 100%(7/7), and clinical success was achieved in all five patients(100%). The patients were followed for 4-33 mo(median: 15 mo). No significant procedural complications or procedurerelated deaths occurred.CONCLUSION Balloon dilatation is an effective and safe therapeutic option for HVOO in children undergoing pediatric liver transplantation. Venous angioplasty is also recommended in cases with recurrent HVOO.

Clinical profile and outcomes of hepatocellular carcinoma in primary Budd-Chiari syndrome

BACKGROUND There is scant literature on hepatocellular carcinoma(HCC)in patients with Budd-Chiari syndrome(BCS).AIM To assess the magnitude,clinical characteristics,feasibility,and outcomes of treatment in BCS-HCC.METHODS A total of 904 BCS patients from New Delhi,India and 1140 from Mumbai,India were included.The prevalence and incidence of HCC were determined,and among patients with BCS-HCC,the viability and outcomes of interventional therapy were evaluated.RESULTS In the New Delhi cohort of 35 BCS-HCC patients,18 had HCC at index presentation(prevalence 1.99%),and 17 developed HCC over a follow-up of 4601 person-years,[incidence 0.36(0.22-0.57)per 100 person-years].BCS-HCC patients were older when compared to patients with BCS alone(P=0.001)and had a higher proportion of inferior vena cava block,cirrhosis,and long-segment vascular obstruction.The median alpha-fetoprotein level was higher in patients with BCS-HCC at first presentation than those who developed HCC at follow-up(13029 ng/mL vs 500 ng/mL,P=0.01).Of the 35 BCS-HCC,26(74.3%)underwent radiological interventions for BCS,and 22(62.8%)patients underwent treatment for HCC[transarterial chemoembolization in 18(81.8%),oral tyrosine kinase inhibitor in 3(13.6%),and transarterial radioembolization in 1(4.5%)].The median survival among patients who underwent interventions for HCC compared with those who did not was 3.5 years vs 3.1 mo(P=0.0001).In contrast to the New Delhi cohort,the Mumbai cohort of BCS-HCC patients were predominantly males,presented with a more advanced HCC[Barcelona Clinic Liver Cancer C and D],and 2 patients underwent liver transplantation.CONCLUSION HCC is not uncommon in patients with BCS.Radiological interventions and liver transplantation are feasible in select primary BCS-HCC patients and may improve outcomes.

Tailoring stepwise treatment for Budd-Chiari syndrome: insights from the Asian Pacific Association for the Study of the Liver (APASL) consensus guidance

Budd-Chiari syndrome(BCS)is a rare disease consisting of obstruction of the hepatic venous outflow tract,which can occur at any level ranging from small hepatic veins to the inferior vena cava(1-4).BCS can result from intravascular thrombosis or membranous obstruction of the hepatic venous outflow tract,or,less commonly,due to external compression from tumors,nodules,abscesses,cysts,or other intrahepatic lesions(1-3).