Transjugular intrahepatic portosystemic shunt in patients treated with a balloon tamponade for variceal hemorrhage without response to high doses of vasoactive drugs: A real-world multicenter retrospective study.

OBJECTIVE: To evaluate the efficacy of transjugular intrahepatic portosystemic shunt (TIPS) and non-TIPS therapy (endoscopy and/or nonselective beta-blockers [NSBB]) in patients with cirrhosis and active variceal hemorrhage who did not respond to high-dose vasoactive drugs and required balloon tamponade for hemostasis. METHODS: Medical records of cirrhotic patients who did not respond to high-dose vasoactive drugs and required balloon tamponade for hemostasis at five university hospitals in China between January 2011 and December 2018 were reviewed. Treatment outcomes were compared between the TIPS and the non-TIPS groups. RESULTS: Treatment failure of variceal hemorrhage within 5 days was reported in six patients of the non-TIPS group (N = 70) and none of the TIPS group (N = 66) (P = .028). The TIPS group had a higher 1-year variceal rebleeding-free rate compared with the non-TIPS group (95.5% vs 60.0%, P < .001). One patient treated with TIPS and nine with non-TIPS therapy experienced rebleeding within 5 days and 6 weeks after the intervention (P = .009). The cumulative 1-year survival rate was higher in the TIPS group than in the non-TIPS group (93.9% vs 78.6%, P = .01). The TIPS group had a higher incidence of hepatic encephalopathy within one year compared with the non-TIPS group (18.2% vs 4.3%, P = .026). CONCLUSION: For patients with cirrhosis and active variceal bleeding who do not respond to high-dose vasoactive agents and require a balloon tamponade for hemostasis, TIPS may be an appropriate treatment choice.

RNA interference-mediated downregulation of phospholipid scramblase 1 expression in primary liver cancer in vitro.

Phospholipid scramblase 1 (PLSCR1) serves a function in the pathogenesis and progression of various types of cancer. However, the role of PLSCR1 in human primary liver cancer remains unknown. The aim of the present study was to evaluate the expression of PLSCR1 in primary liver cancer and analyse the clinical significance. In addition, the present study detected and compared the biological behaviours of HepG2 cells with different levels of activated PLSCR1 or silenced PLSCR1. PLSCR1 expression in primary liver cancer tissue samples was examined using immunohistochemistry. Cultured HepG2 cells were infected with lentiviruses to suppress or activate PLSCR1 expression. Reverse transcription-quantitative PCR and western blotting were performed to analyse the effects of silencing or activating PLSCR1 in cell lines at the mRNA and protein levels, respectively. The effects of PLSCR1 expression on cell proliferation, adhesion, migration and invasion were subsequently determined using Cell Counting Kit 8, adhesion, and Transwell migration and invasion assays. PLSCR1 expression in primary liver cancer tissue samples was higher compared with that in adjacent non-cancerous liver tissue samples and normal tissue samples, and positively correlated with the clinical stage. PLSCR1 was effectively downregulated or overexpressed in HepG2 cells using small interfering RNA and lentivirus techniques, respectively. PLSCR1 upregulation promoted cell proliferation, invasion and migration, while PLSCR1 downregulation inhibited these effects. PLSCR1 is highly expressed in primary liver cancer and associated with the clinical stage. Downregulating the expression of PLSCR1 significantly inhibited the proliferation, adhesion, migration and invasion of cancer cells, suggesting that PLSCR1 may be a potential therapeutic target for preventing the progression of primary liver cancer.