ABSTRACT
Portal vein thrombosis (PVT) is commonly seen in patients with liver cirrhosis. Patients with varices complicated by portal vein thrombosis are more likely to experience bleeding, with higher failure rate of hemostasis and rebleeding rate, and the patients receiving liver transplantation may have a poorer prognosis. There are various risk factors for portal vein thrombosis, such as severity of liver dysfunction, use of non-selective beta blockers, and portal vein blood flow velocity. This article reviews the risk factors for portal vein thrombosis in patients with liver cirrhosis, in order to further understand the mechanism and risk level of portal vein thrombosis.
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Objective To study the effect of ursolic acid (UA) intervention on hepatocyte apoptosis induced by TGF-β1 and its potential mechanism.Methods Primary hepatocytes were extracted from healthy SD rats by in situ perfusion,cultured for 12-24h,then randomly divided into the following groups:blank control group,UA control group (UA 25μmol/L),TGF-β1 group (TGF-β1 2.5ng/ml),UA intervention group (UA 25μmol/L and TGF-β1 2.5ng/ml),DPI intervention group (DPI 0.5μmol/L and TGF-β1 2.5ng/ml).Each group was treated with drugs for corresponding time and their proliferation and apoptosis were detected by flow cytometry,the expression of CD95 (Fas) mRNA was analyzed by RT-qPCR,the expression of protein CD95 and membrane translocation of NADPH oxidase (NOX) subunit p47Phox were analyzed by Western blotting,and the reactive oxygen species (ROS) generation in primary hepatocytes was analyzed with reactive oxygen detection kit.Results UA intervention at 30min before TGF-β1 stimulating hepatocytes markedly reduced hepatocyte apoptosis (63.97 ± 3.19 vs 80.53 ± 1.56,P＜0.01) and promoted hepatocyte proliferation (18.67 ± 1.60 vs 10.83 ± 2.03,P＜0.01).UA intervention notably down-regulated the expressions of CD95 mRNA and protein (1.28 ± 0.15 vs 2.40 ± 0.25,P＜0.01;1.05 ± 0.15 vs 1.37 ± 0.18,P＜0.05),restrained membrane translocation of p47phox (1.13 ± 0.12 vs 1.76 ± 0.22,P＜0.01),and decreased ROS level in primary hepatocytes induced by TGF-β1 (2.12 ± 0.45 vs 3.23 ± 0.53,P＜0.01).Conclusion The mechanism of UA inhibiting hepatocyte apoptosis induced by TGF-β1 is likely to be that UA intervention reduced hepatocyte apoptosis by inhibiting NOX activation and decrease generation of ROS so as to down-regulate expression of CD95 in hepatocytes.
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Objective Dieulafoy's lesion is a rare cause of upper gastrointestinal bleeding. The purpose of this study was to recognize the clinical characteristics of gastric Dieulafoy and to identify possible predictive factors of rebleeding. Methods Retrospective study of patients with gastrointestinal bleeding secondary to Dieulafoy's lesion from January 2009 to June 2016. We analyzed the clinical data and endoscopic findings and the correlated with rebleeding risk factors with Dieulafoy's lesion. Results 111 patients were included in the study, 97 (87.4%) patients were male; the most common location of the bleeding lesions were Proximal stomach of 53 cases (47.7%); According to the Forrest type, 46.8% of the cases were arterial (spurting), 52.3% of the cases were arterial (oozing), there were 101 (91.0%) patients treated by endoscopic combined drug therapy. The success rate of Endoscopic hemostatic treatment was 84.2%, endoscopic hemostatic treatment success rate was as follows: single endoscopic, 85.0%; two endoscopic, 84.8%; three endoscopic, 75.0%. The hemostatic treatment success rate of 101 patients with endoscopic combined drug was as follows: Proximal stomach, 83.7%; mid-stomach, 82.1%; and distal stomach, 88.9%. Age (P = 0.002) and blood transfusion (P = 0.004) were risk factors for rebleeding in the study. Blood transfusion was associated with a higher recurrence rate for bleeding (P = 0.018, OR=37.77, 95% CI = 1.86~766.47) for 101 patients with endoscopic in combination with drug. Conclusion Endoscopic therapy is effective for treating Dieulafoy's lesion. The blood transfusion was associated with a high rate of bleeding recurrence. There were no significant differences between the rebleeding and non-rebleeding groups with respect to bleeding location or hemostatic methods.
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Objective To observe the efficacy and safety of endoscopic variceal ligation (EVL) and esophageal variceal sclerotherapy (EVS) with different hardeners for esophageal variceal bleeding (EVB).Methods Clinical data of 314 patients with EVB were retrospectively reviewed.The patients were divided into 5 groups according to the endoscopic treatments they have received,i.e.,endoscopic variceal ligation (EVL) group (n =112),sodium morrhuate sclerotherapy (EVS1) group (n =48),lauromacrogol sclerotherapy (EVS2) group (n =40),EVL plus sodium morrhuate sclerotherapy (EVLS1) group (n =26) and EVL plus lauromacrogol sclerotherapy (EVLS2) group (n =88).The efficacy,variceal recurrence rate and complication rate were evaluated.Results There was no significant difference in efficacy of stop bleeding among 5 groups,which was 85.7％ (96/112) in EVL group,83.3％ (40/48) in EVS1 group,92.5％(37/40) in EVS2 group,92.3％ (24/26) in EVLS1 group and 94.3％ (83/88) in EVLS2 group (P ＞0.05).The complete cure rates in EVLS1 group (88.5％,23/26) and EVLS2 group (87.5％,77/88)were significantly higher than those in 3 other groups (P ＜ 0.05).Rebleeding rates in EVS1 group (18.8％,9/48) and EVL group (11.6％,13/112) were significantly higher than those in other 3 groups (P ＜0.05).The patients were followed up for 6-18 months,and the varices recurrence rate was highest in group EVL (23.2％,26/112) and lowest in EVLS2 (10.2％,9/88,P ＜0.05).The complication rate in group EVS1 (32.2％,49/152) was significantly higher than that in other 4 groups (P ＜0.05).Conclusion EVL plus EVS,either with sodium morrhuate or lauromacrogol EVS is safe and effective for EVB,especially EVL plus Lauromacrogol EVS,may become an optimal therapy to control esophageal variceal bleeding and rebleeding.
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Objective To compare the predictive value of the model for end-stage liver disease (MELD), MELD-Na and Child-Pugh (CP) for rebleeding in decompensated liver cirrhosis patients with esophageal varices within 3-month and 1-year. Methods A cohort of 365 decompensated liver cirrhotic patients with esophageal varices, who were admitted to hospital between Jan.2003 and Oct.2008, were retroseptively studied and followed up at least for one year. Patients were divided into hyponatremia group and normal group. MELD-Na, MELD and Child-Pugh scores were calculated for each patients on the first day of admission.Receiver operating characteristics curves (ROC) and the area under ROC (AUC) were used to determine the ability of three models for predicting rebleeding in 3-month and 1-year. Z-test was used to compare predictive ability of three models. Results At 3-month and 1 year of enrollment, AUC of MELD-Na was 0.825 and 0.842, respectively, whereas AUC of MELD was 0.779 and 0.802, respectively. MELD-Na and MELD were superior to Child-Pugh in rebleeding prediction (0.678 and 0.634, P＜0.05). But there was no significantly difference between MELD-Na and MELD in rebleeding prediction for 3-month and 1-year (P＞ 0.05). Conclusions MELD-Na and MELD are superior to Child-Pugh score in exactly predicting the rebleeding risk in decompensated liver cirrhosis patients with esophageal varices. MELD-Na compensates a deficiency of MELD.