Introduction: Benefit and risk of anticoagulation in cirrhotic patients with portal vein thrombosis (PVT) remain controversial, especially in those with asymptomatic PVT and in non-liver transplant candidates. Furthermore, the predictors of portal vein recanalization and bleeding events after anticoagulation are critical for making clinical decisions, but still unclear. We conducted a meta-analysis to investigate the outcomes of anticoagulation for PVT in liver cirrhosis and explore the predictors of portal vein recanalization and bleeding events after anticoagulation. Methods: All studies regarding anticoagulation for PVT in liver cirrhosis were searched via PubMed, EMBASE, and Cochrane Library databases. Thrombotic outcomes, bleeding events, and survival were compared between anticoagulation and non-anticoagulation groups. Predictors of portal vein recanalization and bleeding events were pooled. Risk ratios (RRs) or mean differences (MDs) with 95% confidence intervals (CIs) were calculated. Results: Thirty-three studies including 1696 cirrhotic patients with PVT were included. Anticoagulation significantly increased portal Electronic supplementary material The online version of this article (

background: Progesterone-withdrawal (WP)-induced endometrial breakdown occurs in both physiological and pathological processes such as menstruation and abortion. However, the underlying mechanisms are not clearly understood. As the nuclear factor-kB (NF-kB) pathway has been proposed to play a role in endometrial breakdown, we tested this hypothesis using RU486-induced mouse menstruation-like model. methods: The activation of NF-kB was evaluated by immunohistochemistry, western blot and immunofluorescence. The expression of matrix metalloproteinase-9 (MMP9) was analyzed by real-time PCR and its proteins by gelatin zymography and western blot. Chromatin immunoprecipitation was used to investigate the direct binding of NF-kB to MMP9 gene promoter. Inhibitors of NF-kB were used to block its signal in vivo and in vitro to analyze the function of NF-kB in the tissue breakdown process. results: Administration of RU486 resulted in increased phospho-IkB levels and nuclear translocation of p65 in decidual stromal cells, accompanied by the up-regulation of NF-kB inducing kinase and IkB kinase b mRNA. The NF-kB inhibitor, 'pyrrolidine dithiocarbamate' partially suppressed the RU486-induced endometrial breakdown, thus verifying the role of this pathway in vivo. MMP9 was up-and down-regulated following the NF-kB activation and inhibition, respectively. RU486 stimulated recruitment of NF-kB p65 to the MMP9 promoter and further increased its expression. Effects of NF-kB activation and inactivation on MMP9 expression were further explored in human stromal cells in vitro. A similar MMP9 expression pattern was observed in cultured human, as well as mouse, decidual stromal cells following RU486 treatment. conclusions: The activation of the NF-kB pathway induces downstream target genes, including MMP9 from stromal cells to facilitate tissue breakdown in mouse uterus, highlighting the likelihood that this regulatory pattern exists in the human endometrium.

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Background and Aim Spontaneous splenorenal shunt (SSRS) is one of the manifestations of portal hypertension in liver cirrhosis. However, the impact of SSRS on long‐term survival of cirrhotic patients remains unclear. We hypothesize that SSRS may worsen liver dysfunction and deteriorate prognosis in liver cirrhosis by decreasing hepatic perfusion. Methods Patients with liver cirrhosis who were admitted to our department between December 2014 and August 2019 and underwent contrast‐enhanced computed tomography or magnetic resonance imaging scans were prospectively collected. The maximum diameters of SSRS and portal vein system vessels were retrospectively measured. Liver‐to‐abdominal area ratio, Child–Pugh, and model for end‐stage liver disease scores were calculated. Results Overall, 122 cirrhotic patients were included. The prevalence of SSRS was 30.3% (37/122). Median diameter of SSRS was 13.5 mm. Patients with SSRS had significantly thinner diameters of right portal vein (9 mm vs 11.2 mm, P = 0.001) and main portal vein (15.3 mm vs 16.8 mm, P = 0.017) than those without SSRS. Patients with SSRS had significantly lower liver‐to‐abdominal area ratio score (25.39 vs 31.58, P < 0.001) and higher Child–Pugh (7 vs 6, P = 0.046) and model for end‐stage liver disease (12.17 vs 9.79, P < 0.006) scores than those without SSRS. Patients with SSRS had a significantly lower cumulative survival rate than those without SSRS (P = 0.014). Cox regression analysis also showed that SSRS was a risk factor of death of cirrhotic patients (hazard ratio = 4.161, 95% confidence interval = 1.215–14.255, P = 0.023). Conclusions Spontaneous splenorenal shunt may narrow portal vein diameter and shrink liver volume, thereby worsening liver function and increasing mortality in liver cirrhosis.

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Background Portal venous system thrombosis (PVST) will progress in some cases, indicating worse outcome and the necessity of antithrombotic treatment, but will spontaneously improve in others. It is crucial to understand the natural history of PVST in liver cirrhosis. However, the knowledge regarding how to predict the evolution of PVST in cirrhotic patients is very scant. Methods Sixty-nine cirrhotic patients without malignancy, who had undergone repeated contrast-enhanced computed tomography or MRI to evaluate the severity of PVST at the first and last admissions, were included. Logistic regression analysis was performed to identify the risk factors for the evolution of PVST in liver cirrhosis. Odds ratios (ORs) were calculated. Results Among 42 patients without PVST at the first admission, 10 (23.8%) developed PVST at the last admission. Serum albumin level (OR = 0.873), prothrombin time (OR = 1.619), activated partial thromboplastin time (OR = 1.169), Child-Pugh score (OR = 1.560) and model for end-stage liver disease (MELD) score (OR = 1.292) at the last admission were significant risk factors associated with the development of PVST. Among 27 patients with PVST at the first admission, 11 (40.7%), 4 (14.8%) and 12 (44.4%) had improvement, stabilization and progression of PVST at the last admission, respectively. ΔMELD score (OR = 0.714) was the only significant risk factor associated with the improvement of PVST; additionally, serum albumin level at the first admission (OR = 1.236) was the only significant risk factor associated with the progression of PVST. Conclusion Aggravation and amelioration of liver dysfunction may predict the development and improvement of PVST in liver cirrhosis, respectively.

Introduction: Occlusive portal venous system thrombosis (PVT) is significantly associated with poor outcomes in cirrhotic patients. Nonselective b-blockers (NSBBs) may be associated with the development of PVT. However, the role of NSBBs in progressing thrombosis remains unclear. Methods: Forty-three patients on whom contrast-enhanced computed tomography or

Background: Galectins, a family of β-galactoside-binding proteins, are related to the development and progression of various human diseases such as cancer, heart failure, and chronic kidney disease. However, its role in liver diseases is unclear.Methods: The PubMed, Embase, and Cochrane Library databases were searched. Hazard ratios (HRs), odds ratios (ORs), and mean differences (MDs) with 95% CIs were pooled to evaluate the association of the galectins with the outcomes and risk of liver diseases by a random effects model.Results: Thirty three studies involving 43 cohorts and 4,168 patients with liver diseases were included. In the patients with hepatocellular carcinoma (HCC), high expression of galectin-1 and -3 in the tissues was significantly associated with worse overall survival (galectin-1: HR = 1.94, 95% CI = 1.61–2.34, p &lt; 0.001; galectin-3: HR = 3.29, 95% CI = 1.62–6.68, p &lt; 0.001) and positive vascular invasion (galectin-1: OR = 1.74, 95% CI = 1.18–2.58, p = 0.005; galectin-3: OR = 2.98, 95% CI = 1.58–5.60, p = 0.001); but, high expression of galectin-4 and −9 in the tissues was significantly associated with better overall survival (galectin-4: HR = 0.53, 95% CI = 0.36–0.79, p = 0.002; galectin-9: HR = 0.56, 95% CI = 0.44–0.71, p &lt; 0.001) and negative vascular invasion (galectin-4: OR = 0.36, 95% CI = 0.19–0.72, p = 0.003; galectin-9: OR = 0.60, 95% CI = 0.37–0.97, p = 0.037). Serum galectin-3 level was significantly higher in HCC (MD = 3.06, 95% CI = 1.79–4.32, p &lt; 0.001), liver failure (MD = 0.44, 95% CI = 0.23–0.66, p &lt; 0.001), liver cirrhosis (MD = 1.83, 95% CI = 1.15–2.51, p &lt; 0.001), and chronic active hepatitis B (MD = 18.95, 95% CI = 10.91–27.00, p &lt; 0.001); serum galectin-9 level was significantly higher in HCC (MD = 3.74, 95% CI = 2.57–4.91, p &lt; 0.001) and autoimmune hepatitis (MD = 8.80, 95% CI = 7.61–9.99, p &lt; 0.001).Conclusion: High galectin-1 and -3 and low galectin-4 and -9 expression indicate worse outcomes of patients with HCC. Serum galectin-3 and -9 levels are positively associated with the risk of chronic liver diseases.