Mortality and Readmission Rates After Heart Failure: A Systematic Review and Meta-Analysis.

OBJECTIVE: The current work aimed to examine the rates of and risk factors for mortality and readmission after heart failure (HF). SETTING: A systematic search was carried out in PubMed, the Cochrane Library, and EMBASE to identify eligible reports. The random-effects model was utilized to evaluate the pooled results. PARTICIPANTS: A total of 27 studies with 515,238 participants were finally meta-analysed. The HF patients had an average age of 76.3 years, with 51% of the sample being male, in the pooled analysis. PRIMARY AND SECONDARY OUTCOME MEASURES: The outcome measures were 30-day and 1-year readmission rates, mortality, and risk factors for readmission and mortality. RESULTS: The effect sizes for readmission and mortality were estimated as the mean and 95% confidence interval (CI). The estimated 30-day and 1-year all-cause readmission rates were 0.19 (95% CI 0.14-0.23) and 0.53 (95% CI 0.46-0.59), respectively, while the all-cause mortality rates were 0.14 (95% CI 0.10-0.18) and 0.29 (95% CI 0.25-0.33), respectively. Comorbidities were highly prevalent in individuals with HF. CONCLUSION: Heart failure hospitalization is followed by high readmission and mortality rates.

Validation of the six-and-twelve criteria among patients with hepatocellular carcinoma and performance score 1 receiving transarterial chemoembolization.

BACKGROUND: Transarterial chemoembolization (TACE) is recommended for patients with intermediate hepatocellular carcinoma (HCC) according to treatment guidelines. However, a large number of patients with advanced HCC also receive TACE in clinical practice, especially for those with liver-confined HCC and Eastern Cooperative Oncology Group score (ECOG) 1. In view of previous studies, such patients have different prognoses from advanced HCC patients with macrovascular invasion or extrahepatic spread; therefore, patients with ECOG 1 alone might be classified into the intermediate stage and benefit from TACE treatment, but a study particularly focusing on such patients and exploring the effectiveness of TACE therapy is lacking. AIM: To investigate treatment outcomes of TACE in HCC patients with ECOG 1 alone and propose a specific prognostic model. METHODS: Patients from 24 Chinese tertiary hospitals were selected in this nationwide multicenter observational study from January 2010 to May 2016. Overall survival (OS) was estimated using Kaplan-Meier curves and compared by the log-rank test. Multivariate Cox regression was used to develop the potential prognostic models. The discriminatory ability of the models was compared and validated in various patient subgroups. The individual survival prediction for six-and-twelve (6&12) criteria, defined as the algebraic sum of tumor size (cm) and tumor number, was illustrated by contour plot of 3-year survival probability and nomogram. RESULTS: A total of 792 eligible patients were included. During follow-up, median OS reached 18.9 mo [95% confidence interval (CI): 16.9-21.0]. Three independent multivariate analyses demonstrated that tumor size, tumor number, α-fetoprotein level, albumin-bilirubin grade and total bilirubin were prognostic factors of OS (P < 0.05). The previously proposed 6&12 criteria was comparable or even better than currently proposed with the highest predictive ability. In addition, the 6&12 criteria was correlated with OS in various subgroups of patients. The patients were stratified into three strata with score ≤ 6, > 6 but ≤ 12, and > 12 with different median OS of 39.8 mo (95%CI: 23.9-55.7), 21.1 mo (95%CI: 18.4-23.8) and 9.8 mo (95%CI: 8.3-11.3), respectively (P < 0.001). CONCLUSION: TACE is effective for advanced HCC patients with ECOG 1 alone, and the 6&12 criteria may help with clinical decision-making.

Validation and evaluation of clinical prediction systems for first and repeated transarterial chemoembolization in unresectable hepatocellular carcinoma: A Chinese multicenter retrospective study.

BACKGROUND: The treatment outcome of transarterial chemoembolization (TACE) in unresectable hepatocellular carcinoma (HCC) varies greatly due to the clinical heterogeneity of the patients. Therefore, several prognostic systems have been proposed for risk stratification and candidate identification for first TACE and repeated TACE (re-TACE). AIM: To investigate the correlations between prognostic systems and radiological response, compare the predictive abilities, and integrate them in sequence for outcome prediction. METHODS: This nationwide multicenter retrospective cohort consisted of 1107 unresectable HCC patients in 15 Chinese tertiary hospitals from January 2010 to May 2016. The Hepatoma Arterial-embolization Prognostic (HAP) score system and its modified versions (mHAP, mHAP2 and mHAP3), as well as the six-and-twelve criteria were compared in terms of their correlations with radiological response and overall survival (OS) prediction for first TACE. The same analyses were conducted in 912 patients receiving re-TACE to evaluate the ART (assessment for re-treatment with TACE) and ABCR (alpha-fetoprotein, Barcelona Clinic Liver Cancer, Child-Pugh and Response) systems for post re-TACE survival (PRTS). RESULTS: All the prognostic systems were correlated with radiological response achieved by first TACE, and the six-and-twelve criteria exhibited the highest correlation (Spearman R = 0.39, P = 0.026) and consistency (Kappa = 0.14, P = 0.019), with optimal performance by area under the receiver operating characteristic curve of 0.71 [95% confidence interval (CI): 0.68-0.74]. With regard to the prediction of OS, the mHAP3 system identified patients with a favorable outcome with the highest concordance (C)-index of 0.60 (95%CI: 0.57-0.62) and the best area under the receiver operating characteristic curve at any time point during follow-up; whereas, PRTS was well-predicted by the ABCR system with a C-index of 0.61 (95%CI: 0.59-0.63), rather than ART. Finally, combining the mHAP3 and ABCR systems identified candidates suitable for TACE with an improved median PRTS of 36.6 mo, compared with non-candidates with a median PRTS of 20.0 mo (log-rank test P < 0.001). CONCLUSION: Radiological response to TACE is closely associated with tumor burden, but superior prognostic prediction could be achieved with the combination of mHAP3 and ABCR in patients with unresectable liver-confined HCC.

MicroRNA-92a-1-5p increases CDX2 by targeting FOXD1 in bile acids-induced gastric intestinal metaplasia.

BACKGROUND AND AIMS: Gastric intestinal metaplasia (IM) is common in the gastric epithelium of patients with chronic atrophic gastritis. CDX2 activation in IM is driven by reflux of bile acids and following chronic inflammation. But the mechanism underlying how bile acids activate CDX2 in gastric epithelium has not been fully explored. METHODS: We performed microRNA (miRNA) and messenger RNA (mRNA) profiling using microarray in cells treated with bile acids. Data integration of the miRNA/mRNA profiles with gene ontology (GO) analysis and bioinformatics was performed to detect potential miRNA-mRNA regulatory circuits. Transfection of gastric cancer cell lines with miRNA mimics and inhibitors was used to evaluate their effects on the expression of candidate targets and functions. Immunohistochemistry and in situhybridisation were used to detect the expression of selected miRNAs and their targets in IM tissue microarrays. RESULTS: We demonstrate a bile acids-triggered pathway involving upregulation of miR-92a-1-5p and suppression of its target FOXD1 in gastric cells. We first found that miR-92a-1-5p was increased in IM tissues and induced by bile acids. Moreover, miR-92a-1-5p was found to activate CDX2 and downstream intestinal markers by targeting FOXD1/FOXJ1 axis and modulating activation of nuclear factor kappa B (NF-κB) pathway. Furthermore, these effects were found to be clinical relevant, as high miR-92a-1-5p levels were correlated with low FOXD1 levels and high CDX2 levels in IM tissues. CONCLUSION: These findings suggest a miR-92a-1-5p/FOXD1/NF-κB/CDX2 regulatory axis plays key roles in the generation of IM phenotype from gastric cells. Suppression of miR-92a-1-5p and restoration of FOXD1 may be a preventive approach for gastric IM in patients with bile regurgitation.

Long non-coding RNAs AC026904.1 and UCA1: a "one-two punch" for TGF-ß-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer.

Transforming growth factor-ß (TGF-ß) has received much attention as a major inducer of epithelial-mesenchymal transition (EMT) during cancer progression, mainly by activating a set of pleiotropic transcription factors including SNAI2/Slug. However, the involvement of long non-coding RNAs (lncRNAs) in TGF-ß-induced Slug activation and EMT remains largely unknown. Methods: In this study, we used microarray analysis to compare lncRNA expression profiles between TGF-ß treated and untreated breast cancer cells. Then, the clinical significance of lncRNAs in breast cancer was investigated by qPCR and Kaplan-Meier survival analysis. The molecular mechanisms and EMT-promoting effects in vitro were analyzed by confocal laser microscopy, Western blotting, chromosome conformation capture (3C), chromatin isolation by RNA purification (ChIRP), ChIP, luciferase reporter assay and transwell migration assay. Lastly, the pro-metastatic effects in vivo were evaluated by bioluminescent imaging and hematoxylin and eosin (H&E) staining. Results: We observed that TGF-ß induced genome-wide changes in lncRNA levels in breast cancer cells, among which AC026904.1 and UCA1 were highly expressed in metastatic breast cancer and closely associated with poor prognosis. Mechanistic study revealed that AC026904.1 and UCA1 were upregulated by non-canonical and canonical TGF-ß pathways, respectively. Further analysis showed that AC026904.1 functions as an enhancer RNA in the nucleus, whereas UCA1 exerts a competitive endogenous RNA (ceRNA) activity in the cytoplasm. In addition, the biological functions of these two lncRNAs converged on the activation and maintenance of Slug, constituting a one-two punch in promoting EMT and tumor metastasis. Conclusion: These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-ß-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.

Downregulation of gasdermin D promotes gastric cancer proliferation by regulating cell cycle-related proteins.

OBJECTIVE: To explore the relationship between gasdermin D (GSDMD) and gastric cancer (GC) cell proliferation, and to determine whether the downregulated expression of GSDMD contributed to the tumorigenesis and proliferation of GC cells. METHODS: GSDMD expressions in GC tissues and matched adjacent non-cancerous tissues were assessed by quantitative real-time polymerase chain reaction, Western blot and immunohistochemistry. The effect of GSDMD on cell proliferation in vitro was assessed by the colony formation assay and cell viability assays. In vivo, xenografted tumors in nude mice were evaluated. The cell cycle was analyzed by flow cytometry. In addition, the alterations of several cell cycle-related and cell signaling pathway proteins were analyzed by Western blot. RESULTS: GSDMD expression was decreased in GC, and the decreased expression of GSDMD could markedly promote the proliferation of tumors in vivo and in vitro. The downregulation of GSDMD accelerated S/G2 cell transition by activating extracellular signal regulated kinase, signal transducer and activator of transcription 3 and phosphatidylinositol 3 kinase/protein kinase B signaling pathways and regulating cell cycle-related proteins in GC. CONCLUSION: GSDMD may protect against cell proliferation of GC, and it may be used as a diagnostic and treatment strategy for GC.

Promoter methylation of RNF180 is associated with H.pylori infection and serves as a marker for gastric cancer and atrophic gastritis.

Promoter methylation (PM) of RING-finger protein (RNF) 180 affects gastric cancer (GC) prognosis, but its association with risk of GC or atrophic gastritis (AG) is unclear. We investigated relationships between RNF180 PM and GC or AG, and the effects of Helicobactor pylori (H.pylori) infection on RNF180 PM. This study included 513 subjects (159 with GC, 186 with AG, and 168 healthy controls [CON]) for RNF180 PM analysis, and another 55 GC patients for RNF180 gene expression analysis. Methylation was quantified using average methylation rates (AMR), methylated CpG site counts (MSC) and hypermethylated CpG site counts (HSC). RNF180 promoter AMR and MSC increased with disease severity. Optimal cut-offs were GC + AG: AMR > 0.153, MSC > 4 or HSC > 1; GC: AMR > 0.316, MSC > 15 and HSC > 6. Hypermethylation at 5 CpG sites differed significantly between GC/AG and CON groups, and was more common in GC patients than AG and CON groups for 2 other CpG sites. The expression of RNF180 mRNA levels in tumor were significantly lower than those in non-tumor, with the same as in hypermethylation than hypomethylation group. H.pylori infection increased methylation in normal tissue or mild gastritis, and increased hypermethylation risk at 3 CpG sites in AG. In conclusion, higher AMR, MSC and HSC levels could identify AG + GC or GC. Some RNF180 promoter CpG sites could identify precancerous or early-stage GC. H.pylori affects RNF180 PM in normal tissue or mild gastritis, and increases hypermethylation in 3 CpG sites in AG.

POU2F2-oriented network promotes human gastric cancer metastasis.

BACKGROUND AND AIMS: Aberrant upregulation of POU2F2 expression has been discovered in metastatic gastric cancer (GC). However, the mechanisms underlying the aberrant upregulation and the potential functions of POU2F2 remain uncertain. DESIGN: The role and mechanism of POU2F2 in GC metastasis were investigated in gastric epithelial cells, GC cell lines and an experimental metastasis animal model by gain of function and loss of function. Upstream and downstream targets of POU2F2 were selected by bioinformatics and identified by luciferase reporter assay, electrophoretic mobility shift assay and chromatin immunoprecipitation PCR. The influence of miR-218 on its putative target genes (POU2F2, ROBO1 and IKK-ß) and GC metastasis was further explored via in vitro and in vivo approaches. RESULTS: Increased POU2F2 expression was detected in metastatic GC cell lines and patient samples. POU2F2 was induced by the activation of nuclear factor (NF)-κB and, in turn, regulated ROBO1 transcription, thus functionally contributing to GC metastasis. Finally, miR-218 was found to suppress GC metastasis by simultaneously mediating multiple molecules in the POU2F2-oriented network. CONCLUSIONS: This study demonstrated that NF-κB and the SLIT2/ROBO1 interaction network with POU2F2 as the central part may exert critical effects on tumour metastasis. Blocking the activation of the POU2F2-oriented metastasis network using miR-218 precursors exemplified a promising approach that sheds light on new strategies for GC treatment.

MicroRNA-7/NF-κB signaling regulatory feedback circuit regulates gastric carcinogenesis.

MicroRNAs play essential roles in gene expression regulation during carcinogenesis. Here, we investigated the role of miR-7 and the mechanism by which it is dysregulated in gastric cancer (GC). We used genome-wide screenings and identified RELA and FOS as novel targets of miR-7. Overexpression of miR-7 repressed RELA and FOS expression and prevented GC cell proliferation and tumorigenesis. These effects were clinically relevant, as low miR-7 expression was correlated with high RELA and FOS expression and poor survival in GC patients. Intriguingly, we found that miR-7 indirectly regulated RELA activation by targeting the IκB kinase IKKε. Furthermore, IKKε and RELA can repress miR-7 transcription, which forms a feedback circuit between miR-7 and nuclear factor κB (NF-κB) signaling. Additionally, we demonstrate that down-regulation of miR-7 may occur as a result of the aberrant activation of NF-κB signaling by Helicobacter pylori infection. These findings suggest that miR-7 may serve as an important regulator in GC development and progression.

A decline of LAMP- 2 predicts ursodeoxycholic acid response in primary biliary cirrhosis.

Biochemical response to ursodeoxycholic acid (UDCA) in patients with primary biliary cirrhosis (PBC) is variable. We have previously reported that augmented expression of lysosome-associated membrane protein 2 (LAMP-2) was correlated with the severity of PBC. This study aimed to determine whether serum LAMP-2 could serve as a predictor of biochemical response to UDCA. The efficiency of serum LAMP-2 to predict biochemical response was assessed after 1 year of UDCA treatment in PBC patients by a retrospective analysis. We found that the basal serum LAMP-2 level was increased in PBC, especially in patients with stage III-IV (p = 0.010) or TBIL > 1 mg/dL (p = 0.014). Baseline serum LAMP-2 was higher in non-responders than that in responders, but the difference was statistically insignificant. However, after UDCA treatment, serum LAMP-2 level decreased prominently in the first 3 months, which was more obvious in responders. Further studies showed that the 35% decline of LAMP-2 after treatment for 3 months could be stated as an indicator of UDCA response with the sensitivity of 62.9% and specificity of 75.0% by Paris criteria. Meanwhile the specificity and sensitivity were identified as 63.5% and 64.1% by Barcelona criteria. Together, a decline in LAMP-2 might help to predict the response to UDCA.

Reasons for cancer metastasis: A holistic perspective.

Over several years, scientists investigating cancer have focused their efforts on elucidating the mechanisms underlying cancer metastasis, with the aim of finding a way to inhibit this process. These mechanisms, however, only explain the process of cancer metastasis, but do not explain why cancer would metastasize in the first place. Cancer metastasizes due to several factors, namely attack by the immune system, lack of oxygen and necessary nutrients, large amounts of lactic acid produced by glycolysis and increased cell death. Therefore, the majority of the presently available treatments for cancer also bear the potential to induce metastasis. Thus, it is crucial in medical practice to minimize the risk of cancer metastasis during a time when there are no effective means to inhibit this process.

The association between bile salt export pump single-nucleotide polymorphisms and primary biliary cirrhosis susceptibility and ursodeoxycholic acid response.

BACKGROUND: Primary biliary cirrhosis (PBC) is a chronic and progressive cholestasis liver disease. Bile salt export pump (BSEP) is the predominant bile salt efflux system of hepatocytes. BSEP gene has been attached great importance in the susceptibility of PBC and the response rate of ursodeoxycholic acid (UDCA) treatment of PBC patients. METHODS: In this study, TaqMan assay was used to genotype four variants of BSEP, and the Barcelona criteria were used for evaluating the response rate of UDCA treatment. RESULTS: Variant A allele of BSEP rs473351 (dominant model, OR = 2.063; 95% CI, 1.254-3.393; P = 0.004) was highly associated with PBC susceptibility. On the contrary, variant A allele of BSEP rs2287618 (dominant model, OR = 0.617; 95% CI, 0.411-0.928; P = 0.020) provided a protective role and Barcelona evaluation criterion indicated that the frequency of variant allele at BSEP rs2287618 was significantly decreased in UDCA-responsive PBC patients (P = 0.021). CONCLUSION: These results suggested that BSEP rs473351 was closely associated with the susceptibility of PBC and if people with BSEP rs2287618 were diagnosed as PBC, the UDCA treatment was not satisfactory. Larger studies with mixed ethnicity subjects and stratified by clinical and subclinical characteristics are needed to validate our findings.

Selection of treatment modalities for Budd-Chiari Syndrome in China: a preliminary survey of published literature.

AIM: To evaluate the frequency of use of various treatment modalities for Budd-Chiari syndrome (BCS) in China by conducting a preliminary survey of relevant literature. METHODS: All papers regarding the treatment of BCS in Chinese patients were identified by searching PubMed, Chinese Scientific and Technological Journal, and China National Knowledge Infrastructure databases. Data regarding the number of BCS patients treated with different treatment modalities over time were collected. The proportions of BCS patients undergoing various treatment modalities were calculated. RESULTS: Overall, 300 of 3005 papers initially retrieved were included. These papers included 23352 BCS patients treated with different treatment modalities. The treatment modalities include surgery (n = 8625), interventional treatment (n = 13940), surgery combined with interventional treatment (n = 363), medical therapy (n = 277), other treatments (n = 91), and no treatment (n = 56). After 2005, the number of BCS patients treated with surgery was drastically decreased, but the number of BCS patients who underwent interventional treatment was almost maintained. Shunt surgery was the most common type of surgery (n = 3610). Liver transplantation was rarely employed (n = 2). Balloon angioplasty with or without stenting was the most common type of interventional treatment (n = 13747). Transjugular intrahepatic portosystemic shunt was rarely employed (n = 81). CONCLUSION: Selection of treatment modalities for BCS might be different between China and Western countries. Further work should be necessary to establish a unanimous therapeutic strategy for BCS in China.

Nonselective ß-blockers may induce development of portal vein thrombosis in cirrhosis.

Currently, nonselective ß-blockers (NSBBs) are commonly used for the prevention of variceal bleeding in liver cirrhosis. The beneficial effects of NSBBs are primarily attributed to the reduction in cardiac output by blockade of ß1 receptors and vasoconstriction of the splanchnic circulation by the blockade of ß2 receptors. The prognostic value of occlusive portal vein thrombosis (PVT) in cirrhotic patients has been increasingly recognized. The most important risk factor for the development of PVT in liver cirrhosis is the decreased portal vein inflow velocity. Collectively, we propose that the use of NSBBs potentially increases the development of portal vein thrombosis by reducing portal vein inflow velocity. The hypothesis should be confirmed by prospective cohort studies, in which cirrhotic patients without prior PVT treated with and without NSBBs are enrolled, and the development of PVT during follow-up is compared between the two groups. Additionally, subgroup analyses should be performed according to the dosage of NSBBs and the reduction of portal inflow velocity after use of NSBBs.

Selection of a TIPS stent for management of portal hypertension in liver cirrhosis: an evidence-based review.

Nowadays, transjugular intrahepatic portosystemic shunt (TIPS) has become a mainstay treatment option for the management of portal hypertension-related complications in liver cirrhosis. Accumulated evidence has shown that its indications are being gradually expanded. Notwithstanding, less attention has been paid for the selection of an appropriate stent during a TIPS procedure. Herein, we attempt to review the current evidence regarding the diameter, type, brand, and position of TIPS stents. Several following recommendations may be considered in the clinical practice: (1) a 10-mm stent may be more effective than an 8-mm stent for the management of portal hypertension, and may be superior to a 12-mm stent for the improvement of survival and shunt patency; (2) covered stents are superior to bare stents for reducing the development of shunt dysfunction; (3) if available, Viatorr stent-grafts may be recommended due to a higher rate of shunt patency; and (4) the placement of a TIPS stent in the left portal vein branch may be more reasonable for decreasing the development of hepatic encephalopathy. However, given relatively low quality of evidence, prospective well-designed studies should be warranted to further confirm these recommendations.

Hepatic venous pressure gradient measurement before TIPS for acute variceal bleeding.

Hepatic venous pressure gradient (HVPG) is an independent predictor of variceal rebleeding in patients with cirrhosis. After pharmacological and/or endoscopic therapy, the use of a transjugular intrahepatic portosystemic shunt (TIPS) may be necessary in HVPG non-responders, but not in responders. Thus, HVPG measurement may be incorporated into the treatment algorithm for acute variceal bleeding, which further identifies the candidates that should undergo early insertion of TIPS or maintain the traditional pharmacological and/or endoscopic therapy. The potential benefits are to reduce the cost and prevent TIPS-related complications.

EVS vs TIPS shunt for gastric variceal bleeding in patients with cirrhosis: A meta-analysis.

AIM: To evaluate the clinical effects of transjugular intrahepatic portosystemic shunt (TIPS) vs endoscopic variceal sclerotherapy (EVS) in the management of gastric variceal (GV) bleeding in terms of variceal rebleeding, hepatic encephalopathy (HE), and survival by meta-analysis. METHODS: Medline, Embase, and CNKI were searched. Studies compared TIPS with EVS in treating GV bleeding were identified and included according to our predefined inclusion criteria. Data were extracted independently by two of our authors. Studies with prospective randomized design were considered to be of high quality. Hazard ratios (HRs) or odd ratios (ORs) were calculated using a fixed-effects model when there was no inter-trial heterogeneity. Oppositely, a random-effects model was employed. RESULTS: Three studies with 220 patients who had at least one episode of GV bleeding were included in the present meta-analysis. The proportions of patients with viral cirrhosis and alcoholic cirrhosis were 39% (range 0%-78%) and 36% (range 12% to 41%), respectively. The pooled incidence of variceal rebleeding in the TIPS group was significantly lower than that in the EVS group (HR = 0.3, 0.35, 95%CI: 0.17-0.71, P = 0.004). However, the risk of the development of any degree of HE was significantly increased in the TIPS group (OR = 15.97, 95%CI: 3.61-70.68). The pooled HR of survival was 1.26 (95%CI: 0.76-2.09, P = 0.36). No inter-trial heterogeneity was observed among these analyses. CONCLUSION: The improved effect of TIPS in the prevention of GV rebleeding is associated with an increased risk of HE. There is no survival difference between the TIPS and EVS groups. Further studies are needed to evaluate the survival benefit of TIPS in cirrhotic patients with GV bleeding.

TIPS improves liver transplantation-free survival in cirrhotic patients with refractory ascites: an updated meta-analysis.

AIM: To compare the liver transplantation-free (LTF) survival rates between patients who underwent transjugular intrahepatic portosystemic shunts (TIPS) and those who underwent paracentesis by an updated meta-analysis that pools the effects of both number of deaths and time to death. METHODS: MEDLINE, EMBASE, and the Cochrane Library were searched from the inception to October 2012. LTF survival, liver transplantation, liver disease-related death, non-liver disease-related death, recurrent ascites, hepatic encephalopathy (HE) and severe HE, and hepatorenal syndrome were assessed as outcomes. LTF survival was estimated using a HR with a 95%CI. Other outcomes were estimated using OR with 95%CIs. Sensitivity analyses were performed to assess the effects of potential outliers in the studies according to the risk of bias and the study characteristics. RESULTS: Six randomized controlled trials with 390 patients were included. In comparison to paracentesis, TIPS significantly improved LTF survival (HR = 0.61, 95%CI: 0.46-0.82, P < 0.001). TIPS also significantly decreased liver disease-related death (OR = 0.62, 95%CI: 0.39-0.98, P = 0.04), recurrent ascites (OR = 0.15, 95%CI: 0.09-0.24, P < 0.001) and hepatorenal syndrome (OR = 0.32, 95%CI: 0.12-0.86, P = 0.02). However, TIPS increased the risk of HE (OR = 2.95, 95%CI: 1.87-4.66, P = 0.02) and severe HE (OR = 2.18, 95%CI: 1.27-3.76, P = 0.005). CONCLUSION: TIPS significantly improved the LTF survival of cirrhotic patients with refractory ascites and decreased the risk of recurrent ascites and hepatorenal syndrome with the cost of increased risk of HE compared with paracentesis. Further studies are warranted to validate the survival benefit of TIPS in clinical practice settings.

Shunting branch of portal vein and stent position predict survival after transjugular intrahepatic portosystemic shunt.

AIM: To evaluate the effect of the shunting branch of the portal vein (PV) (left or right) and the initial stent position (optimal or suboptimal) of a transjugular intrahepatic portosystemic shunt (TIPS). METHODS: We retrospectively reviewed 307 consecutive cirrhotic patients who underwent TIPS placement for variceal bleeding from March 2001 to July 2010 at our center. The left PV was used in 221 patients and the right PV in the remaining 86 patients. And, 224 and 83 patients have optimal stent position and sub-optimal stent positions, respectively. The patients were followed until October 2011 or their death. Hepatic encephalopathy, shunt dysfunction, and survival were evaluated as outcomes. The difference between the groups was compared by Kaplan-Meier analysis. A Cox regression model was employed to evaluate the predictors. RESULTS: Among the patients who underwent TIPS to the left PV, the risk of hepatic encephalopathy (P = 0.002) and mortality were lower (P < 0.001) compared to those to the right PV. Patients who underwent TIPS with optimal initial stent position had a higher primary patency (P < 0.001) and better survival (P = 0.006) than those with suboptimal initial stent position. The shunting branch of the portal vein and the initial stent position were independent predictors of hepatic encephalopathy and shunt dysfunction after TIPS, respectively. And, both were independent predictors of survival. CONCLUSION: TIPS placed to the left portal vein with optimal stent position may reduce the risk of hepatic encephalopathy and improve the primary patency rates, thereby prolonging survival.

Preoperative infliximab use and postoperative complications in Crohn's disease: a systematic review and meta-analysis.

BACKGROUND: Infliximab revolutionized the treatment paradigm of Crohn's disease (CD), but did not reduce the need for surgery. The impact of biologic agents on surgical complication rates remains debated. The aim of this study was to determine the effect of preoperative infliximab use on early postoperative complications in patients with CD undergoing abdominal surgery. METHOD: PubMed and Embase databases were searched to identify comparative studies that investigated postsurgical morbidity in CD patients receiving infliximab preoperatively with those not on infliximab. We used meta-analysis with random-effects model to calculate the pooled odds ratios (ORs) with 95% confidence intervals (CIs) for total complication rate as well as major, minor, infectious, and non-infectious complications. RESULTS: A total of 18 studies involving 5769 patients included in this systematic review. There was significant association between infliximab therapy prior to surgery and total (OR = 1.45, 95% CI 1.04-2.02; 13 studies, 2538 patients), infectious (OR = 1.47, 95% CI 1.08-1.99; 10 studies, 2116 patients) and non-infectious (OR = 2.29, 95% CI 1.14-4.61; 3 studies, 729 patients) postoperative complications respectively. There was no significant disparity in the major (OR = 1.39, 95% CI 0.85-2.27; 9 studies, 3696 patients) and minor (OR = 1.39, 95% CI 0.57-3.40; 5 studies, 753 patients) complication rates between infliximab and control groups. No publication bias was detected. CONCLUSION: Preoperative infliximab use modestly increases the risk of total early postoperative complications, and particularly infectious complications in CD patients.