Proportion Of Cirrhotic Patients Research Articles

Outcomes of laparoscopic radiofrequency ablation versus percutaneous radiofrequency ablation for hepatocellular carcinoma.

Few studies have compared the therapeutic outcomes in patients with HCC who underwent laparoscopic radiofrequency ablation (LRFA) versus percutaneous radiofrequency ablation (PRFA) for hepatocellular carcinoma (HCC). Therefore, this study compared the recurrence and survival outcomes of the two RFA methods in patients with HCC. Recurrence and overall survival outcomes were evaluated in 307 patients who underwent LRFA (n = 151) or PRFA (n = 156) as a treatment method for de novo HCC. Inverse probability of treatment weighting (IPTW) analysis was performed to reduce the impact of treatment selection bias. There were no significant differences in major baseline characteristics between the LRFA and PRFA groups. However, the proportion of cirrhotic patients was higher in the LRFA group, whereas the LRFA group had more tumors and a more advanced tumor-node-metastasis stage. Moreover, the mean tumor size was significantly larger in the LRFA group than in the PRFA group. In a multivariate analysis, serum albumin level, more than three tumors, and the RFA method were identified as significant predictors of recurrence-free survival. Moreover, for the overall survival of HCC patients, serum albumin levels, days of hospital stay during RFA, and the RFA method were independent predictors. In the IPTW-adjusted analysis, the LRFA group showed significantly higher recurrence-free survival and overall survival. Our study revealed that compared with PRFA, LRFA was associated with longer recurrence-free survival and favorable overall survival in patients with HCC. Therefore, LRFA should be considered the primary therapy in patients with HCC eligible for RFA.

Clinical Decompensation and Outcomes in Patients With Compensated Cirrhosis and a Hepatic Venous Pressure Gradient ≥20 mm Hg.

Hepatic venous pressure gradient (HVPG) of ≥10 mm Hg predicts clinical decompensation (CD) in compensated cirrhosis. A proportion of cirrhotic patients at presentation have high HVPG (≥20 mm Hg) and are compensated. The natural history, spectrum of CD, and mortality in this group is largely unknown. Consecutive compensated cirrhotic patients with HVPG ≥6 mm Hg (n = 741) were followed up for 3-6 months for the development of any CD. Patients were classified based on the baseline HVPG (6 to <12 mm Hg [low HVPG, Gr.A, n = 163], 12 to <20 mm Hg [intermediate HVPG, Gr.B, n = 437] and ≥20 mm Hg [high HVPG, Gr.C, n = 141]). We analyzed the predictors of first CD, HVPG response to carvedilol, and mortality in these groups. CD developed in 217 (29.3%) patients during a mean follow-up of 1.6 ± 0.4 years, and those who developed CD had higher baseline HVPG (17.02 ± 4.79 vs 14.28 ± 4.86; P < 0.001). First CD was seen earlier (1.3 ± 0.7 years vs 1.5 ± 0.6 years and 1.6 ± 0.5 years, P = 0.02) and more frequently (44.7% vs 11% and 31.1%, P < 0.01) in high HVPG groups compared with low and intermediate HVPG groups, with higher mortality rates. Patients in the high HVPG group compared with the low HVPG group more often had NASH-cirrhosis (35.5% vs 19.6%; P 0.001), higher liver stiffness values (45.06 ± 20.46 vs 20.09 ± 5.47 kPa, P < 0.001), and lower platelet counts (113.37 ± 72.57 vs 151.7 ± 87.30/cmm, P < 0.001). Patients with HVPG ≥12 mm Hg received carvedilol, and a repeat HVPG performed in a proportion after 9.3 ± 2.4 months showed response (≥20% reduction in HVPG or <12 mm Hg) in 31.6% patients (Gr. B, 44.9% > Gr. C, 22.2%, P < 0.05). Baseline HVPG (HVPG ≥12 to <20 mm Hg [Hazard ratio: 2.73] and HVPG ≥20 mm Hg [Hazard ratio: 4.48], P < 0.001) independently predicted CD. HVPG ≥20 mm Hg in patients with compensated cirrhosis independently predicts early and more frequent CD and poor outcomes. These patients should be labeled as "high-risk compensated cirrhosis," and early and effective interventions to reduce portal pressure should be initiated to improve long-term outcomes.

Prevalence of prolonged QT interval in patients with HCV-related chronic liver disease

BackgroundHepatitis C virus (HCV) is a common disease in Egypt with a high socioeconomic burden and extra-hepatic manifestations as QT prolongation, but previous studies included mainly patients with advanced liver disease, so in this study, we aimed to delineate the prevalence of QT prolongation in early-stage HCV patients.ResultsThe study included 874 HCV patients with early cirrhosis; in Child’s class A, 57 (6.5%) patients had prolonged QT interval corrected (QTc). There was significant higher proportion of cirrhotic patients in the prolonged QTc group (31.6%) vs. in the normal QTc group (11.5%). QTc was 424.39 ± 36.6 vs. 411.51 ± 32.89 ms in cirrhotic and non-cirrhotic patients, respectively (P, 0.001). There was significant higher proportion of Fibrosis 4 (FIB-4) ≥ 1.45 score in the prolonged QTc (77.2%) vs. in the normal QTc group (56.8%) (P, 0.003). QTc interval was 417.76 ± 34.12 ms in patients with FIB-4 score ≥ 1.45 vs. 406.78 ± 31.95 ms in those with FIB-4 < 1.45 (P, < 0.001). FIB-4 score value of 2.108 predicted prolonged QTc with a sensitivity of 63.2% and a specificity of 64.5% (P, < 0.001). Twenty-four patients of long QTc group sent ECGs after HCV eradication, and 19 patients (79%) showed QTc normalization.ConclusionsHCV is associated with QTc prolongation even in patients with early chronic liver disease stages without significant fibrosis. Also, it is related to the degree of fibrosis and cirrhosis. At a cutoff value of 2.108, FIB-4 score can predict prolonged QTc. HCV eradication is associated with a high incidence of QTc normalization.

THU-054-Acute variceal bleed leads to acute on chronic liver failure like syndrome in a small proportion of cirrhotic patients: an analysis of 3845 patients from AARC data base

THU-054-Acute variceal bleed leads to acute on chronic liver failure like syndrome in a small proportion of cirrhotic patients: an analysis of 3845 patients from AARC data base

Trends in HCV treatment uptake, efficacy and impact on liver fibrosis in the Swiss HIV Cohort Study.

Hepatitis C virus (HCV) therapies with interferon-free second-generation direct-acting antivirals (DAAs) are highly effective and well tolerated. They have the potential to increase treatment eligibility and efficacy in HIV-infected patients. We assessed the impact of DAAs on treatment uptake and efficacy, as well as its impact on the burden of liver disease in the Swiss HIV Cohort Study (SHCS). We describe clinical and virological characteristics of patients treated with second-generation DAAs. We compared treatment incidence, sustained virological response (SVR)12 and liver fibrosis stages between three time periods: period 1, 01/2009-08/2011 (prior to the availability of DAAs); period 2, 09/2011-03/2014 (first generation DAAs); period 3, 04/2014-12/2015 (second generation DAAs). At the beginning of the third period, 876 SHCS participants had a chronic HCV infection of whom 180 (20%) started treatment with a second-generation DAA. Three-quarters of them had advanced liver fibrosis (Metavir≥F3) of whom 80% were cirrhotics. SVR12 was achieved in 173/180 (96%) patients, three patients died and four experienced a virological failure. Over the three time periods, treatment uptake (4.5/100py, 5.7/100py, 22.4/100py) and efficacy (54%, 70%, 96% SVR12) continuously increased. The proportion of cirrhotic patients with replicating HCV infection in the SHCS declined from 25% at the beginning to 12% at the end of the last period. After the introduction of second-generation DAAs, we observed an increase in treatment uptake and efficacy which resulted in a significant reduction in the number of cirrhotic patients with a replicating HCV infection in the SHCS.

Proton pump inhibitor intake neither predisposes to spontaneous bacterial peritonitis or other infections nor increases mortality in patients with cirrhosis and ascites.

Background and AimThe aim of this study was to assess the impact of proton pump inhibitor (PPI) intake on the development of spontaneous bacterial peritonitis (SBP) or other infections, as well as on mortality, in a thoroughly documented cohort of patients with cirrhosis and ascites.Patients and MethodsWe performed a retrospective analysis of follow-up data from 607 consecutive patients with cirrhosis undergoing their first paracentesis at a tertiary center. A binary logistic regression model investigating the association between PPI intake and SBP at the first paracentesis was calculated. Competing risk analyses and Cox models were used to investigate the effect of PPIs on the cumulative incidence of SBP or other infections and transplant-free survival, respectively. Adjustments were made for age, hepatocellular carcinoma, history of variceal bleeding, varices and model of end-stage liver disease score.ResultsEighty-six percent of patients were receiving PPIs. After adjusting for potential confounding factors, PPI intake was neither associated with increased SBP prevalence at the first paracentesis (odds ratio (OR):1.11,95% confidence interval (95%CI):0.6–2.06; P = 0.731) nor cumulative incidence of SBP (subdistribution hazard ratio (SHR): 1.38; 95%CI:0.63–3.01; P = 0.42) and SBP or other infections (SHR:1.71; 95%CI:0.85–3.44; P = 0.13) during follow-up. Moreover, PPI intake had no impact on transplant-free survival in both the overall cohort (hazard ratio (HR):0.973,95%CI:0.719–1.317; P = 0.859) as well as in the subgroups of patients without SBP (HR:1.01,95%CI:0.72–1.42; P = 0.971) and without SBP or other infections at the first paracentesis (HR:0.944,95%CI:0.668–1.334; P = 0.742).ConclusionsThe proportion of cirrhotic patients with PPI intake was higher than in previous reports, suggesting that PPI indications were interpreted liberally. In our cohort with a particularly high prevalence of PPI intake, we observed no association between PPIs and SBP or other infections, as well as mortality. Thus, the severity of liver disease and other factors, rather than PPI treatment per se may predispose for infectious complications.

Methods of decreasing infection to improve outcomes after liver resections

Infections cause both morbidity and mortality in patients undergoing liver resection. Various methods have been advocated to decrease the infectious complications after liver resection. We do not know if they are of any benefit to the patient or the health-care funder. To determine the benefits and harms of different interventions in decreasing the infectious complications and improving the outcomes after liver resection. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library, MEDLINE, EMBASE, and Science Citation Index Expanded until August 2011. We included all randomised clinical trials that were performed to compare interventions aimed at decreasing the infectious complications after liver resection. Two authors independently identified the trials and extracted the data. We analysed the data with both the fixed-effect and the random-effects model using RevMan Analysis. For each outcome we calculated the risk ratio (RR), rate ratio, or mean difference (MD) with 95% confidence intervals (CI) based on available patient data analysis. We included seven trials including 521 patients for this review. The sample size in the trials varied from 12 to 180 patients. All the trials were of high risks of systematic errors and of random errors. Four trials included patients who underwent liver resection only. In the remaining three trials, patients underwent combined liver resection with extrahepatic biliary resection resulting in a biliary enteric anastomosis. Four trials included only major liver resection. The remaining three trials included a mixture of major and minor liver resections. It appears that the proportion of cirrhotic patients in the trials was very low. The comparisons performed included whether antibiotics are necessary routinely during the peri-operative period of liver resection, the duration of antibiotics, the use of prebiotics and probiotics in the perioperative period, use of recombinant bactericidal-permeability increasing protein 21 (rBPI21), and the use of topical povidone iodine gel at the time of wound closure. Only one or two trials were included under each comparison. There was no significant differences in mortality or severe morbidity in any of the comparisons. Quality of life was not reported in any of the trials. There is currently no evidence to support or refute the use of any treatment to reduce infectious complications after liver resections. Further well designed trials with low risk of systematic error and low risk of random errors are necessary.

Relationship Between Steatosis, Inflammation, and Fibrosis in Chronic Hepatitis C: A Meta-Analysis of Individual Patient Data

Steatosis is a frequent histologic finding in chronic hepatitis C (CHC), but it is unclear whether steatosis is an independent predictor for liver fibrosis. We evaluated the association between steatosis and fibrosis and their common correlates in persons with CHC and in subgroup analyses according to hepatitis C virus (HCV) genotype and body mass index. We conducted a meta-analysis on individual data from 3068 patients with histologically confirmed CHC recruited from 10 clinical centers in Italy, Switzerland, France, Australia, and the United States. Steatosis was present in 1561 patients (50.9%) and fibrosis in 2688 (87.6%). HCV genotype was 1 in 1694 cases (55.2%), 2 in 563 (18.4%), 3 in 669 (21.8%), and 4 in 142 (4.6%). By stepwise logistic regression, steatosis was associated independently with genotype 3, the presence of fibrosis, diabetes, hepatic inflammation, ongoing alcohol abuse, higher body mass index, and older age. Fibrosis was associated independently with inflammatory activity, steatosis, male sex, and older age, whereas HCV genotype 2 was associated with reduced fibrosis. In the subgroup analyses, the association between steatosis and fibrosis invariably was dependent on a simultaneous association between steatosis and hepatic inflammation. In this large and geographically different group of CHC patients, steatosis is confirmed as significantly and independently associated with fibrosis in CHC. Hepatic inflammation may mediate fibrogenesis in patients with liver steatosis. Control of metabolic factors (such as overweight, via lifestyle adjustments) appears important in the management of CHC.

Impairment of psychomotor responses after conscious sedation in cirrhotic patients undergoing therapeutic upper GI endoscopy

OBJECTIVES: The aim of this study was to determine whether the number connection test (NCT) times of a group of cirrhotic patients without clinically overt hepatic encephalopathy and a group of healthy patients without liver disease who were undergoing endoscopy were prolonged after sedation with short acting i.v. benzodiazepines. METHODS: All patients were administered the NCT in a standard fashion for 30 min before sedation for an upper GI endoscopy and then 2 h after sedation postprocedure. Two NCTs were carried out before and 2 h after sedation, and the mean of the tests pre- and postsedation calculated. Based on the upper limit of the 95% CI of the presedation NCT of patients without liver disease as the cut-off level for hepatic encephalopathy, the proportion of cirrhotic patients with subclinical encephalopathy before and after sedation were also determined. RESULTS: A total of 61 consecutive cirrhotic patients who underwent therapeutic upper GI endoscopy completed the study. The mean presedation NCT time was 43.5 s (95% CI = 39.0–48.1 s) and the mean postsedation NCT time 60.0 s (95% CI = 50.7–69.3 s). The difference between the mean pre- and postsedation NCT times was 16.4 s (95% CI = 9.8–23.1 s; p < 0.001). A total of 38 consecutive patients without clinical or biochemical evidence of liver disease who presented for upper GI endoscopy completed the NCT as described for the group of cirrhotic patients. The mean (± SD) baseline NCT time was 34.7 ± 7.9 s (95% CI = 32.1–37.2 s), whereas the mean postsedation NCT time was 33.7 ± 8.5 s (95% CI = 30.9–36.5 s). This difference was not statistically significant ( p = 0.177). Using the upper limit of the 95% CI of the mean (37.4 s) of the presedation time in the patients without liver disease as the cut-off between normal and encephalopathy, the number of cirrhotic patients with abnormal presedation NCT times was 33 patients (54.1%), and this number rose to 46 patients (75.4%) after sedation with midazolam. This increase in proportion of cirrhotic patients with prolonged NCT time was statistically significant ( p < 0.001). CONCLUSIONS: Sedation with i.v. midazolam prolongs NCT times in cirrhotic patients but not in healthy individuals without liver disease. The proportion of patients with prolonged NCT times increased in patients with cirrhosis following sedation, whereas this did not occur in those without liver disease.

Impairment of psychomotor responses after conscious sedation in cirrhotic patients undergoing therapeutic upper GI endoscopy.

The aim of this study was to determine whether the number connection test (NCT) times of a group of cirrhotic patients without clinically overt hepatic encephalopathy and a group of healthy patients without liver disease who were undergoing endoscopy were prolonged after sedation with short acting i.v. benzodiazepines. All patients were administered the NCT in a standard fashion for 30 min before sedation for an upper GI endoscopy and then 2 h after sedation postprocedure. Two NCTs were carried out before and 2 h after sedation, and the mean of the tests pre- and postsedation calculated. Based on the upper limit of the 95% CI of the presedation NCT of patients without liver disease as the cut-off level for hepatic encephalopathy, the proportion of cirrhotic patients with subclinical encephalopathy before and after sedation were also determined. A total of 61 consecutive cirrhotic patients who underwent therapeutic upper GI endoscopy completed the study. The mean presedation NCT time was 43.5 s (95% CI = 39.0-48.1 s) and the mean postsedation NCT time 60.0 s (95% CI = 50.7-69.3 s). The difference between the mean pre- and postsedation NCT times was 16.4 s (95% CI = 9.8-23.1 s; p < 0.001). A total of 38 consecutive patients without clinical or biochemical evidence of liver disease who presented for upper GI endoscopy completed the NCT as described for the group of cirrhotic patients. The mean (+/- SD) baseline NCT time was 34.7+/-7.9 s (95% CI = 32.1-37.2 s), whereas the mean postsedation NCT time was 33.7+/-8.5 s (95% CI = 30.9-36.5 s). This difference was not statistically significant (p = 0.177). Using the upper limit of the 95% CI of the mean (37.4 s) of the presedation time in the patients without liver disease as the cut-off between normal and encephalopathy, the number of cirrhotic patients with abnormal presedation NCT times was 33 patients (54.1%), and this number rose to 46 patients (75.4%) after sedation with midazolam. This increase in proportion of cirrhotic patients with prolonged NCT time was statistically significant (p < 0.001).