Risk Of Hepatic Decompensation Research Articles

Effects of Statins on the Hepatic Decompensation, Mortality, Complications and Drug Safety in Liver Cirrhosis: A Systematic Review and Meta-Analysis

Background and Aim: Evidence indicates statins seem to improve outcomes in cirrhotic patients. Systematic review and meta-analysis are performed to evaluate the effect and safety of statins in the setting of cirrhosis. Methods: We searched PubMed, EMBASE, and the Cochrane Library from inception through January 2018 to identify comparative studies evaluating the role of statins in cirrhosis. Pooled risk estimates with 95% confidence intervals were calculated using a random effects model. Results: Eight studies (4 retrospective cohort studies and 4 randomized controlled trials) involving 3,966 cirrhotic patients were included. Statin use was associated with 56% lower risk of progression to decompensated cirrhosis (RR, 0.44; 95% CI, 0.36–0.54) and 47% lower risk of mortality (RR, 0.53; 95% CI, 0.47–0.61). Subgroup analyses showed that these results were generally consistent regardless of study design, etiology of cirrhosis, stage of cirrhosis, follow-up time, method of identifying cirrhosis. For initial variceal bleeding, pooled RR was 0.48 (0.35–0.67). For ascites, pooled RR was 0.66 (0.45–0.99). For portal hypertension, using statins could increase the HVPG response rate, pooled RR was 2.61(1.03–6.62). For hepatocellular carcinoma, pooled RR was 0.47(0.36–0.63). For any adverse event and serious adverse events, using statins was almost equivalent to nonusers, pooled RR was 1.06 (0.50-2.25) and 0.77 (0.31–1.95). Conclusions: Statin use may be associated with reduced risk of hepatic decompensation and mortality in cirrhosis with well tolerated. Additionally, statin use appears to decrease portal hypertension and reduce the risk of initial variceal bleeding, ascites and hepatocellular carcinoma. Further RCTs will be required to confirm our findings.

Liver Surface Nodularity Score Allows Prediction of Cirrhosis Decompensation and Death.

Purpose To determine whether use of the liver surface nodularity (LSN) score, a quantitative biomarker derived from routine computed tomographic (CT) images, allows prediction of cirrhosis decompensation and death. Materials and Methods For this institutional review board-approved HIPAA-compliant retrospective study, adult patients with cirrhosis and Model for End-Stage Liver Disease (MELD) score within 3 months of initial liver CT imaging between January 3, 2006, and May 30, 2012, were identified from electronic medical records (n = 830). The LSN score was measured by using CT images and quantitative software. Competing risk regression was used to determine the association of the LSN score with hepatic decompensation and overall survival. A risk model combining LSN scores (<3 or ≥3) and MELD scores (<10 or ≥10) was created for predicting liver-related events. Results In patients with compensated cirrhosis, 40% (129 of 326) experienced decompensation during a median follow-up period of 4.22 years. After adjustment for competing risks including MELD score, LSN score (hazard ratio, 1.38; 95% confidence interval: 1.06, 1.79) was found to be independently predictive of hepatic decompensation. Median times to decompensation of patients at high (1.76 years, n = 48), intermediate (3.79 years, n = 126), and low (6.14 years, n = 152) risk of hepatic decompensation were significantly different (P < .001). Among the full cohort with compensated or decompensated cirrhosis, 61% (504 of 830) died during the median follow-up period of 2.26 years. After adjustment for competing risks, LSN score (hazard ratio, 1.22; 95% confidence interval: 1.11, 1.33) and MELD score (hazard ratio, 1.08; 95% confidence interval: 1.06, 1.11) were found to be independent predictors of death. Median times to death of patients at high (0.94 years, n = 315), intermediate (2.79 years, n = 312), and low (4.69 years, n = 203) risk were significantly different (P < .001). Conclusion The LSN score derived from routine CT images allows prediction of cirrhosis decompensation and death. ©RSNA, 2016 Online supplemental material is available for this article.

Paritaprevir/Ritonavir, Ombitasvir, Dasabuvir Combination and the Rate and Risk of Hepatic Decompensation: Results From ERCHIVES

Paritaprevir/Ritonavir, Ombitasvir, Dasabuvir Combination and the Rate and Risk of Hepatic Decompensation: Results From ERCHIVES

193 Isolated lung transplantation (LT) for cystic fibrosis patients with portal hypertension (PHT)

Objectives PHT is the main manifestation of liver disease in adults CF patients. The risk of hepatic decompensation after isolated LT is unknown. The model for end-stage liver disease (MELD) score is not relevant for the indication to combined lungs-liver transplantation. We presented the postoperative outcome of isolated lung transplantation in CF patients with asymptomatic PHT. Methods From 2008 to 2014, 14 isolated LT (over 299) were proceeded over CF patients with PHT. Results All Patients had asymptomatic liver disease before LT but all had PHT on the CT scan: splenomegaly (14–19 cm) in 10 patients, portosystemic collaterals in 8, all had portal vein dilatation >14 (diameter 17±2.3 mm). The liver stiffness measurement (LMS) was elevated 18±8 kPa when in our adult CF center median LSM was 5.9 kPa in 241 CF patients. Thirteen patients had normal liver and renal function. Gastroesophageal varices were absents in 10 screened patients. After LT, 4 patients required ECMO, 6 developed easy to treat ascites associated with transient renal insufficiency (4) or intestinal complications (2). One developed transient ascitis 7 months after LT associated with sepsis and renal dysfunction. Hepatocellular function remain normal in all patients. Every patient is still alive (mean time 42±22 months). Conclusion Carefully selected CF patients with end-stage lung disease and portal hypertension can tolerate isolated lung transplantation. The non-invasive evaluation of the severity of PHT has to be evaluated. Prospective multicentric study is need to clearly define the indications of combined lung–liver transplantation.

P0122 : Type 2 diabetes reduces overall survival and increases the risk of hepatic decompensation in HCV-related liver cirrhosis. Results from a prospective long-term study during 8 years

P0122 : Type 2 diabetes reduces overall survival and increases the risk of hepatic decompensation in HCV-related liver cirrhosis. Results from a prospective long-term study during 8 years

Relative effects of heavy alcohol use and Hepatitis C in decompensated chronic liver disease in a hospital inpatient population

Background: Heavy alcohol use has been hypothesized to accelerate disease progression to end-stage liver disease in patients with hepatitis C virus (HCV) infection. In this study, we estimated the relative influences of heavy alcohol use and HCV in decompensated chronic liver disease (CLD). Methods: Retrospectively, 904 patients with cirrhotic disease admitted to our hospitals during January 2010–December 2012 were identified based on ICD9 codes. A thorough chart review captured information on demographics, viral hepatitis status, alcohol use and progression of liver disease (i.e. decompensation). Decompensation was defined as the presence of ascites due to portal hypertension, bleeding esophageal varices, hepatic encephalopathy or hepatorenal syndrome. Heavy alcohol use was defined as a chart entry of greater than six daily units of alcohol or its equivalent. Results: 347 patients were included based on our selection criteria of documented heavy alcohol use (n = 215; 62.0%), hepatitis titers (HCV: n = 182; 52.5%) and radiological evidence of CLD with or without decompensation (decompensation: n = 225; 64.8%). Independent of HCV infection, heavy alcohol use significantly increased the risk of decompensation (OR = 1.75, 95% CI 1.11–2.75, p < 0.02) relative to no heavy alcohol use. No significance was seen with age, sex, race, HIV, viral hepatitis and moderate alcohol use for risk for decompensation. Additionally, dose-relationship regression analysis revealed that heavy, but not moderate alcohol use, resulted in a three-fold increase (p = 0.013) in the risk of decompensation relative to abstinence. Conclusions: While both heavy alcohol use and HCV infection are associated with risk of developing CLD, our data suggest that heavy, but not moderate, alcohol consumption is associated with a greater risk for hepatic decompensation in patients with cirrhosis than does HCV infection.

Liver Stiffness Is Associated With Risk of Decompensation, Liver Cancer, and Death in Patients With Chronic Liver Diseases: A Systematic Review and Meta-analysis

Liver stiffness measurement (LSM), using elastography, can independently predict outcomes of patients with chronic liver diseases (CLDs). However, there is much variation in reporting and consistency of findings. We performed a systematic review and meta-analysis to evaluate the association between LSM and outcomes of patients with CLDs. We performed a systematic review of the literature, through February 2013, for studies that followed up patients with CLDs prospectively for at least 6 months and reported the association between baseline LSM and subsequent development of decompensated cirrhosis or hepatocellular carcinoma (HCC), as well as mortality. Summary relative risk (RR) estimates per unit of LSM and 95% confidence intervals (CIs) were estimated using the random effects model. Our final analysis included 17 studies, reporting on 7058 patients with CLDs. Baseline LSM was associated significantly with risk of hepatic decompensation (6 studies; RR, 1.07; 95% CI, 1.03-1.11), HCC (9 studies; RR, 1.11; 95% CI, 1.05-1.18), death (5 studies; RR, 1.22; 95% CI, 1.05-1.43), or a composite of these outcomes (7 studies; RR, 1.32; 95% CI, 1.16-1.51). We observed considerable heterogeneity among studies-primarily in the magnitude of effect, rather than the direction of effect. This heterogeneity could not be explained by variations in study locations, etiologies and stages of CLD, techniques to measure liver stiffness, adjustment for covariates, or method of imputing relationship in the meta-analysis. Based on a meta-analysis of cohort studies, the degree of liver stiffness is associated with risk of decompensated cirrhosis, HCC, and death in patients with CLDs. LSM therefore might be used in risk stratification.

Antiviral Therapy for Chronic Hepatitis B in Pregnancy

The management of chronic hepatitis B (CHB) during pregnancy remains a challenge and involves various aspects of maternal-fetal care. Despite the standard immunoprophylaxis, a significant portion of infants born to highly viremic mothers remain infected with hepatitis B virus (HBV). Emerging data suggest that antiviral therapy in the third trimester can prevent immunoprophylaxis failure. To minimize fetal exposure to antiviral agents, antiviral therapy during pregnancy should be reserved for mothers with advanced disease or who are at risk for hepatic decompensation. Current safety data suggest that lamivudine, telbivudine, or tenofovir may be used during pregnancy. However, the timing in initiating antiviral therapy requires careful assessment of risks and benefit. The authors provide a systematic review of the features of HBV during pregnancy, risk factors for vertical transmission, and evidence-based data on antiviral use during pregnancy. They propose an algorithm to assess the need of antiviral treatment and monitor mothers with CHB.

Tipranavir in the Protease Inhibitors Arena

Tipranavir in the Protease Inhibitors Arena

Editorial : Treatment of Patients With HCV-Related Cirrhosis With Peginterferon and Ribavirin: Swinging the Pendulum Toward Treatment

Patients with hepatitis C virus-related cirrhosis are at increased risk for hepatic decompensation and hepatocellular carcinoma (HCC). They also responded less well to standard therapy compared with those without cirrhosis. Several recent studies have demonstrated that patients with cirrhosis can be safely treated and those who achieve a sustained virological response have better clinical outcomes compared with nonresponders. These results support treatment for patients with compensated cirrhosis. In addition, cirrhotic patients should be monitored after a sustained virological response is obtained, because some patients remain at risk for complications of liver disease, particularly HCC. Newer, more effective therapy is needed for patients with cirrhosis.

Recurrent Hepatitis C After Liver Transplantation

Decompensated cirrhosis from hepatitis C virus (HCV) genotype 1 is the leading indication for liver transplantation in the United States, accounting for nearly 50% of all liver transplants. Recurrent HCV is universal after liver transplantation in patients viremic at the time of transplantation and leads to cirrhosis in up to 30% of patients by five years. Once cirrhosis develops, the risk of hepatic decompensation is 42% per year. This has led to recurrent HCV emerging as an important yet controversial indication for liver retransplantation and a renewed interest in the role of anti-viral therapies. Since the first report of interferon for recurrent HCV treatment in 1996, there have been several reports in the literature of interferon-based therapies for this silent epidemic. However, these studies are limited by a paucity of randomized controlled trials. Despite encouraging results with pegylated interferon and ribavirin in the non-transplant HCV population, these findings have not translated to transplant recipients where viral eradication is frequently unsuccessful ( < 40%). Although stimulating factors are often used to treat the side effects of anti-viral therapy, they are expensive and their use remains controversial. Rejection due to anti-viral therapy, although rare, continues to be a significant concern. Despite successful HCV eradication in a small percentage of patients, progressive cryptogenic fibrosis can still develop leading to hepatic decompensation requiring retransplantation. The lack of effective therapies, severe side effects and reports of hepatic decompensation despite HCV eradication raises the question of whether recurrent HCV genotype 1 should be treated with interferon-based therapies. Clinical trials of newer antiviral medications are urgently required in these patients who are at risk of rapid development of cirrhosis.

Comparison of outcomes between patients with alcoholic cirrhosis and those with hepatitis C virus‐related cirrhosis

The natural history of alcoholic cirrhosis, especially in Asian countries, has not been completely understood thus far. We retrospectively compared the outcomes of compensated cirrhosis between Japanese alcoholic and hepatitis C virus (HCV)-infected patients. A total of 227 patients (75 alcoholic and 152 HCV-infected patients) with compensated cirrhosis were enrolled. The median follow-up period was 4.9 years. The cumulative rates of hepatocellular carcinoma (HCC) development were significantly lower in the alcoholic patients than in the HCV-infected patients (6.8% vs 50.3% at 10 years, P = 0.0003), while the cumulative rates of hepatic decompensation (37.4% vs 51.7% at 10 years) and survival (53.8% vs 47.4% at 10 years) did not significantly differ between the two groups (Kaplan-Meir analysis). The main causes of death were hepatic failure and non-hepatic diseases in the alcoholic patients and HCC and hepatic failure in the HCV-infected patients. Multivariate analyses using the Cox proportional hazard model revealed that the risk of HCC was lower in alcoholic cirrhosis than in HCV-related cirrhosis (hazard ratio (HR), 0.46), while the risk of hepatic decompensation and mortality was the same. Predictors of decreased survival were non-abstinence (HR, 2.53) in the alcoholic patients and low serum albumin level (1.58) in the HCV-infected patients. Survival of patients with alcoholic cirrhosis was similar to that of patients with HCV-related cirrhosis. The risk of HCC development was lower in alcoholic cirrhosis than in HCV-related cirrhosis. Abstinence from alcohol was important for improving the survival of patients with alcoholic cirrhosis.

Management of HBV-related cirrhosis: Role of nucleoside analogs

In the management of HBV related cirrhosis of the liver, viral suppression with safe and effective antiviral agents is essential. Besides, antiviral therapy for long term use in cirrhotics should be safe and affordable with low risk of drug resistance. Treatment of compensated HBV cirrhosis can diminish the risk of hepatic decompensation and progression to hepatocellular carcinoma [HCC]. Regression of fibrosis and reversal of cirrhosis have also been reported with antiviral therapy. Further, in decompensated cirrhosis, although liver transplantation is considered as the definitive therapy, inhibition of viral replication before transplantation can delay the need for liver transplant and also prevent HBV recurrence in the post-transplantation period. These patients while on antiviral therapy need close monitoring for viral resistance and adverse events, besides continued surveillance for HCC. This article reviews the literature on the role of nucleoside analogues in the management of HBV related chronic liver disease.

Sudden Progression to Liver Failure in a Stable Cirrhotic Patient

Purpose: Patients with cirrhosis are at risk for hepatic decompensation in case of superimposed acute liver damage. Surgical procedures in cirrhotics can also precipitate hepatic decompensation. We present a case of a stable cirrhotic patient who developed hepatic failure after acquiring acute hepatitis A (HAV) infection, and undergoing surgical procedures. Methods: A clinical vignette case report is presented. Results: A 54 year old male with no known liver disease presented with right upper quadrant pain. Laboratory data showed only a mild increase in his transaminases. Right upper quadrant ultrasound showed gallstones. He underwent an uneventful laporascopic cholecystectomy without mention of liver morphology. He presented eight days later with jaundice, malaise, lethargy, and ascites. Laboratory tests revealed bilirubin of 18.8 mg/dl, INR of 1.7, and creatinine of 4.2. No viral serologies were obtained. Imaging studies were inconclusive and the patient underwent exploratory laparotomy for possible retained biliary stone or iatrogenic bile duct damage. Operative findings included a grossly cirrhotic liver, but no biliary obstruction. Biopsy revealed micronodular cirrhosis with extensive acute necrosis. The patient was transferred for liver transplant evaluation. The patient had recently traveled to the Caribbean and his wife had contracted acute HAV infection. Serology confirmed acute HAV infection in our patient. Despite supportive care he did not improve, and subsequently underwent successful liver transplantation. Conclusion: This case illustrates several important points relating to the care of cirrhotic patients. First, acute HAV infection can have devastating effects in a cirrhotic patient. The overall case-fatality rate of acute HAV is 0.01% to 0.3%, but can reach up to 11.6% in patients with underlying chronic liver disease. Fulminant hepatic failure secondary to superinfection with HAV has been well-documented in patients with cirrhosis and chronic viral hepatitis. The CDC recommends widespread vaccination for HAV in patients with known chronic liver disease. Second, cirrhotic patients undergoing emergent intra-abdominal surgery have a high risk of morbidity and mortality. Prior data has shown peri-operative mortalities in the 10%, 30%, and 70% range for patients with Child's A, B, and C cirrhosis, respectively. Finally, there can be significant mortality (approximately 10%) in any patient undergoing surgery in the face of acute viral hepatitis. In conclusion, patients with chronic liver disease should be vaccinated against hepatitis A and B. Also, clinicians should recognize the high risk of morbidity and mortality in cirrhotic patients and patients with acute viral hepatitis undergoing surgical procedures.

Asian Pacific Association for the Study of the Liver consensus statements on the diagnosis, management and treatment of hepatitis C virus infection

Asian Pacific Association for the Study of the Liver consensus statements on the diagnosis, management and treatment of hepatitis C virus infection