Liver cirrhosis

doi:10.1016/S0140-6736(14)60121-5

The Lancet

Volume 383, Issue 9930, 17–23 May 2014, Pages 1749-1761

https://doi.org/10.1016/S0140-6736(14)60121-5 Get rights and content

Summary

Cirrhosis is an increasing cause of morbidity and mortality in more developed countries, being the 14th most common cause of death worldwide but fourth in central Europe. Increasingly, cirrhosis has been seen to be not a single disease entity, but one that can be subclassified into distinct clinical prognostic stages, with 1-year mortality ranging from 1% to 57% depending on the stage. We review the current understanding of cirrhosis as a dynamic process and outline current therapeutic options for prevention and treatment of complications of cirrhosis, on the basis of the subclassification in clinical stages. The new concept in management of patients with cirrhosis should be prevention and early intervention to stabilise disease progression and to avoid or delay clinical decompensation and the need for liver transplantation. The challenge in the 21st century is to prevent the need for liver transplantation in as many patients with cirrhosis as possible.

Introduction

Cirrhosis results from different mechanisms of liver injury that lead to necroinflammation and fibrogenesis; histologically it is characterised by diffuse nodular regeneration surrounded by dense fibrotic septa with subsequent parenchymal extinction and collapse of liver structures, together causing pronounced distortion of hepatic vascular architecture.1, 2 This distortion results in increased resistance to portal blood flow and hence in portal hypertension and in hepatic synthetic dysfunction. Clinically, cirrhosis has been regarded as an end-stage disease that invariably leads to death, unless liver transplantation is done, and the only preventive strategies have been screening for oesophageal varices and hepatocellular carcinoma.

Lately, this perception has been challenged, because 1-year mortality in cirrhosis varies widely, from 1% to 57%, depending on the occurrence of clinical decompensating events.³ Histopathologists have proposed that the histological term cirrhosis should be substituted by advanced liver disease, to underline the dynamic processes and variable prognosis of the disorder.⁴ Moreover, fibrosis, even in the cirrhotic range, regresses with specific therapy if available, such as antiviral treatment for chronic hepatitis B⁵ or C.⁶

Here, we review the current understanding of cirrhosis as a dynamic process and outline current therapeutic options for prevention and treatment of complications of cirrhosis, on the basis of the subclassification in clinical prognostic stages.3, 7 The new concept in management of patients with cirrhosis is the use of non-specific therapies for prevention and early intervention to stabilise disease progression and to avoid or delay decompensation and the need for liver transplantation.

Section snippets

Epidemiology

Cirrhosis is an increasing cause of morbidity and mortality in more developed countries. It is the 14th most common cause of death in adults worldwide but the fourth in central Europe; it results in 1·03 million deaths per year worldwide,⁸ 170 000 per year in Europe,⁹ and 33 539 per year in the USA.¹⁰ Cirrhosis is the main indication for 5500 liver transplants each year in Europe.⁹ The main causes in more developed countries are infection with hepatitis C virus, alcohol misuse, and,

Pathophysiology

The transition from chronic liver disease to cirrhosis involves inflammation, activation of hepatic stellate cells with ensuing fibrogenesis, angiogenesis, and parenchymal extinction lesions caused by vascular occlusion.¹¹ This process leads to pronounced hepatic microvascular changes, characterised by sinusoidal remodelling (extracellular matrix deposition from proliferating activated stellate cells resulting in capillarisation of hepatic sinusoids), formation of intrahepatic shunts (due to

Diagnosis

Most chronic liver disease is notoriously asymptomatic until cirrhosis with clinical decompensation occurs. Decompensating events include ascites, sepsis, variceal bleeding, encephalopathy, and non-obstructive jaundice. Imaging by ultrasonography, CT, or MRI of an irregular and nodular liver together with impaired liver synthetic function is sufficient for the diagnosis of cirrhosis. Other findings include small and shrunken liver, splenomegaly, and evidence of portosystemic collaterals.

Natural course

Cirrhosis should no longer be regarded as a terminal disease and the concept of a dynamic process is increasingly accepted. A prognostic clinical subclassification with four distinct stages has been proposed with substantially differing likelihoods of mortality: stage 1 (compensated with no oesophageal varices) has an estimated mortality of 1% per year, and stages 2 (compensated with varices), 3 (decompensated with ascites), and 4 (decompensated with gastrointestinal bleeding) have annual

Prevention and treatment of complications

The focus of this Seminar is on prevention and therapy in the initial stages of cirrhosis, including the first decompensating event.

Future therapies

Currently licensed drugs, such as non-selective β blockers, statins, oral antibiotics, and anticoagulants are likely to be used in various combinations to prevent and treat complications of cirrhosis in the near future.42, 132 Statins reduce HVPG and are associated with reduced incidence of hepatocellular carcinoma. Anticoagulation used to be considered a contraindication in cirrhosis; however, stable cirrhosis is characterised by normal thrombin generation and even hypercoagulability.¹³³

Conclusions—future directions

Cirrhosis should no longer be considered as a single disease stage, because it has distinct clinical prognostic stages with substantial differences in 1-year survival.⁷ Preventive and therapeutic strategies are summarised in figure 5. Clinicians should try to diagnose advanced liver disease as early as possible and to prevent the progression to further clinical stages and the advent of complications. We have previously reviewed the potential expansion of current indications of widely used drugs

Search strategy and selection criteria

We searched Medline (2000–13) using the search term “liver cirrhosis”. We largely selected publications from the past 5 years, but we did not exclude highly relevant older publications. We selected further relevant publications from the reference lists of articles identified by this search strategy. Review articles and book chapters are cited to provide more details and references than can be cited here.

References (140)

D Schuppan et al.
Liver cirrhosis
Lancet
(2008)
G D'Amico et al.
Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies
J Hepatol
(2006)
P Hytiroglou et al.
Beyond “cirrhosis”: a proposal from the International Liver Pathology Study Group
Am J Clin Pathol
(2012)
P Marcellin et al.
Regression of cirrhosis during treatment with tenofovir disoproxil fumarate for chronic hepatitis B: a 5-year open-label follow-up study
Lancet
(2013)
TR Morgan et al.
Outcome of sustained virological responders with histologically advanced chronic hepatitis C
Hepatology
(2010)
G Garcia-Tsao et al.
Now there are many (stages) where before there was one: in search of a pathophysiological classification of cirrhosis
Hepatology
(2010)
R Lozano et al.
Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010
Lancet
(2012)
M Blachier et al.
The burden of liver disease in Europe: a review of available epidemiological data
J Hepatol
(2013)
DL Hoyert et al.
Deaths: preliminary data for 2011
Natl Vital Stat Rep
(2012)

IR Wanless et al.

Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension

Hepatology

(1995)

M Fernández et al.

Angiogenesis in liver disease

J Hepatol

(2009)

JC García-Pagán et al.

Functional aspects on the pathophysiology of portal hypertension in cirrhosis

J Hepatol

(2012)

E Cholongitas et al.

Transjugular liver biopsy: how good is it for accurate histological interpretation?

Gut

(2006)

L Castera

Noninvasive methods to assess liver disease in patients with hepatitis B or C

Gastroenterology

(2012)

V Arvaniti et al.

Infections in patients with cirrhosis increase mortality four-fold and should be used in determining prognosis

Gastroenterology

(2010)

G Fede et al.

Renal failure and cirrhosis: a systematic review of mortality and prognosis

J Hepatol

(2012)

R Moreau et al.

Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis

Gastroenterology

(2013)

SU Kim et al.

The Laennec staging system for histological sub-classification of cirrhosis is useful for stratification of prognosis in patients with liver cirrhosis

J Hepatol

(2012)

P Manousou et al.

Digital image analysis of liver collagen predicts clinical outcome of recurrent hepatitis C virus 1 year after liver transplantation

Liver Transpl

(2011)

J Parkes et al.

Enhanced liver fibrosis test can predict clinical outcomes in patients with chronic liver disease

Gut

(2010)

J Vergniol et al.

Noninvasive tests for fibrosis and liver stiffness predict 5-year outcomes of patients with chronic hepatitis C

Gastroenterology

(2011)

DB Rein et al.

The cost-effectiveness of birth-cohort screening for hepatitis C antibody in U.S. primary care settings

Ann Intern Med

(2012)

P Angulo et al.

The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD

Hepatology

(2007)

N Sheron et al.

Developing a ‘traffic light’ test with potential for rational early diagnosis of liver fibrosis and cirrhosis in the community

Br J Gen Pract

(2012)

D Roulot et al.

Transient elastography as a screening tool for liver fibrosis and cirrhosis in a community-based population aged over 45 years

Gut

(2011)

EA Tsochatzis et al.

Elastography for the diagnosis of severity of fibrosis in chronic liver disease: a meta-analysis of diagnostic accuracy

J Hepatol

(2011)

S Naveau et al.

Excess weight risk factor for alcoholic liver disease

Hepatology

(1997)

E Tsochatzis et al.

Metabolic syndrome is associated with severe fibrosis in chronic viral hepatitis and non-alcoholic steatohepatitis

Aliment Pharmacol Ther

(2008)

A Berzigotti et al.

Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis

Hepatology

(2011)

M Stepanova et al.

Components of metabolic syndrome are independent predictors of mortality in patients with chronic liver disease: a population-based study

Gut

(2010)

G Nkontchou et al.

Insulin resistance, serum leptin, and adiponectin levels and outcomes of viral hepatitis C cirrhosis

J Hepatol

(2010)

HB El-Serag et al.

Diabetes increases the risk of chronic liver disease and hepatocellular carcinoma

Gastroenterology

(2004)

TM Welzel et al.

Metabolic syndrome increases the risk of primary liver cancer in the United States: a study in the SEER-Medicare database

Hepatology

(2011)

LD Plank et al.

Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial

Hepatology

(2008)

A Luca et al.

Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis

Gastroenterology

(1997)

EASL clinical practical guidelines: management of alcoholic liver disease

J Hepatol

(2012)

J Westin et al.

Moderate alcohol intake increases fibrosis progression in untreated patients with hepatitis C virus infection

J Viral Hepat

(2002)

A Forner et al.

Hepatocellular carcinoma

Lancet

(2012)

MS Ascha et al.

The incidence and risk factors of hepatocellular carcinoma in patients with nonalcoholic steatohepatitis

Hepatology

(2010)

K Moriarty et al.

Alcohol-related disease: meeting the challenge of improved quality of care and better use of resources

EA Tsochatzis et al.

New therapeutic paradigm for patients with cirrhosis

Hepatology

(2012)

CO Zein

Clearing the smoke in chronic liver diseases

Hepatology

(2010)

C Hézode et al.

Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C

Hepatology

(2005)

JA Leithead et al.

Smoking-related morbidity and mortality following liver transplantation

Liver Transpl

(2008)

ND Freedman et al.

Association of coffee drinking with total and cause-specific mortality

N Engl J Med

(2012)

DM Torres et al.

Is it time to write a prescription for coffee? Coffee and liver disease

Gastroenterology

(2013)

SC Larsson et al.

Coffee consumption and risk of liver cancer: a meta-analysis

Gastroenterology

(2007)

A De Gottardi et al.

Postprandial effects of dark chocolate on portal hypertension in patients with cirrhosis: results of a phase 2, double-blind, randomized controlled trial

Am J Clin Nutr

(2012)

M Hernández-Guerra et al.

Ascorbic acid improves the intrahepatic endothelial dysfunction of patients with cirrhosis and portal hypertension

Hepatology

(2006)

Cited by (1396)

Beta-blockers and cirrhosis: Striking the right balance
2024, American Journal of the Medical Sciences
Decompensated cirrhosis is associated with a significantly increased risk of mortality. Variceal hemorrhage (VH) further increases the risk of mortality, and of future variceal bleed events. Non-selective beta-blockers (NSBBs) are effective therapy for primary and secondary prophylaxis of VH and have become the cornerstone of pharmacologic therapy in cirrhosis. Beta-blockers are associated with reduced overall mortality and GI-bleeding related mortality in patients with decompensated cirrhosis; they may also confer hemodynamically independent beneficial effects. Long-term treatment with beta-blockers may improve decompensation-free survival in compensated cirrhosis with clinically significant portal hypertension (CSPH). Carvedilol more effectively lowers the hepatic vein portal gradient than traditional NSBBs and has been shown to improve survival in compensated cirrhosis. Treatment goals in compensated cirrhosis with CSPH should focus on early utilization of beta-blockers to prevent decompensation and reduce mortality.
Cirrhotic cardiomyopathy: Pathogenesis, clinical features, diagnosis, treatment and prognosis
2024, Revista Portuguesa de Cardiologia
Cardiac dysfunction among cirrhotic patients has long been recognized in the medical community. While it was originally believed to be a direct result of alcohol toxicity, in the last 30 years cirrhotic cardiomyopathy (CCM) has been described as a syndrome characterized by chronic cardiac dysfunction in cirrhotic patients in the absence of known cardiac disease, regardless of the etiology of cirrhosis. CCM occurs in about 60% of patients with cirrhosis and plays a critical role in disease progression and treatment outcomes. Due to its predominantly asymptomatic course, diagnosing CCM is challenging and requires a high index of suspicion and a multiparametric approach. Patients with CCM usually present with the following triad: impaired myocardial contractile response to exercise, inadequate ventricular relaxation, and electrophysiological abnormalities (notably prolonged QT interval). In recent years, research in this area has grown expeditiously and a new set of diagnostic criteria has been developed by the Cirrhotic Cardiomyopathy Consortium, to properly identify patients with CCM. Nevertheless, CCM is still largely unknown among clinicians, and a major part of its pathophysiology and treatment is yet to be understood. In the present work, we aim to compile and summarize the available data on the pathogenesis, clinical features, diagnosis, treatment, and prognosis of CCM.
A disfunção cardíaca observada em doentes cirróticos é reconhecida há muito tempo pela comunidade médica. Embora originalmente se acreditasse ser o resultado direto da toxicidade pelo álcool, nos últimos trinta anos a cardiomiopatia cirrótica (CCM) foi descrita como uma síndrome de disfunção cardíaca em doentes cirróticos na ausência de doença cardíaca conhecida, independentemente da etiologia da cirrose. A CCM está presente em até 60% dos doentes com cirrose e desempenha um papel crítico na progressão da doença e no resultado do tratamento. Devido ao seu curso predominantemente assintomático, o diagnóstico de CCM é desafiante e requer um elevado índice de suspeição e uma abordagem multiparamétrica. Doentes com CCM geralmente apresentam a seguinte tríade: resposta contrátil do miocárdio ao exercício anormal, perturbação do relaxamento ventricular e anomalias eletrofisiológicas (nomeadamente, prolongamento do intervalo QT). Nos últimos anos, a pesquisa nesta área aumentou rapidamente e um novo conjunto de critérios diagnósticos foi desenvolvido pelo Consórcio da Cardiomiopatia Cirrótica, para melhor identificar estes doentes. No entanto, este tema é ainda amplamente desconhecido por muitos clínicos e a grande parte da sua fisiopatologia e tratamento estão ainda por esclarecer. Nesta revisão, o nosso objetivo é compilar e sumariar a informação disponível sobre a patogénese, apresentação clínica, diagnóstico, tratamento e prognóstico da CCM.
Impacts of the development of acute-on-chronic liver failure and bacterial infections on β-cell function and glucose homeostasis in patients with liver cirrhosis
2024, Digestive and Liver Disease
The pathogenesis involved in glucose metabolism disorders (GMDs) in patients with liver cirrhosis remains unclear.
We investigated the effects of acute-on-chronic liver failure (ACLF) development and bacterial infections (BIs) on pancreatic β-cell function and glucose homeostasis in individuals with liver cirrhosis.
A retrospective analysis was conducted on 327 patients experiencing acute deterioration of liver cirrhosis. Oral glucose tolerance tests (OGTTs) and OGTT-based β-cell function indices were employed to assess β-cell function and glucose homeostasis. Univariate and multivariate logistic regression analyses were employed to identify GMD-associated risk factors.
Both the development of ACLF and BIs significantly increased the prevalence of GMDs. Both ACLF and BIs markedly elevated the homeostasis model of assessment 2-insulin resistance (HOMA2-IR). ACLF significantly impaired glucose-stimulated insulin secretion, as evidenced by reduced insulinogenic index (IGI). Patients with GMDs exhibited significantly lower IGI levels than those without GMDs. Independent risk factors associated with GMDs were prothrombin activity (odds ratio [OR]=0.981, 95% confidence interval [CI]: 0.960–0.995), HOMA2-IR (OR=1.749, 95% CI: 1.130–2.707), and IGI (OR=0.963, 95% CI: 0.947–0.978).
In liver cirrhosis, the onset of ACLF impairs glucose-stimulated insulin secretion from β-cells. Both liver impairment and BIs contribute to increased insulin resistance, ultimately disturbing glucose homeostasis.
D-dimer-to-platelet count ratio as a novel indicator for predicting prognosis in HBV-related decompensated cirrhosis
2024, Heliyon
Hepatitis B virus-related decompensated cirrhosis (HBV-DC) is a critical illness with a low survival rate. Timely identification of prognostic indicators is crucial for risk stratification and personalized management of patients. The present study aimed to investigate the potential of the D-dimer-to-platelet count ratio (DPR) as a prognostic indicator for HBV-DC.
A retrospective review of medical records was conducted for 164 patients diagnosed with HBV-DC. Baseline clinical and laboratory characteristics were extracted for analysis. The endpoint was 30-day mortality. Disease severity was assessed by the Model for End-stage Liver Disease (MELD) score. A multivariate logistic regression model and receiver operating characteristic curve analysis (ROC) were used to evaluate the predictive value of DPR for mortality.
During the 30-day follow-up period, 30 (18.3%) patients died. Non-survivors exhibited significantly higher DPR values than survivors, and a high DPR had a strong association with increased mortality. Importantly, DPR was identified as an independent risk factor for mortality in HBV-DC patients after adjustments for confounding factors (Odds ratio = 1.017; 95% Confidence interval, 1.006–1.029; p = 0.003). The cut-off value of DPR as a predictor of mortality was>57.6 (sensitivity = 57%, specificity = 86%, p < 0.001). The area under ROC curve for DPR for 30-day mortality was 0.762, comparable to the MELD score (p = 0.100). Furthermore, the combined use of DPR and MELD score further increased the area under the ROC curve to 0.897.
Elevated DPR was demonstrated to have a correlation with unfavorable outcomes in HBV-DC patients, suggesting its potential utility as an effective biomarker for assessment of prognosis in these patients.
Tianhuang formula ameliorates liver fibrosis by inhibiting CCL2-CCR2 axis and MAPK/NF-κB signaling pathway
2024, Journal of Ethnopharmacology
In the progression of chronic liver diseases, liver fibrosis is a reversible pathophysiologic event for liver diseases prognosis and risk of cirrhosis. Liver injury factors of different etiologies mediate this process. There is still a lack of effective medications for treating liver fibrosis. Additionally, the ameliorative effects of traditional herbs on liver fibrosis have been commonly reported. Tianhuang formula (THF) is a drug combination consisting of 2 traditional Chinese herbs, which has been showing significant improvement in metabolic liver diseases. However, the hepatoprotective effect and mechanism of THF in ameliorating liver fibrosis are still unclear.
This study aimed to investigate the effects of THF on carbon tetrachloride (CCl₄)-induced and methionine-choline-deficient (MCD) diet-induced liver fibrosis model and to reveal the potential mechanisms. It can provide experimental evidence for THF as a therapeutic candidate for liver fibrosis.
In this study, CCl₄-induced mice were treated with THF (80 mg/kg, 160 mg/kg) or Fuzheng Huayu (FZHY) capsules (4.8 g/kg) for 6 weeks. MCD-induced mice received the same doses of THF or FZHY for 4 weeks. FZHY is used as a comparative study in these two models. Following that, using kit reagents detected changes in relevant serum and liver biochemical indicators. Histological changes in mouse liver were measured by staining of H&E and Sirius Red. The markers expression of liver fibrosis and inflammation were detected using qRT-PCR, western blotting and immunohistochemical staining analysis. The potential regulatory mechanism of THF to ameliorate liver fibrosis was performed by RNA-sequencing analysis. Finally, the analysis results were verified by immunofluorescence co-staining, qRT-PCR and western blotting.
Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and hepatic triglyceride (TG) levels in CCl₄ and MCD-induced liver fibrosis mice were significantly improved after THF treatment. Meanwhile, the expression of fibrosis and inflammation markers were significantly suppressed. Furthermore, THF downregulated the expression of the macrophage marker CD68. According to RNA-sequencing analysis, we found the CCL2-CCR2 axis and MAPK/NF-κB as the potential signaling pathway for THF against liver fibrosis.
This study revealed that THF ameliorated liver injury, inflammation and fibrotic process by inhibiting CCL2-CCR2 axis and its downstream MAPK/NF-κB signaling pathway.
Utility of laryngoscopy in liver failure
2024, American Journal of Otolaryngology - Head and Neck Medicine and Surgery
To determine the utility of laryngoscopy in the evaluation of liver transplant patients.
This study is a single center retrospective cohort review of patients with a diagnosis of liver failure who underwent laryngoscopy or stroboscopy exam as part of a pre-transplant evaluation from 1/1/2010 to 12/31/2022. Patients were identified using ICD 9 and 10 codes for liver failure and CPT codes for flexible laryngoscopy and stroboscopy. Only patients who underwent preoperative liver transplant evaluation were included. Demographic data was collected. Cohort analysis between patients who did or did not undergo further diagnostic intervention was undertaken.
1824 patients were identified. 243 of these patients underwent pre-transplant laryngoscopy or stroboscopy. 26 of the 243 (10.7 %) patients had further diagnostic work up for findings during laryngoscopy, stroboscopy, or head and neck examination. There was one patient who was found to have head and neck cancer and was excluded from the transplant list until this was treated.
Otolaryngologic evaluation of liver transplant patients may be beneficial to identify head and neck pathology.

View all citing articles on Scopus

View full text

SeminarLiver cirrhosis

Summary

Introduction

Section snippets

Epidemiology

Pathophysiology

Diagnosis

Natural course

Prevention and treatment of complications

Future therapies

Conclusions—future directions

Search strategy and selection criteria

Liver cirrhosis

Lancet

Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies

J Hepatol

Beyond “cirrhosis”: a proposal from the International Liver Pathology Study Group

Am J Clin Pathol

Regression of cirrhosis during treatment with tenofovir disoproxil fumarate for chronic hepatitis B: a 5-year open-label follow-up study

Lancet

Outcome of sustained virological responders with histologically advanced chronic hepatitis C

Hepatology

Now there are many (stages) where before there was one: in search of a pathophysiological classification of cirrhosis

Hepatology

Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010

Lancet

The burden of liver disease in Europe: a review of available epidemiological data

J Hepatol

Deaths: preliminary data for 2011

Natl Vital Stat Rep

Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension

Hepatology

Angiogenesis in liver disease

J Hepatol

Functional aspects on the pathophysiology of portal hypertension in cirrhosis

J Hepatol

Transjugular liver biopsy: how good is it for accurate histological interpretation?

Gut

Noninvasive methods to assess liver disease in patients with hepatitis B or C

Gastroenterology

Infections in patients with cirrhosis increase mortality four-fold and should be used in determining prognosis

Gastroenterology

Renal failure and cirrhosis: a systematic review of mortality and prognosis

J Hepatol

Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis

Gastroenterology

The Laennec staging system for histological sub-classification of cirrhosis is useful for stratification of prognosis in patients with liver cirrhosis

J Hepatol

Digital image analysis of liver collagen predicts clinical outcome of recurrent hepatitis C virus 1 year after liver transplantation

Liver Transpl

Enhanced liver fibrosis test can predict clinical outcomes in patients with chronic liver disease

Gut

Noninvasive tests for fibrosis and liver stiffness predict 5-year outcomes of patients with chronic hepatitis C

Gastroenterology

The cost-effectiveness of birth-cohort screening for hepatitis C antibody in U.S. primary care settings

Ann Intern Med

The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD

Hepatology

Developing a ‘traffic light’ test with potential for rational early diagnosis of liver fibrosis and cirrhosis in the community

Br J Gen Pract

Transient elastography as a screening tool for liver fibrosis and cirrhosis in a community-based population aged over 45 years

Gut

Elastography for the diagnosis of severity of fibrosis in chronic liver disease: a meta-analysis of diagnostic accuracy

J Hepatol

Excess weight risk factor for alcoholic liver disease

Hepatology

Metabolic syndrome is associated with severe fibrosis in chronic viral hepatitis and non-alcoholic steatohepatitis

Aliment Pharmacol Ther

Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis

Hepatology

Components of metabolic syndrome are independent predictors of mortality in patients with chronic liver disease: a population-based study

Gut

Insulin resistance, serum leptin, and adiponectin levels and outcomes of viral hepatitis C cirrhosis

J Hepatol

Diabetes increases the risk of chronic liver disease and hepatocellular carcinoma

Gastroenterology

Metabolic syndrome increases the risk of primary liver cancer in the United States: a study in the SEER-Medicare database

Hepatology

Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial

Hepatology

Seminar
Liver cirrhosis