Drs. Stephen A. Harrison and Salvatore Petta discuss the paper: The severity of steatosis influences liver stiffness measurement in patients with nonalcoholic fatty liver disease from the November 2015 issue of HEPATOLOGY.

The Severity Of Steatosis Influences Liver Stiffness Measurement In Patients With NAFLD

Note: Published earlier in 2015.Drs. Stephen A. Harrison and Saleh A. Alqahtani discuss the paper: Safety and Tolerability of Ledipasvir/Sofosbuvir With and Without Ribavirin in Patients with Chronic Hepatitis C Virus Genotype 1 Infection: Analysis of Phase III ION Trials.

Note: Published earlier in 2015. Drs. Stephen A. Harrison and Saleh A. Alqahtani discuss the paper: Safety and Tolerability of Ledipasvir/Sofosbuvir With and Without Ribavirin in Patients with Chronic Hepatitis C Virus Genotype 1 Infection: Analysis of Phase III ION Trials.

Ledipasvir/Sofosbuvir Safety+Tolerability With&Without Ribavirin in Chronic HCV Infection

Drs. Stephen A. Harrison and Lisa B. VanWagner discuss the paper: Association of nonalcoholic fatty liver disease with subclinical myocardial remodeling and dysfunction: A population-based study.

Association of NAFLD with Subclinical Myocardial Remodeling and Dysfunction

Drs. Stephen A. Harrison and Sasan Roayaie discuss the paper: The Role of Hepatic Resection in the Treatment of Hepatocellular Cancer.

The Role of Hepatic Resection in Liver Cancer

Drs. Stephen A. Harrison and Saleh A. Alqahtani discuss the paper:  Safety and Tolerability of Ledipasvir/Sofosbuvir With and Without Ribavirin in Patients with Chronic Hepatitis C Virus Genotype 1 Infection: Analysis of Phase III ION Trials.

Drs. Stephen A. Harrison and Leon A. Adams discuss the paper: The Impact of Phlebotomy in Nonalcoholic Fatty Liver Disease: A Prospective, Randomized, Controlled Trial.

The Impact of Phlebotomy in Nonalcoholic Fatty Liver Disease

Drs. Stephen A. Harrison and Annalisa Berzigotti discuss the paper: Portal hypertension and the outcome of surgery for hepatocellular carcinoma in compensated cirrhosis: A systematic review and meta-analysis from the Februrary issue of HEPATOLOGY.

Portal Hypertension and the Outcome of Surgery for HCC

Drs. Stephen A. Harrison and Eric M. Yoshida discuss the paper: Concordance of sustained virological response 4, 12, and 24 weeks post-treatment with sofosbuvir-containing regimens for hepatitis C virus from the January issue of HEPATOLOGY.

Concordance Of Sustained Virological Response With Sofosbuvir - Containing Regimens For HCV

Drs. Stephen A. Harrison and Karim J. Hazalun discuss the paper: Standing the test of time: Outcomes of a decade of prioritizing patients with hepatocellular carcinoma, results of the UNOS natural geographic experiment from the December issue of HEPATOLOGY.

Prioritizing HCC Patients -- Results Of The UNOS National Geographic Experiment

Stephen A. Harrison, MD and Taro Yamashita, MD, PhD, discuss Gd-EOB-DTPA-enhanced MRI and Alpha-fetoprotein Predict Prognosis of Early Early Stage HCC.

Enhanced MRI Prognosis Of Early Early Stage HCC

VisionTo Prevent and Cure Liver DiseaseMissionTo advance and disseminate the science and practice of hepatology, and to promote liver health and quality patient careAASLD is the leading organization of scientists and healthcare professionals committed to preventing and curing liver disease. AASLD was founded in 1950 by a small group of leading liver specialists (including Hans Popper, Leon Schiff, Fred Hoffbauer, Cecil Watson, Jesse Bollman, and Sheila Sherlock, to name a few) to bring together those who had contributed to the field of hepatology. AASLD has grown to an international society responsible for all aspects of hepatology, and our annual meeting, The Liver Meeting®, has grown in attendance from 12 to over 9,500 physicians, surgeons, researchers, and allied health professionals from around the world.Hepatology has been recognized as a discipline only in the last few decades, and AASLD played a seminal and unifying role in focusing interest on hepatological problems, as well as the founding of other hepatological societies. Our three monthly journals, HEPATOLOGY, Liver Transplantation, and Clinical Liver Disease provide the latest research findings for hepatology and surgery of the liver.AASLD's membership includes ALL professionals dedicated to hepatobiliary discoveries and patient care. Mentoring, the sharing of knowledge, and dedication to professional growth and development are among the core values of AASLD and its members.

Vision To Prevent and Cure Liver Disease Mission To advance and disseminate the science and practice of hepatology, and to promote liver health and quality patient care AASLD is the leading organization of scientists and healthcare professionals committed to preventing and curing liver disease. AASLD was founded in 1950 by a small group of leading liver specialists (including Hans Popper, Leon Schiff, Fred Hoffbauer, Cecil Watson, Jesse Bollman, and Sheila Sherlock, to name a few) to bring together those who had contributed to the field of hepatology. AASLD has grown to an international society responsible for all aspects of hepatology, and our annual meeting, The Liver Meeting®, has grown in attendance from 12 to over 9,500 physicians, surgeons, researchers, and allied health professionals from around the world. Hepatology has been recognized as a discipline only in the last few decades, and AASLD played a seminal and unifying role in focusing interest on hepatological problems, as well as the founding of other hepatological societies. Our three monthly journals, HEPATOLOGY, Liver Transplantation, and Clinical Liver Disease provide the latest research findings for hepatology and surgery of the liver. AASLD's membership includes ALL professionals dedicated to hepatobiliary discoveries and patient care. Mentoring, the sharing of knowledge, and dedication to professional growth and development are among the core values of AASLD and its members.

HEPATOLOGY Podcast

Heart failure (HF) is, after cirrhosis, the second-most common cause of ascites. Serum B-type natriuretic peptide (BNP) plays an important role in the diagnosis of HF. Therefore, we hypothesized that BNP would be useful in the differential diagnosis of ascites. Consecutive patients with new onset ascites were prospectively enrolled in this cross-sectional study. All patients had measurements of serum-ascites albumin gradient (SAAG), total protein concentration in ascitic fluid, serum, and ascites BNP. We enrolled 218 consecutive patients with ascites resulting from HF (n = 44), cirrhosis (n = 162), peritoneal disease (n = 10), and constrictive pericarditis (n = 2). Compared to SAAG and/or total protein concentration in ascites, the test that best discriminated HF-related ascites from other causes of ascites was serum BNP. A cutoff of &gt;364 pg/mL (sensitivity 98%, specificity 99%, and diagnostic accuracy 99%) had the highest positive likelihood ratio (168.1); that is, it was the best to rule in HF-related ascites. Conversely, a cutoff ≤182 pg/mL had the lowest negative likelihood ratio (0.0) and was the best to rule out HF-related ascites. These findings were confirmed in a 60-patient validation cohort. Conclusions: Serum BNP is more accurate than ascites analyses in the diagnosis of HF-related ascites. The workup of patients with new onset ascites could be streamlined by obtaining serum BNP as an initial test and could forego the need for diagnostic paracentesis, particularly in cases where the cause of ascites is uncertain and/or could be the result of HF.

Ascites: Is the Etiology Cirrhosis or Cardiac?

Extensive population-based studies are much needed to accurately establish epidemiology and disease course in patients with primary sclerosing cholangitis (PSC). We aimed to obtain population-based prevalence and incidence figures, insight in disease course with regard to survival, liver transplantation (LT), and occurrence of malignancies, as well as risk factors thereof. Four independent hospital databases were searched in 44 hospitals in a large geographically defined area of the Netherlands, comprising 50% of the population. In addition, all PSC patients in the three Dutch liver transplant centers and all inflammatory bowel disease (IBD) patients in the adherence area of a large district hospital were identified. All medical records were reviewed on-site, verifying diagnosis. Five hundred and ninety PSC patients were identified, resulting in an incidence of 0.5 and a point prevalence of 6.0 per 100,000. Median follow up was 92 months. Estimated median survival from diagnosis until LT or PSC-related death in the entire cohort was 21.3 years, as opposed to 13.2 years in the combined transplant centers cohort (n = 422; P &lt; 0.0001). Colorectal carcinoma (CRC) risk was 10-fold increased, as compared to ulcerative colitis controls, and developed at a much younger age (39 years; range, 26-64), compared to IBD controls (59 years; range, 34-73; P = 0.019). Colonoscopic surveillance was associated with significantly better outcome. Conclusion: This study exemplifies that, for relatively rare diseases, it is paramount to collect observational data from large, population-based cohorts, because incidence and prevalence rates of PSC are markedly lower and survival much longer than previously reported. The selection of a bias-free, population-based cohort showed a significantly longer survival, compared to the tertiary referral cohort. CRC can develop at an early age, warranting surveillance from time of PSC diagnosis.

Steroid Use In Acute Liver Failure

Acute kidney injury (AKI) is common in patients with cirrhosis and associated with significant mortality. The most common etiologies of AKI in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS). Accurately distinguishing the etiology of AKI is critical, as treatments differ markedly. However, establishing an accurate differential diagnosis is extremely challenging. Urinary biomarkers of kidney injury distinguish structural from functional causes of AKI and may facilitate more accurate and rapid diagnoses. We conducted a multicenter, prospective cohort study of patients with cirrhosis and AKI assessing multiple biomarkers for differential diagnosis of clinically adjudicated AKI. Patients (n = 36) whose creatinine returned to within 25% of their baseline within 48 hours were diagnosed with PRA. In addition, 76 patients with progressive AKI were diagnosed by way of blinded retrospective adjudication. Of these progressors, 39 (53%) patients were diagnosed with ATN, 19 (26%) with PRA, and 16 (22%) with HRS.  Median values for neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), liver-type fatty acid binding protein (L-FABP), and albumin differed between etiologies and were significantly higher in patients adjudicated with ATN. The fractional excretion of sodium (FENa) was lowest in patients with HRS, 0.10%, but did not differ between those with PRA, 0.27%, or ATN, 0.31%, P = 0.54. The likelihood of being diagnosed with ATN increased step-wise with the number of biomarkers above optimal diagnostic cutoffs. Conclusion: Urinary biomarkers of kidney injury are elevated in patients with cirrhosis and AKI due to ATN. Incorporating biomarkers into clinical decision making has the potential to more accurately guide treatment by establishing which patients have structural injury underlying their AKI. Further research is required to document biomarkers specific to HRS.

Kidney Biomarkers and Differential Diagnosis of Patients with Cirrhosis and Acute Kidney Injury

Ursodeoxycholic acid (UDCA) is no longer recommended for management of adult patients with primary sclerosing cholangitis (PSC). We undertook a prospective evaluation of UDCA withdrawal in a group of consecutive patients with PSC. Twenty six patients, all treated with UDCA (dose range: 10-15 mg/kg/day) were included. Paired blood samples for liver biochemistry, bile acids, and fibroblast growth factor 19 (FGF19) were collected before UDCA withdrawal and 3 months later. Liquid chromatography/tandem mass spectrometry was used for quantification of 29 plasma bile acid metabolites. Pruritus and health-related quality of life (HRQoL) were assessed with a 10-point numeric rating scale, the Medical Outcomes Study Short Form-36 (SF-36), and PBC-40 questionnaires. UDCA withdrawal resulted in a significant deterioration in liver biochemistry (increase of alkaline phosphatase of 75.6%; P &lt; 0.0001; gamma-glutamyl transpeptidase of 117.9%, P &lt; 0.0001; bilirubin of 50.0%, P &lt; 0.001; alanine aminotransferase of 63.9%, P &lt; 0.005; and aspartate aminotransferase of 45.0%, P &lt; 0.005) and increase of Mayo Risk Score for PSC (change from baseline of +0.5 point; P &lt; 0.003). Bile acid analysis revealed a significant decrease in lithocholic acid and its derivatives after UDCA withdrawal, but no effect on concentrations of primary bile acids aside from an increased accumulation of their taurine conjugates. After UDCA removal cholestatic parameters, taurine species of cholic acid and chenodeoxycholic acid correlated with serum FGF19 levels. No significant effect on HRQoL after UDCA withdrawal was observed; however, 42% of patients reported a deterioration in their pruritus. Conclusion: At 3 months, discontinuation of UDCA in patients with PSC causes significant deterioration in liver biochemistry and influences concentrations of bile acid metabolites. A proportion of patients report increased pruritus, but other short-term markers of quality of life are unaffected.

Ursodeoxycholic Acid and PSC, Revisited

Nonalcoholic steatohepatitis (NASH) is currently the third leading indication for liver transplantation (LT) in the U.S. and is predicted to become the leading indication for LT in the near future. The trends in NASH-related hepatocellular carcinoma (HCC) among LT recipients in the U.S. remain undefined. We performed a retrospective cohort study to evaluate trends in the etiology of HCC among adult LT recipients in the U.S. from 2002 to 2012, using national data from the United Network for Organ Sharing registry. From 2002-2012, there were 61,868 adults who underwent LT in the U.S., including 10,061 patients with HCC. The total number and proportion of HCC LT recipients demonstrated a significant increase following the implementation of the Model for Endstage Liver Disease (MELD) scoring system in 2002 (3.3%, n?=?143 in 2000 versus 12.2%, n?=?714 in 2005 versus 23.3%, n?=?1336 in 2012). The proportion of hepatitis C virus (HCV)-related HCC increased steadily from 2002 to 2012, and HCV remained the leading etiology of HCC throughout the MELD era (43.4% in 2002 versus 46.3% in 2007 versus 49.9% in 2012). NASH-related HCC also increased significantly, and NASH is the second leading etiology of HCC-related LT (8.3% in 2002 versus 10.3% in 2007 versus 13.5% in 2012). From 2002 to 2012, the number of patients undergoing LT for HCC secondary to NASH increased by nearly 4-fold, and the number of LT patients with HCC secondary to HCV increased by 2-fold. Conclusion: NASH is the second leading etiology of HCC leading to LT in the U.S. More important, NASH is currently the most rapidly growing indication for LT in patients with HCC in the U.S.

NASH and HCC: A Growing Role for Liver Transplantation

Minimal Hepatic Encephalopathy: Making Diagnosis Easier by AASLD

Minimal Hepatic Encephalopathy: Making Diagnosis Easier

Sclerosingcholangitis

Integrating host and HBV characteristics, this study aimed to develop models for predicting long-term cirrhosis and hepatocellular carcinoma (HCC) risk in chronic hepatitis B virus (HBV) patients. This analysis included hepatitis B surface antigen (HBsAg)-seropositive and anti-HCV-seronegative participants from the Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer in HBV (R.E.V.E.A.L.-HBV) cohort. Newly developed cirrhosis and HCC were ascertained through regular follow-up ultrasonography, computerized linkage with national health databases, and medical chart reviews. Two-thirds of the participants were allocated for risk model derivation and another one-third for model validation. The risk prediction model included age, gender, HBV e antigen (HBeAg) serostatus, serum levels of HBV DNA, and alanine aminotransferase (ALT), quantitative serum HBsAg levels, and HBV genotypes. Additionally, the family history was included in the prediction model for HCC. Cox's proportional hazards regression coefficients for cirrhosis and HCC predictors were converted into risk scores. The areas under receiver operating curve (AUROCs) were used to evaluate the performance of risk models. Elder age, male, HBeAg, genotype C, and increasing levels of ALT, HBV DNA, and HBsAg were all significantly associated with an increased risk of cirrhosis and HCC. The risk scores estimated from the derivation set could accurately categorize participants with low, medium, and high cirrhosis and HCC risk in the validation set (P &lt; 0.001). The AUROCs for predicting 3-year, 5-year, and 10-year cirrhosis risk ranged 0.83-0.86 and 0.79-0.82 for the derivation and validation sets, respectively. The AUROC for predicting 5-year, 10-year, 15-year risk of HCC ranged 0.86-0.89 and 0.84-0.87 in the derivation and validation sets, respectively. Conclusion: The risk prediction models of cirrhosis and HCC by integrating host and HBV profiles have excellent prediction accuracy and discriminatory ability. They may be used for clinical management of chronic hepatitis B patients.

Predictive Models of Cirrhosis and HCC in CHB

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Best Episodes on Physical Health & Your Body

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