Risk Of Hepatic Decompensation Research Articles

Long-term outcome and risk stratification in compensated advanced chronic liver disease after HCV-cure.

Around 750,000 patients per year will be cured of HCV infection until 2030. Those with compensated advanced chronic liver disease remain at risk for hepatic decompensation and de novo HCC. Algorithms have been developed to stratify risk early after cure; however, data on long-term outcomes and the prognostic utility of these risk stratification algorithms at later time points are lacking. We retrospectively analyzed a cohort of 2335 patients with compensated advanced chronic liver disease (liver stiffness measurement≥10kPa) who achieved HCV-cure by interferon-free therapies from 15 European centers (median age 60.2±11.9y, 21.1% obesity, 21.2% diabetes).During a median follow-up of 6 years, first hepatic decompensation occurred in 84 patients (3.6%, incidence rate: 0.74%/y, cumulative incidence at 6y: 3.2%); 183 (7.8%) patients developed de novo HCC (incidence rate: 1.60%/y, cumulative incidence at 6y: 8.3%), with both risks being strictly linear over time.Baveno VII criteria to exclude (FU-liver stiffness measurement <12kPa and follow-up platelet count >150g/L) or rule-in (FU-liver stiffness measurement ≥25kPa) clinically significant portal hypertension (CSPH) stratified the risk of hepatic decompensation with proportional hazards. Estimated probability of CSPH discriminated patients developing versus not developing hepatic decompensation in the gray zone (ie, patients meeting none of the above criteria).Published HCC risk stratification algorithms identified high-incidence and low-incidence groups; however, the size of the latter group varied substantially (9.9%-69.1%). A granular "HCC-sustained virologic response" model was developed to inform an individual patient's HCC risk after HCV-cure. In patients with compensated advanced chronic liver disease, the risks of hepatic decompensation and HCC remain constant after HCV-cure, even in the long term (>3y). One-time post-treatment risk stratification based on noninvasive criteria provides important prognostic information that is maintained during long-term follow-up, as the hazards remain proportional over time.

Evaluation of mucosal-associated invariant T-cells as a potential biomarker to predict infection risk in liver cirrhosis.

Infection is a serious complication in patients with cirrhosis. Mucosal-associated invariant T (MAIT) cells are involved in the immune defense against infections and known to be impaired in several chronic conditions, including cirrhosis. Here, we evaluated if MAIT cell levels in peripheral blood are associated with risk of bacterial infections in patients with cirrhosis. Patients with cirrhosis seen at the Karolinska University Hospital, Stockholm, Sweden, between 2016 and 2019 were included. Levels of MAIT cells in peripheral blood were determined using flow cytometry. Baseline and follow-up data after at least two years of follow-up were collected by chart review for the primary outcome (bacterial infection) and secondary outcomes (decompensation and death). Competing risk and Cox regression were performed. We included 106 patients with cirrhosis. The median MAIT cells fraction in the circulation was 0.8% in cirrhosis compared to 6.1% in healthy controls. In contrast to our hypothesis, we found an association in the adjusted analysis between relatively preserved MAIT cell levels, and a slightly higher risk to develop bacterial infections (adjusted subdistribution hazard ratio (aSHR) 1.15 (95%CI = 1.01-1.31). However, MAIT cell levels were not associated with the risk of hepatic decompensation (aSHR 1.19 (95%CI = 0.91-1.56)) nor with death (adjusted hazard ratio 1.10 (95%CI = 0.97-1.22)). Relatively preserved MAIT cell levels in blood of patients with cirrhosis were associated with a somewhat higher risk of bacterial infections. The clinical relevance of this might not be strong. MAIT cells might however be an interesting biomarker to explore in future studies.

Diabetes impairs the haemodynamic response to non-selective betablockers in compensated cirrhosis and predisposes to hepatic decompensation.

Non-selective betablockers (NSBBs) reduce the risk of hepatic decompensation in patients with compensated advanced chronic liver disease (cACLD). Metabolic co-morbidities (MetC) are increasingly observed in cACLD patients. To investigate the impact of MetC on the haemodynamic effects of NSBB and hepatic decompensation in cACLD. cACLD patients undergoing paired hepatic venous pressure gradient (HVPG) measurements before/under NSBB therapy were retrospectively considered for this study. We recorded baseline characteristics on MetC (obesity, dyslipidaemia and diabetes), as well as hepatic decompensation and liver-related mortality during follow-up. We included 92 patients (Child-A n = 80, 87%; Child-B n = 12, 13%). MetC were found in 34 (37%) patients: 19 (20.7%) with obesity, 14 (15.2%) with dyslipidaemia and 23 (34.8%) with diabetes. The median baseline HVPG of 18 (IQR:15-21) mmHg decreased to 15 (IQR:9-12) mmHg under NSBB. HVPG-response (decrease ≥10% or to ≤12 mmHg) was achieved in 60 (65.2.%) patients. Patients with diabetes (OR: 0.35, p = 0.021) and higher BMI (OR: 0.89 per kg/m2 , p = 0.031) were less likely to achieve HVPG-response. During a median follow-up of 2.3 (0.5-4.2) years, 18 (19.5%) patients experienced hepatic decompensation. Child-B (adjusted subdistribution hazard ratio, aSHR: 4.3 [95% CI:1.5-12.2], p = 0.006), HVPG-response (aSHR: 0.3 [95% CI:0.1-0.9], p = 0.037) and diabetes (aSHR: 2.8 [95% CI:1.1-7.2], p = 0.036) were independently associated with hepatic decompensation. In patients with cACLD, diabetes and a higher BMI impair the HVPG-response to NSBB. Furthermore, diabetes-independently from Child B and lack of HVPG-response-increases the risk ofhepatic decompensation.

Stronger Neo‐Minophagen C (SNMC): A stronger adjuvant for TACE?

Stronger <scp>Neo‐Minophagen</scp> C (<scp>SNMC</scp>): A stronger adjuvant for <scp>TACE</scp>?

COVID-19: Has the Liver Been Spared?

The liver is a secondary and often collateral target of COVID-19 disease but can lead to important consequences. COVID-19 might directly cause a high number of complications in patients with pre-existing chronic liver disease, increasing their risk of hepatic decompensation. Moreover, it also determines indirect consequences in the management of patients with liver disease, especially in those suffering from decompensated cirrhosis and HCC, as well as in the execution of their follow-up and the availability of all therapeutic possibilities. Liver imaging in COVID-19 patients proved to be highly nonspecific, but it can still be useful for identifying the complications that derive from the infection. Moreover, the recent implementation of telemedicine constitutes a possible solution to both the physical distancing and the re-organizational difficulties arising from the pandemic. The present review aims to encompass the currently hypothesized pathophysiological mechanisms of liver injury in patients with COVID-19 mediated by both the direct invasion of the virus and its indirect effects and analyze the consequence of the pandemic in patients with chronic liver disease and liver tumors, with particular regard to the management strategies that have been implemented to face this worldwide emergency and that can be further improved.

Risk of hepatic decompensation but not hepatocellular carcinoma decreases over time in patients with hepatitis B surface antigen loss

We examined the long-term incidence of hepatocellular carcinoma (HCC) and hepatic decompensation among chronic hepatitis B (CHB) patients who have achieved hepatitis B surface antigen (HBsAg) seroclearance. All adult CHB-monoinfected patients who cleared HBsAg between January 2000 and December 2020 were identified using a territory-wide database in Hong Kong. Patients who underwent liver transplantation and/or developed HCC before HBsAg seroclearance or less than 6 months follow-up were excluded. The primary and secondary endpoints were HCC and hepatic decompensation respectively. We identified 9,769 patients with CHB who achieved HBsAg seroclearance (mean age 57 years, 60.0% male, 13.2% cirrhosis); most had compensated liver function at HBsAg loss. At a median (25th-75th percentile) follow-up of 4.6 (2.2-8.4) years, 106 (1.1%) patients developed HCC. Patients who developed HCC were older, more likely to be male and have cirrhosis, and had higher alanine aminotransferase and lower platelets at the time of HBsAg loss than patients without HCC. The cumulative incidence of HCC remained steady 0-7 and 8-12 years after HBsAg loss (p= 0.898) (crude annual incidence drop:-0.04%, 95% CI-0.13% to 0.04%, p= 0.265). Moreover, 124/9,640 (1.3%) patients developed hepatic decompensation. The growth in cumulative incidence of hepatic decompensation decelerated 8-12 years after HBsAg loss (p= 0.009) (crude annual incidence drop:-0.23%, 95% CI-0.40% to-0.06%, p= 0.012). In multivariable analysis, HBsAg loss for over 7 years was associated with a reduced risk of hepatic decompensation (adjusted subdistribution hazard ratio [aSHR] 0.55, 95% CI 0.31-0.97, p= 0.039) but not HCC (aSHR 1.35, 95% CI 0.83-2.19, p= 0.230). HCC risk persists in patients after HBsAg loss, whereas the risk of hepatic decompensation decreases over time. Patients with chronic hepatitis B (CHB) still have a non-negligible risk of hepatocellular carcinoma (HCC) after 12 years of HBsAg seroclearance, especially among those with cirrhosis. The risk of developing hepatic decompensation decreases over time after HBsAg seroclearance. In clinical practice, although patients with CHB who cleared HBsAg have a more favourable clinical outcome than those who remain chronically infected, long-term HCC surveillance would still be necessary for patients with cirrhosis and other high-risk subgroups after HBsAg seroclearance.

Fully automated AI-based splenic segmentation for predicting survival and estimating the risk of hepatic decompensation in TACE patients with HCC

ObjectivesSplenic volume (SV) was proposed as a relevant prognostic factor for patients with hepatocellular carcinoma (HCC). We trained a deep-learning algorithm to fully automatically assess SV based on computed tomography (CT) scans. Then, we investigated SV as a prognostic factor for patients with HCC undergoing transarterial chemoembolization (TACE).MethodsThis retrospective study included 327 treatment-naïve patients with HCC undergoing initial TACE at our tertiary care center between 2010 and 2020. A convolutional neural network was trained and validated on the first 100 consecutive cases for spleen segmentation. Then, we used the algorithm to evaluate SV in all 327 patients. Subsequently, we evaluated correlations between SV and survival as well as the risk of hepatic decompensation during TACE.ResultsThe algorithm showed Sørensen Dice Scores of 0.96 during both training and validation. In the remaining 227 patients assessed with the algorithm, spleen segmentation was visually approved in 223 patients (98.2%) and failed in four patients (1.8%), which required manual re-assessments. Mean SV was 551 ml. Survival was significantly lower in patients with high SV (10.9 months), compared to low SV (22.0 months, p = 0.001). In contrast, overall survival was not significantly predicted by axial and craniocaudal spleen diameter. Furthermore, patients with a hepatic decompensation after TACE had significantly higher SV (p < 0.001).ConclusionAutomated SV assessments showed superior survival predictions in patients with HCC undergoing TACE compared to two-dimensional spleen size estimates and identified patients at risk of hepatic decompensation. Thus, SV could serve as an automatically available, currently underappreciated imaging biomarker.Key Points• Splenic volume is a relevant prognostic factor for prediction of survival in patients with HCC undergoing TACE, and should be preferred over two-dimensional surrogates for splenic size.• Besides overall survival, progression-free survival and hepatic decompensation were significantly associated with splenic volume, making splenic volume a currently underappreciated prognostic factor prior to TACE.• Splenic volume can be fully automatically assessed using deep-learning methods; thus, it is a promising imaging biomarker easily integrable into daily radiological routine.

S1034 The Effect of Cholangiocarcinoma on the Hepatic Outcomes of Hospitalized Patients With Liver Cirrhosis: A Nationwide Analysis

INTRODUCTION: Patients with cirrhosis can develop cholangiocarcinoma (CCA) due to shared comorbidities including primary sclerosing cholangitis and metabolic risk factors. Since cirrhotic patients with CCA are at particular risk of hepatic decompensation with CCA involvement of the biliary/portal structures, it is important to evaluate the effect of CCA on the hepatic outcomes of these patients. METHODS: Patients with CCA were selected from the 2011 to 2017 National Inpatient Sample and were stratified by the presence of cirrhosis. The control patients were matched by age, gender, and race using a 1:4 propensity score matching algorithm. The two cohorts were compared using the following study endpoints: mortality, length of stay (LOS), hospitalization costs, and hepatic events. RESULTS: Of the 790014 patients with cirrhosis identified from the database 1470 (0.19%) patients were identified as having cholangiocarcinoma and 5880 were identified as matched controls. The two cohorts were both on average 63.4 years of age and both had a gender ratio of 68.8/31.2% male/female. The mortality rate was higher in the CCA cohort (9.32 vs 6.26% P < 0.01, OR 1.54 95%CI 1.25–1.89), as were the LOS (7.15 vs 6.19d P < 0.01) and hospitalization costs ($73,913 vs $63,149 P < 0.01). The CCA cohort had higher incidences of ascites (39.4 vs 27.4% P < 0.01, OR 1.72 95%CI 1.53–1.94), SBP (4.49 vs 2.76% P < 0.01, OR 1.66 95%CI 1.24–2.22), hepatorenal syndrome (5.99 vs 4.05% P < 0.01, OR 1.51 95%CI 1.17–1.94), and portal vein thrombosis (7.55 vs 2.01% P < 0.01, OR 3.99 95%CI 3.06–5.20). While the CCA cohort had a lower incidence of variceal bleeding (3.27 vs 4.73% P = 0.02, OR 0.68 95%CI 0.50–0.93), no difference between cohorts was found in the incidences of hepatic encephalopathy (17.2 vs 17.9% P = 0.58, OR 0.96 95%CI 0.82–1.11), and liver transplant rates (1.22 vs 0.80% P = 0.16, OR 1.54 95%CI 0.89-2.66). In a multivariate model, the presence of CCA was associated with higher hospital mortality (P < 0.01, aOR 1.41 95%CI 1.11–1.78) despite controlling for comorbidities and hepatic events. CONCLUSION: The presence of CCA in patients with cirrhosis is associated with increased hospital mortality and hepatic events, including ascites-related complications and PVT. These patients therefore require proactive surveillance of hepatic complications, followed by multidisciplinary management with oncology-hepatology specialty evaluation.Figure 1.: Multivariate model: the presence of cholangiocarcinoma is associated with increased mortality in hospitalized patients with cirrhosis.

Noninvasively Predicting Liver-Related Outcomes in Patients with Advanced Liver Disease Who Cleared HCV Infection

After clearance of chronic hepatitis C virus (HCV) infection, patients with advanced liver fibrosis are still at risk for hepatic decompensation. Few

Spleen Stiffness Measurements Predict the Risk of Hepatic Decompensation After Direct-Acting Antivirals in HCV Cirrhotic Patients.

Little evidence is available regarding the risk of hepatic decompensation (HD) after direct-acting antivirals (DAAs) in patients with advanced chronic liver disease. Our aim was to assess the risk of decompensation and the prognostic role of noninvasive tests, such as liver (LSM) and spleen (SSM) stiffness measurements, in the prediction of decompensation after sustained virologic response (SVR) by DAAs. A cohort study involving 146 cirrhotic patients treated with DAAs in our tertiary center with LSM and SSM available both before and six months after treatment (SVR24). A historical cohort of 92 consecutive cirrhotic patients with active HCV was used as a control group. A propensity score inverse probability weighting method was used to account for differences between the groups. Time-dependent models for the prediction of decompensation were applied to account for changes in noninvasive tests after therapy. The decompensation incidence in the DAA cohort was 7.07 (4.56-10.96) per 100 person-years (PYs), which was significantly lower than in the active HCV cohort. The DAA therapy was an independent protective factor for HD development (SHR: 0.071, 95 %-CI: 0.015-0.332). SSM ≥ 54 kPa was independently associated with decompensation despite SVR achievement (SHR: 4.169, 95 %-CI: 1.050-16.559), alongside with a history of decompensation (SHR: 7.956, 95 %-CI: 2.556-24.762). SSM reduction < 10 % also predicted the risk of decompensation after SVR24. The risk of decompensation was markedly reduced after DAA therapy, but it was not eliminated. Paired SSM values stratified the risk of decompensation after SVR better than other noninvasive tests.

Issue highlights

Issue highlights

Predictive Factors and Time to Development of Hepatic Decompensation in Patients with Non-alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of cirrhosis in the USA. We aimed to determine the time to develop hepatic events in patients with NAFLD and develop a simple model to identify patients at risk for hepatic decompensation. Retrospective cohort study. Seven hundred patients with NAFLD met inclusion criteria for the study. Patients were divided into model construction (n = 450) and validation (n = 250) cohorts. Demographic, clinical, and laboratory variables were gathered at the time of diagnosis of NAFLD. Kaplan-Meier analysis determined the time to development of hepatic events from initial diagnosis. A time-to-event prediction model was established in the model construction cohort using the multivariate Cox proportional hazards model and was then internally validated. Forty-nine (7%) patients developed hepatic events at a mean duration of 6.2 ± 4.2years from initial diagnosis. Kaplan-Meier probability of developing a hepatic event at 5-, 10-, and 12-year intervals was 4.8%, 10.6%, and 11.3%, respectively. Age, presence of diabetes, and platelet count were identified as significant variables to predict hepatic events. NAFLD decompensation risk score was developed as "age × 0.06335 + presence of diabetes (yes = 1, no = 0) × 0.92221 - platelet count × 0.01522" to predict the probability of hepatic decompensation. Risk score model had an area under the curve of 0.89 (95% CI = 0.92, 0.86) and it performed well in both the validation (0.91, 0.87-0.94) and the overall cohort (0.89, 0.87-0.91). A significant proportion of patients with NAFLD developed hepatic decompensation. We have provided a simple, objective model to help identify "at-risk" patients.

The von Willebrand Factor antigen to platelet ratio (VITRO) score predicts hepatic decompensation and mortality in cirrhosis.

The ratio of von Willebrand Factor to platelets (VITRO) reflects the severity of fibrosis and portal hypertension and might thus hold prognostic value. Patients with compensated cirrhosis were recruited. VITRO, Child-Pugh score (CPS) and MELD were determined at study entry. Hepatic decompensation was defined as variceal bleeding, ascites or hepatic encephalopathy. Liver transplantation and death were recorded. One hundred and ninety-four patients with compensated cirrhosis (CPS-A 89%, B 11%; 56% male; median age 56years; 50% with varices) were included. During a median follow-up of 45months (IQR 29-61), decompensation occurred in 35 (18%) patients and 14 (7%) patients deceased. The risk of hepatic decompensation was significantly increased in the n = 88 (45%) patients with a VITRO ≥ 2.5 (p < 0.001). Patients with a VITRO ≥ 2.5 had a higher probability of decompensation at 1-year 9% (95% CI 3-16) vs. 0% (95% CI 0-0) and at 2-years 18% (95% CI 10-27%), vs. 4% (95% CI 0-8%) as compared to patients with VITRO < 2.5. Patients with VITRO ≥ 2.5, the estimated 1-year/2-year survival rates were at 98% (95% CI 95-100%) and 94% (95% CI 88-99%) as compared to 100% (95% CI 100-100%) both in the patients with a VITRO < 2.5 (p < 0.001). After adjusting for age, albumin and MELD, VITRO ≥ 2.5 remained as significant predictor of transplant-free mortality (HR 1.38, CI 1.09-1.76; p = 0.007). Patients with compensated cirrhosis and VITRO > 2.1 after hepatitis C eradication remained at significantly increased risk for decompensation (p = 0.033). VITRO is a valuable prognostic tool for estimating the risk of decompensation and mortality in patients with compensated cirrhosis-including the setting after hepatitis C eradication.

Proton pump inhibitor use increases mortality and hepatic decompensation in liver cirrhosis.

BACKGROUNDProton pump inhibitors (PPIs) are widely prescribed, often without clear indications. There are conflicting data on its association with mortality risk and hepatic decompensation in cirrhotic patients. Furthermore, PPI users and PPI exposure in some studies have been poorly defined with many confounding factors.AIMTo examine if PPI use increases mortality and hepatic decompensation and the impact of cumulative PPI dose exposure.METHODSData from patients with decompensated liver cirrhosis were extracted from a hospital database between 2013 to 2017. PPI users were defined as cumulative defined daily dose (cDDD) ≥ 28 within a landmark period, after hospitalisation for hepatic decompensation. Cox regression analysis for comparison was done after propensity score adjustment. Further risk of hepatic decompensation was analysed by Poisson regression.RESULTSAmong 295 decompensated cirrhosis patients, 238 were PPI users and 57 were non-users. PPI users had higher mortality compared to non-users [adjusted HR = 2.10, (1.20-3.67); P = 0.009]. Longer PPI use with cDDD > 90 was associated with higher mortality, compared to non-users [aHR = 2.27, (1.10-5.14); P = 0.038]. PPI users had a higher incidence of hospitalization for hepatic decompensation [aRR = 1.61, (1.30-2.11); P < 0.001].CONCLUSIONPPI use in decompensated cirrhosis is associated with increased risk of mortality and hepatic decompensation. Longer PPI exposure with cDDD > 90 increases the risk of mortality.

SAT-225-The risk of hepatic decompensation is reduced, but not abolished after direct-acting antivirals: The role of portal hypertension

SAT-225-The risk of hepatic decompensation is reduced, but not abolished after direct-acting antivirals: The role of portal hypertension

The risk of hepatic decompensation is reduced, but not abolished after direct-acting antivirals: the role of spleen stiffness measurement

The risk of hepatic decompensation is reduced, but not abolished after direct-acting antivirals: the role of spleen stiffness measurement

The role of liver and spleen stiffness measurement in predicting hepatic decompensation after HCV eradication with direct-acting antiviral agents therapy

Introduction: To date few evidences are available on the risk of hepatic decompensation (HD) related to portal hypertension (PH) after therapy with new direct-acting antivirals (DAAs) in patients with HCV-related advanced chronic liver disease (ACLD). Furthermore, the predictive role of liver (LSM) and spleen (SSM) stiffness measurement after DAA therapy is still debated. We previously reported that SSM 54 kPa was able to predict HD in untreated HCV patients.

Vitamin D deficiency is associated with hepatic decompensation and inflammation in patients with liver cirrhosis: A prospective cohort study.

BackgroundVitamin D is required to maintain the integrity of the intestinal barrier and inhibits inflammatory signaling pathways.ObjectiveVitamin D deficiency might be involved in cirrhosis-associated systemic inflammation and risk of hepatic decompensation in patients with liver cirrhosis.MethodsOutpatients of the Hepatology Unit of the University Hospital Frankfurt with advanced liver fibrosis and cirrhosis were prospectively enrolled. 25-hydroxyvitamin D (25(OH)D3) serum concentrations were quantified and associated with markers of systemic inflammation / intestinal bacterial translocation and hepatic decompensation.ResultsA total of 338 patients with advanced liver fibrosis or cirrhosis were included. Of those, 51 patients (15%) were hospitalized due to hepatic decompensation during follow-up. Overall, 72 patients (21%) had severe vitamin D deficiency. However, patients receiving vitamin D supplements had significantly higher 25(OH)D3 serum levels compared to patients without supplements (37 ng/mL vs. 16 ng/ml, P<0.0001). Uni- and multivariate analyses revealed an independent association of severe vitamin D deficiency with the risk of hepatic decompensation during follow-up (multivariate P = 0.012; OR = 3.25, 95% CI = 1.30–8.2), together with MELD score, low hemoglobin concentration, low coffee consumption, and presence of diabetes. Of note, serum levels of C-reactive protein, IL-6 and soluble CD14 were significantly higher in patients with versus without severe vitamin D deficiency, and serum levels of soluble CD14 levels declined in patients with de novo supplementation of vitamin D (median 2.15 vs. 1.87 ng/mL, P = 0.002).ConclusionsIn this prospective cohort study, baseline vitamin D levels were inversely associated with liver-cirrhosis related systemic inflammation and the risk of hepatic decompensation.

Assessment of Advanced Liver Fibrosis and the Risk for Hepatic Decompensation in Patients With Congestive Hepatopathy.

Congestive hepatopathy (CH) arises from chronically elevated right-sided heart pressures transmitted to the liver by passive venous congestion. Over time, CH can lead to hepatic bridging fibrosis, decompensated cirrhosis, and hepatocellular carcinoma. Currently, there are no evidence-based guidelines to direct appropriate screening or management of patients with CH, partly because of the inability of current clinical tools (serum tests, imaging studies, liver stiffness measurements, and liver biopsy) to accurately estimate hepatic fibrosis or the risk for hepatic decompensation. The Model for End-Stage Liver Disease excluding international normalized ratio (MELD-XI) score is the only validated serum-based test to predict clinical outcomes in CH. Noninvasive liver stiffness measurements are proving to be of minimal utility as all patients with CH have elevated values that currently cannot differentiate between congestion and fibrosis. In addition, fibrosis staging by liver biopsy is difficult to standardize because of heterogeneous collagen deposition in CH. Moreover, liver biopsy results have little predictive value for post-heart transplant hepatic outcomes in patients with CH. Evaluating liver nodules and masses is also complicated in CH as the finding of delayed venous washout in nodules is not specific for hepatocellular carcinoma in the background of a congested liver, and these lesions may require biopsy to confirm the diagnosis. The lack of effective clinical tools for predicting liver fibrosis and liver function suggests the need for the development of novel biomarkers in patients with CH to assist in the management of this complicated disease. (Hepatology 2018; 00:000-000).

Non-Invasive Markers (ALBI and APRI) Predict Pregnancy Outcomes in Women With Chronic Liver Disease.

Rates of pregnancy in women with cirrhosis are increasing. Risk of hepatic decompensation during pregnancy, therefore, merits tailored obstetric and hepatology care. Prognostic markers that determine pregnancy outcomes are lacking. Medical records of women who attended hepatology clinic at King's College Hospital with chronic liver disease (CLD) who became pregnant from 1983 to 2017 were reviewed. Information on demographics, clinical history, serology, and outcome of pregnancy was collected. In all, 165 pregnancies occurred in 100 women with CLD including 80 pregnancies in 48 women with cirrhosis. Median age of conception in cirrhotic and non-cirrhotic women were 26 years (16-44) and 28 years (16-51) respectively (p = 0.015). Whilst women with cirrhosis had similar live birth rate to non-cirrhotic women (75 vs. 85% p = 0.119), they were significantly less likely to proceed beyond 37 weeks gestation (45 vs. 58% p = 0.033). Women who received preconception counseling were more likely to have stable liver disease at conception (100 vs 86% p = 0.02). Compared with preconception MELD (model for end stage liver disease), preconception Albumin-Bilirubin score (ALBI) more accurately predicted live birth with an area under the receiver-operator curve (AUROC) of 0.741 (p < 0.001), and preconception AST to platelet ratio index (APRI) more accurately predicted ability to proceed beyond 37 weeks gestation with an AUROC of 0.700 (p < 0.001). Most women with cirrhosis who conceived achieved a successful pregnancy outcome. ALBI and APRI scores can prognosticate pregnancy outcomes in women with CLD. Preconception counseling by a hepatologist or specialist obstetrician improved patient care in this group.