PLAN OF TALK 18/09/2012. Core Curriculum In Hepatology And Liver Transplantation September 11 th, 2012
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1 Core Curriculum In Hepatology And Liver Transplantation September 11 th, 2012 ALCOHOL-RELATED LIVER DISEASES Pathogenesis And Treatment Stephen Stewart Mater Misericordiae University Hospital Normal (0-30%) STAGES OF ALCOHOLIC LIVER DISEASE Cirrhosis Mortality Steatosis (60-100%) Steatohepatitis (20-40%) Rising mortality reflects rising alcohol consumption Leon. Lancet, January 2006 Fibrosis/ cirrhosis (<10%) PLAN OF TALK Pathogenesis modes of liver injury Alcoholic hepatitis key points ALD cirrhosis key points Case Nutrition in Liver Disease 1
2 O2 + NADPH MEOS (CYP2E1) H2O + NADP NAD NADH ETHANOL Alcohol Dehydrogenase H2O2 Peroxisomal catalase H2O WHY IS ALCOHOL HEPATOTOXIC? Alcohol induces hepatic steatosis NAD NADH ACETALDEHYDE Aldehyde Dehydrogenase Alcohol increases gut permeability Alcohol metabolism produces oxidative stress ACETATE Alcohol metabolism produces acetaldehyde H20 + CO2 Substrate supply MECHANISMS OF HEPATOCYTE INJURY IN ASH -oxidation (PPAR-α inhibition) Fatty acid synthesis (SREBP-1c induction) FREE FATTY ACIDS Dietary fat intake Lipolysis of adipose fat NADH/NAD GLYCEROL-3-PHOSPHATE gut permeability CYP2E1/Fe alcohol metabolism ADH Esterification endotoxin oxidative stress acetaldehyde TRIGLYCERIDE Phosphatidate Phosphohydrolase host protein Export from the liver KC lipid peroxidation adducts Increased by alcohol Inhibited by alcohol VLDL cytokines necroinflammation apoptosis & fibrosis protein function ER stress immune mechanisms Acetaldehyde and ER stress ALD SUSCEPTIBILITY Acetaldehyde (+ homocysteine)?unfolded proteins ER stress Dose, timing and type of alcohol Reduces protein synthesis Increases fat and cholesterol synthesis Increases transcription of pro-apoptotic genes Diet Gender Decreases GSH transport through Mt membrane Non-gender linked genetic susceptibility Sensitizes to TNF-induced killing From Lluis JM Gastroenterology
3 Blood alcohol (mg/100mls) 18/09/ On an empty stomach Following a meal ANIMAL MODELS OF ALD (Km) of liver alcohol dehydrogenase activity Only primates closely resemble human disease! Time min Mice intragastric feeding model Rats intragastric feeding model Guinea pig Micropig Primates - develop cirrhosis 3
4 ALCOHOLIC HEPATITIS CLINICAL FEATURES ACUTE ALCOHOLIC HEPATITIS Range from none to liver failure Some correlation with histology Mild/Mod histology: non-specific Anorexia/fatigue, RUQ pain, hepatomegaly. Severe histology: liver specific Ascites (30-60%), splenomegaly (15%), jaundice (50%), pyrexia (50%), tender hepatomegaly. ALCOHOLIC HEPATITIS - DIAGNOSIS HISTOLOGY Is it alcoholic hepatitis? Recent onset of jaundice in a heavy drinker on the background of recent alcohol consumption Liver cell damage (ballooning degeneration) Inflammatory cell infiltrate (neutrophils) Fibrosis (pericellular Chicken-wire ) Perivenular distribution ALCOHOLIC HEPATITIS PROGNOSTICATION PROGNOSTICATION Prognosticate prior to specific treatment DF 1989 GAHS 2005 DF = 4.6 (PT - Control PT) + Bi/17 DF > 32 = 35% 28 day mortality DF > 32 get benefit from steroid treatment 4
5 GLASGOW ALCOHOLIC HEPATITIS SCORE (GAHS) THERAPEUTIC OPTIONS FOR ACUTE ALCOHOLIC HEPATITIS Score Value Age < WCC (10 9 /l) < Urea (mmol/l) <5 5 - Bilirubin ( mol/l) < >250 PT (ratio) < >2.0 Score 28d mortality 84d mortality < 9 13% 21% 9 54% 60% Score 5-12 Derived from 241 patients with ASH Verified in 195 patients GAHS correctly predicted 28 day outcome in 81% Forrest Gut Steroids 2. Pentoxifylline 3. Antioxidants 4. Enteral nutrition STOPAH N = 101 STEROIDS OR PENTOXIFYLLINE FOR ALCOHOLIC HEPATITIS 5
6 4 MORE POINTS 1. Is a biopsy necessary prior? 2. Can we finer tune who gets steroids? 3. What about those that present with sepsis? 4. Can we prognosticate on steroids? Carithers 1989 Ann Int Med Methylprednisolone therapy in patients with severe alcoholic hepatitis. A randomized multicenter trial. Carithers RL Jr, Herlong HF, Diehl AM, Shaw EW, Combes B, Fallon HJ, Maddrey WC. Medical College of Virginia, Richmond. 66 patients with clinical AH (no biopsy) HE or DF > 32 32mg prednisolone/day for 28 days tapered for 2 weeks Compared with placebo 1 month survival 94% v 65% N Engl J Med Feb 20;326(8): A randomized trial of prednisolone in patients with severe alcoholic hepatitis. Ramond MJ, Poynard T, Rueff B, Mathurin P, Théodore C, Chaput JC, Benhamou JP. Service d'hépatologie, Hôpital Beaujon, Clichy, France. 61 patients with biopsy proven AH HE or DF > 32 40mg prednisolone/day for 28 days Compared with placebo 4 MORE POINTS 1. Is a biopsy necessary prior? 2. Can we fine tune who gets steroids? 3. What about those that present with sepsis? 4. Can we prognosticate on steroids? 2 month survival 88% v 44% 6
7 GAHS, STEROIDS AND 28 DAY SURVIVAL 4 MORE POINTS GAHS <9 9 Corticosteroid Treated: 80% * 77.4% No Corticosteroids: 87.5% * 40.7% *p< patients with ASH (Glasgow, King s, Newcastle) All DF > 32 GAHS 9 (64%) poor prognosis when steroids not given for whatever reason Patients with GAHS < 9 have an excellent prognosis without treatment Forrest Gut Is a biopsy necessary prior? 2. Can we finer tune who gets steroids? 3. What about those that present with sepsis? 4. Can we prognosticate on steroids? 4 MORE POINTS 1. Is a biopsy necessary prior? 2. Can we finer tune who gets steroids? 3. What about those that present with sepsis? 4. Can we prognosticate on steroids? CAN WE PREDICT OUTCOME ON STEROIDS? (ECBL) WHAT DO WE DO WHEN STEROIDS FAIL? 238 patients, all DF>32 All treated with steroids ECBL = any fall in bilirubin at 7 days (73%) Highly predictive of 6 month outcome? Stop steroids at 7 days Mathurin Hepatology 2003 Pentoxifylline? 29 switched at day 7. No better survival than matched retrospective cohort Mathurin J Hep 2008 MARS? RCT 19 v 19; no benefit Transplantation? Mathurin AASLD 2007 Mathurin NEJM
8 COHORT First episode of acute alcoholic hepatitis Steroid non responders Super-selected patients (<2% of AH admissions) Listed for transplantation First episode of acute alcoholic hepatitis Steroid non responders Super-selected patients (<2% of AH admissions) Listed for transplantation Early transplantation can significantly improve survival in patients not responding to medical therapy Ongoing debate on whether this is an appropriate use of organs STRATEGY/RESEARCH DRINKER WITH ALD Ask do you want to stop drinking? No Discharge Bili at 7d, No C/I Continue 4w Yes GAHS 9 No C/I Pred 40mg/d No Bili at 7d?Stop Offer help to stop drinking Unsuccessful Discharge GAHS 9 C/I?Treat New C/I Stage Successful Decompensated cirrhosis Compensated cirrhosis Non-cirrhotic GAHS <9 Trials of new therapies Trials of new therapies Assess for OLTx Surveillance Discharge Supportive care Ask do you want to stop drinking? DRINKER WITH ALD No Discharge WHAT FACTORS PREDICT MORTALITY? Yes Offer help to stop drinking Unsuccessful Discharge Ongoing alcohol consumption Successful Liver biopsy Smoking Decompensated cirrhosis Stage Compensated cirrhosis Non-cirrhotic Age Albumin Assess for OLTx Surveillance Discharge 8
9 TRANSPLANTATION IN ALD ALD transplant recipients do at least as well as other aetiologies 6 month rule does not help to predict long term abstinence Return to drinking rarely impacts on mortality Mortality is mainly cardiovascular and malignant CASE 1 Day 1 Day 1 32 male heavy drinker Admission with jaundice, spider naevi, tremor Bi 300 PT 22 DF 64 Treatment? Ur 3 WCC 15 Pl 63 GAHS 9 No bleeding, encephalopathy or sepsis USS enlarged fatty liver Treatment? Day 1 Day 1 Ur 3 WCC 4 Pl 63 GAHS 8 32 male Heavy drinker Admission with jaundice, spider naevi, tremor Bi 170 PT 17 DF 33 No bleeding, encephalopathy or sepsis Treatment? 9
10 Day 1 Day 1 Ur 3 WCC 4 Pl 63 GAHS 8 32 male heavy drinker Admission with jaundice, spider naevi Bi 300 PT 22 DF 64 No bleeding, encephalopathy or sepsis Treatment? Day 1 Day 2 Ur 3 WCC 15 Pl 63 50ml bright red fresh blood PR GAHS 9 No bleeding, encephalopathy or sepsis USS enlarged fatty liver Day 2 500ml haematemesis Management? 10
11 Day 7 Bi 400 PT 25 Cr 300 Oliguria Treatment? Increasing confusion/agitation Day 10 Moderate noradrenaline requirements Terlipressin Bi 500 PT 28 Cr 500 Oliguria Treatment? ITU Survival/Non Survival Survivors Non Survivors p value Child-Pugh score 11 (10-12) 13 (11-13) < MELD 17 (10-28) 31 (23-37) < APACHE II 17 (14-23) 27 (21-31) < SOFA 9 (7-11) 13 (10-16) < Requirement for RRT 27% 73% < Requirement for Vasopressors 20% 80% < Requirement for Ventilation 44 % 56% < WHEN TO SWITCH TO PALLIATION? NUTRITION IN LIVER DISEASE Beware the very high DF, GAHS, MELD score ICU scores are even better predictors of mortality Limited options in those that are not candidates for steroids Poor survival in steroid non-responders and limited alternative treatments HRS not responding to albumin and terlipressin Requirement for renal replacement and vasopressors also poor prognostic indicators in the ITU liver patient Reduced nutrient intake Increased energy requirements Altered substrate utilization Protein calorie malnutrition Micronutrient malnutrition Difficult to assess Beware the patient with terminal addiction 11
12 NUTRITION IN LIVER DISEASE General Management NUTRITION IN LIVER DISEASE Specific Cases Frequent feeding switches off early fat/protein utilization Assessment and replacement of micronutrient deficiencies Enteral feeding in alcoholic hepatitis TIPS for refractory ascites Avoid protein restriction 12
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