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home - Liver - Alcohol - Alcoholic Hepatitis Written by Dr Sebastian Zeki

Recognises the rising incidence of acute and chronic liver disease in
the UK related alcohol abuse and in particular the increasing alcohol
consumption in adole nts young adults women and growth in

Recognises alcoholic hepatitis and understands the prognostic
scores determined by Maddrey’s discriminant function the Glasgow
alcoholic hepatitis score and their role in identifying which patients
may benefit from corticosteroids Can treat alcohol withdrawal

Aware of appropriate use of benzodiazepines in alcohol withdrawal
and can recognise the early signs of delirium tremens

Is able to take a relevant history and perform appropriate examination
Recognises those patients who would benefit from corticosteroids
instituting treatment and has awareness of indications for withdrawing
their use
Aware of the potential complications of alcoholic hepatitis chronic
liver disease and able to prevent or intervene where appropriate

Appreciates the role of other specialists nurse specialists
intensivists radiologists dieticians psychiatrists and addiction

Communicates effectively with patients their relatives in the context
of their disease its severity prognosis and substance abuse

Identifies the abstinent alcoholic who would benefit from

Considers all therapeutic modalities and preparedness to refer to
specialist centre where diagnosis remains in doubt or appropriate
management cannot be performed as per national guidelines

Alcoholic Hepatitis

Death Fatty liver TPN DM Steroids B R U I T -Liver cell necrosis Distinguishing features in alc hep: Written by Dr Sebastian Zeki Nonalcoholic steatohepatitis Hepatic Imaging Prognosis Abstinent decomp cirrhosis has 5y transplant-free survival of approxi-mately 60 vs 30 % for those who do not. -Other possible tests for alcohol intakeCarbohydrate deficient transferrin (CDT) can be used for the diagnosis of alcoholic liver disease- Se 65% %, and sp 85%.False +ve CDT tests occur (sepsis, anorexia nervosa, and airway diseases).-Ethyl glucuronide (EtG), a direct ethanol metabolite formed by conjugation of EtOH to glucuronic acid, can be detected in various body fluids, tissue, and hair up to 80hrs after the complete elimination of alcohol from the body. An ELISA EtG test gives a serum Se of 92% and Sp of 91% for EtOH intake. Liver transplantation — Post-op quality of life and survival are excellent. Alcoholic Hepatitis CirrhosisAbstinence alters prognosis from 30% to 70% survival at five years.Micronodular cirrhosis worse than macronodular cirrhosis. Other nonessential histologic features include: Bridging necrosis, fatty changes, bile duct proliferation, cholestasis, and perivenular fibrosis. Chronic hepatitisAbstinence does not stop progression. Treatments:Librium- for withdrawal.Vitamin K — For coagulopathy, although usually intrinsic liver damage so not useful.Prophylaxis of gastric mucosal bleeding - should be considered-use a H2-blocker/sucralfate.Corticosteroids — If improvement, happens in the first 7 days.Nutritional- Feed NG. Dont restrict proteins. If get protein related encephalopathy use of branched-chain amino acids.Pentoxifylline- Alc hep is TNFalpha driven, pentoxifylline is aTNF synthesis inhibitor ). Mortality reduction of 20% by reducing hepatorenal syndrome. Not useful in steroid non-responders.Etanercept — Soluble TNF receptor:FC fusion protein- Showed 92% 30 day survival but associated with many side effects.Infliximab — Not useful as high rate of sepsis especially if also on steroids.Hepatic regeneration therapy — Hepatocyte regeneration growth factors (eg insulin and glucagon) are not useful.Propylthiouracil -Used to reduced pericentral hypoxia- not useful.Colchicine — Inhibits hepatic fibrogenesis.Polyunsaturated lecithins — May alter collagenase activity/ reduce stellate cell activation.S-adenosylmethionine — A glutathione precursor. Not useful.Metadoxine — A combination of 2 antioxidants, pyridoxine and pyrrolidone (metadoxine) ;has been approved for the treatment of alcoholic liver disease in some countries.Complementary medicinesSilymarin (from milk thistle)- antioxidant but not useful Alcoholic Hepatitis Progresses to panlobular fibrosis in those who continue to drink.- fibrosis is potentially reversibleBridging fibrosis between central vein and portal tract Alcoholic fibrosis (extracellular matrix) starts in pericentral zoneEarly pericentral fibrosis, also called hyaline necrosis, predicts a high likelihood of eventual Regenerative nodules (true cirrhosis)- irreversible damage 40% Fever, Hepatomegaly (fatty liver and swollen hepatocytes)Jaundice,Anorexia.Hepatic encephalopathy and bleeding.Sometimes asymptomatic30% have ascitesLiver bruit heard if severe in >50 % of patients. -Perivenular distribution of inflammation -Infiltration by neutr-phils (hallmark of alc hep) -Mallory bodies (eosinophilic accumulations of intracellular cytokeratins) Pathology —-Centrilobular accumulation of membrane-bound (macrovesicular ) steatosis-The fat is composed of non-toxic triglycerides as oppose-Proliferation of smooth endoplasmic reticulum-Gradual distortion of mitochondria.-Minimal inflammation Liver lobule Macrovesicular fat Alcohol Malnutrition Obesity Diabetes mellitus (DM) Corticosteroids (Steroids)Total parenteral nutrition (TPN) Alcoholic/ Fatty LiverClinical manifestations —The only complaint may be mild, tender hepatomegaly.Diagnosis —Liver tests are generally normal or modestly elevated, and jaundice is unusual General Laboratory Findings:The AST (SGOT):ALT (SGPT) >2.0 - values for both usually <400 IU/L- ALT is lower as alcoholics have less hepaticpyridoxal-6-phosphate (cofactor for ALT enzyme).Patients may have a macrocytosis/thrombocytopenia/leukocytosis (WCC correlates with hepatic damage).A raised ALP/GGT and bilirubin may be present-this can persist for weeks after the ALT has returned to normal. Liver transplantation 20% of liver transplants are for alcoholic cirrhosis.There is a 5y survival of 75% vs 25% without transplant.Patients require 6 m abstinence pretransplantation.50 % drink EtOH pos-op/ 5% excessive.Psychiatric addiction programmes can reduce recidivism.There is an increased rate of lung, liver, and oropharyngeal cancer in Differentating Alc Hep for other conditionsUSS/CT and MRI all can show fatty liver or cirrhosis.MRI findings for alcoholic cirrhosis vs viral cirrhosis= higher volume index of the caudate lobe, smaller size of regenerative nodules of the liver, and more frequent visualization of the right posterior hepatic notch.Macrovesicular steatosis and inflammation, with Mallory bodies occur in NASH and alc hepCanalicular cholestasis, marked ductular reaction, acute inflammation in the portal regions, and periportal fibrosis occur in alcoholic hepatitis.Steatosis is not always seen in alcoholic liver disease while NASH is generally associated with a greater degree of steatohepatitis and nuclear vacuolization.Cholestasis is often reported in alcoholic liver disease but not in NASH.A formula has been proposed to distinguish NASH from alcoholic liver disease that incorpo-rates the MCV, BMI, and AST/ALT ratio. Predictors of Poor Prognosis:Continued alcohol ingestion.Histologic findings such as inflamm-tion esp neutrophils.Perivenular fibrosis and a mixed pattern of macrovesicular and microvesicular fat.Laboratory findings eg. 15% of those with persistent leukocytosis progress to subfulminant hepatic failure even if alcohol is discontinued (reflect hepatic inflammation in absence of other causes).Maddrey's discriminant function = (4.6 x [prothrombin time - control PT]) + (serum bilirubin).MELD.Glasgow alcoholic hepatitis score.Lille model (for stopping steroids). Causes of a fatty liverMicrovesicular fat Alcoholic foamy degeneration Acute fatty liver of pregnancyReye's syndrome Valproic acid Tetracycline Jamaican vomiting sickness Also seen in NASH Indian childhood cirrhosisStarvationJejunoileal bypass surgery for morbid obesityAmiodarone 4% 25% 95% of heavy drinkersFatty liver can occur within hours after a large alcohol binge.It represents a direct effect of ethanol and can occur despite an adequate nutritional state.

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