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ALCOHOLIC FATTY LIVER DISEASE Diana Alcantara-Payawal, MD
Histologic Spectrum Fatty  Liver FAT Fat  + Inflam +/- Fibrosis Scar + Nodules +/-  Fat Alcoholic Hepatitis ? 40% Cirrhosis 10- 35 % 8-20% NORMAL 90-100 %
Risk factors for alcoholic liver disease: ,[object Object],[object Object],[object Object],[object Object],[object Object]
Major forms of alcoholic liver disease: ,[object Object],[object Object],[object Object],Time to develop liver disease = to amount of alcohol  consumed One beer, 4 ounces of wine, one ounce of 80% spirits = 12 grams of alcohol Men:60-80 gm/day for 10 years Women 20-40 gm/day for 10 years
Women’s Risk of ALD ,[object Object],[object Object],[object Object]
Susceptibility of females to hepatotoxicity of ethanol ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Enzymatic pathways of ethanol metabolism Ethanol Acetaldehyde Acetate NAD+ NADH NAD+ NADH Acetaminophen CCl4 Toxic metabolites, reactive oxygen species CYP2E1 ADH ALDH
New mechanism for control of lipid metabolism FFA Induction of FFA oxidation, transport and export genes PPAR/RXR Sterol SREBP Induction of sterol/fat synthesizing genes + + + - Ethanol - +
FFA HOOC(CH 2 ) N CH 3 L-FABP FFA Triglycerides PL,CE Peroxismal B Oxidation AOX Microsomal B Oxidation CYP4A1 Mitochondrial B Oxidation CPT-1 HOOC(CH 2 ) N CH 3 Hepatic Fatty Acid  Metabolism
HC ROS TNFa TGFb IL-6 IL-1 TXA2 HSC Inflammation; Hypoxia KC Ethanol and acetaldehyde EC Injury Death (necrosis, apoptosis) Fibrogenesis Adhesion Molecule cytokines ROS TNFa Activating factors
Activated HSC Irreversible activation maybe mediated by HSC products, retinoid depletion, and changes in the matrix ECM protein collagen I, fibronectin Activation of HSC TGF B
Interactions of ethanol and endotoxin Endotoxin Scavenger receptor Ethanol Activation of Kupffer cell LBP Endotoxin CD14 Ethanol induces LBP and CD14 Kupffer cell FIRST HIT Second Hit
Activation of Hepatic Stellate Cells The very earliest event in HSC activation is unknown Receptors present TNFa, IL-1 Matrix changes ? Activation of NF kB Via degradation of IkB Induction of PDGF-R, TGFB-Rs, ICAM-1
Consequences of Kupffer cell activation  by ethanol Cytokines TNFa IL-1, IL-6 PDGF Eicosanoids ROS MIP2, IL-8 Activated Kupffer Cell
CHRONIC ETHANOL INGESTION Acetaldehyde Lipid peroxidation Aldehydes Protein adducts MAA adducts Autoantibodies Autoimmune response Collagen Fibrotic response Intestine + Endotoxin Kuppfer cells Hepatocyte PPARg/RXR Stellate cell TNF-a TGF-B IL-1  IL-6 Inflammatory Response
Laboratory findings ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Maddrey’s discriminatory function 4.6(protime- control in seconds) + bilirubin (umol/L)/17 >32 assess severity of AH Alcoholic hepatitis has poor prognosis Presence of ascites, variceal hemmorrhage,  deep encephalopathy or hepatorenal syndrome has dismal prognosis
Lifestyle modification EtOH intake Obesity Smoking

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Alcoholic liver 2005 ust

  • 1. ALCOHOLIC FATTY LIVER DISEASE Diana Alcantara-Payawal, MD
  • 2. Histologic Spectrum Fatty Liver FAT Fat + Inflam +/- Fibrosis Scar + Nodules +/- Fat Alcoholic Hepatitis ? 40% Cirrhosis 10- 35 % 8-20% NORMAL 90-100 %
  • 3.
  • 4.
  • 5.
  • 6.
  • 7. Enzymatic pathways of ethanol metabolism Ethanol Acetaldehyde Acetate NAD+ NADH NAD+ NADH Acetaminophen CCl4 Toxic metabolites, reactive oxygen species CYP2E1 ADH ALDH
  • 8. New mechanism for control of lipid metabolism FFA Induction of FFA oxidation, transport and export genes PPAR/RXR Sterol SREBP Induction of sterol/fat synthesizing genes + + + - Ethanol - +
  • 9. FFA HOOC(CH 2 ) N CH 3 L-FABP FFA Triglycerides PL,CE Peroxismal B Oxidation AOX Microsomal B Oxidation CYP4A1 Mitochondrial B Oxidation CPT-1 HOOC(CH 2 ) N CH 3 Hepatic Fatty Acid Metabolism
  • 10. HC ROS TNFa TGFb IL-6 IL-1 TXA2 HSC Inflammation; Hypoxia KC Ethanol and acetaldehyde EC Injury Death (necrosis, apoptosis) Fibrogenesis Adhesion Molecule cytokines ROS TNFa Activating factors
  • 11. Activated HSC Irreversible activation maybe mediated by HSC products, retinoid depletion, and changes in the matrix ECM protein collagen I, fibronectin Activation of HSC TGF B
  • 12. Interactions of ethanol and endotoxin Endotoxin Scavenger receptor Ethanol Activation of Kupffer cell LBP Endotoxin CD14 Ethanol induces LBP and CD14 Kupffer cell FIRST HIT Second Hit
  • 13. Activation of Hepatic Stellate Cells The very earliest event in HSC activation is unknown Receptors present TNFa, IL-1 Matrix changes ? Activation of NF kB Via degradation of IkB Induction of PDGF-R, TGFB-Rs, ICAM-1
  • 14. Consequences of Kupffer cell activation by ethanol Cytokines TNFa IL-1, IL-6 PDGF Eicosanoids ROS MIP2, IL-8 Activated Kupffer Cell
  • 15. CHRONIC ETHANOL INGESTION Acetaldehyde Lipid peroxidation Aldehydes Protein adducts MAA adducts Autoantibodies Autoimmune response Collagen Fibrotic response Intestine + Endotoxin Kuppfer cells Hepatocyte PPARg/RXR Stellate cell TNF-a TGF-B IL-1 IL-6 Inflammatory Response
  • 16.
  • 17. Maddrey’s discriminatory function 4.6(protime- control in seconds) + bilirubin (umol/L)/17 >32 assess severity of AH Alcoholic hepatitis has poor prognosis Presence of ascites, variceal hemmorrhage, deep encephalopathy or hepatorenal syndrome has dismal prognosis
  • 18. Lifestyle modification EtOH intake Obesity Smoking