Non Alcoholic Steatohepatitis

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Information about Non Alcoholic Steatohepatitis

Published on April 8, 2008

Author: hanash

Source: slideshare.net

Description

Non Alcoholic Steatohepatitis

Non Alcoholic Steatohepatitis

What is it? Epidemiology Pathogenesis Clinical Features and Diagnosis Clinical Course Treatment

What is it?

Epidemiology

Pathogenesis

Clinical Features and Diagnosis

Clinical Course

Treatment

Non alcoholic fatty liver disease Clinico-histopathological entity Histological features resemble alcohol induced liver disease Associated with negligible or no alcohol intake Spectrum of disease Steatosis Steatohepatitis cirrhosis Leading cause of cryptogenic cirrhosis Increasingly recognised

Clinico-histopathological entity

Histological features resemble alcohol induced liver disease

Associated with negligible or no alcohol intake

Spectrum of disease

Steatosis

Steatohepatitis

cirrhosis

Leading cause of cryptogenic cirrhosis

Increasingly recognised

Epidemiology Occurs worldwide Greater in western populations USA 3% of lean individuals 19% of obese 50% of morbidly obese/diabetics ♀ > ♂ Associated with type 2 diabetes, obesity, hypertension and hyperlipidaemia

Occurs worldwide

Greater in western populations

USA

3% of lean individuals

19% of obese

50% of morbidly obese/diabetics

♀ > ♂

Associated with type 2 diabetes, obesity, hypertension and hyperlipidaemia

Pathogenesis Not fully known Insulin resistance Additional oxidative injury

Not fully known

Insulin resistance

Additional oxidative injury

Excessive Triglyceride accumulation Excessive import of free fatty acids Increased delivery (obesity, rapid weight loss) Excess conversion of carbohydrates and proteins to triglycerides (overfeeding, TPN) Reduced export of FFA Impaired VLDL synthesis or secretion Impaired beta-oxidation of FFA to ATP

Excessive import of free fatty acids

Increased delivery (obesity, rapid weight loss)

Excess conversion of carbohydrates and proteins to triglycerides (overfeeding, TPN)

Reduced export of FFA

Impaired VLDL synthesis or secretion

Impaired beta-oxidation of FFA to ATP

Fatty Acids in the Hepatocyte

Insulin Resistance Key role Insulin resistance leads to changes in lipid metabolism Increased peripheral lipolysis, triglyceride synthesis and hepatic uptake of FFA Shift from carbohydrate to FFA beta oxidation Free fatty acids Inducers of cytochrome p-450 Leads to hepatotoxic free oxygen radical species

Key role

Insulin resistance leads to changes in lipid metabolism

Increased peripheral lipolysis, triglyceride synthesis and hepatic uptake of FFA

Shift from carbohydrate to FFA beta oxidation

Free fatty acids

Inducers of cytochrome p-450

Leads to hepatotoxic free oxygen radical species

Insulin Resistance

 

 

Additional defects Antioxidants Free radicals deplete antioxidants Glutathione, vit E, beta-carotene, vit C Iron Insulin resistance associated with increased hepatic iron levels Heterozygous for the haemochromatosis gene mutation Leptin Deficiency leads to massive obesity Leptin may contribute to development of fibrosis Intestinal Microbes Endogenous ethanol and acetaldehyde production which leads to hepatic injury Endotoxin production

Antioxidants

Free radicals deplete antioxidants

Glutathione, vit E, beta-carotene, vit C

Iron

Insulin resistance associated with increased hepatic iron levels

Heterozygous for the haemochromatosis gene mutation

Leptin

Deficiency leads to massive obesity

Leptin may contribute to development of fibrosis

Intestinal Microbes

Endogenous ethanol and acetaldehyde production which leads to hepatic injury

Endotoxin production

Clinical Features and Diagnosis Usually asymptomatic Fatigue, malaise, abdominal pain Often incidental diagnosis AST and ALT elevated in 90% AST/ALT < 1 Liver biopsy

Usually asymptomatic

Fatigue, malaise, abdominal pain

Often incidental diagnosis

AST and ALT elevated in 90%

AST/ALT < 1

Liver biopsy

Clinical Course NAFLD have only slightly lower overall survival than the general population Better prognosis than alcoholic hepatitis Alcoholic hepatitis 38 to 50% progress to cirrhosis NASH 8 to 26 % progress to cirrhosis Little change in LFTs throughout course of disease Can recur following transplant

NAFLD have only slightly lower overall survival than the general population

Better prognosis than alcoholic hepatitis

Alcoholic hepatitis

38 to 50% progress to cirrhosis

NASH

8 to 26 % progress to cirrhosis

Little change in LFTs throughout course of disease

Can recur following transplant

Treatment No proven effective treatment Gradual weight loss 10% over 6-12 months Associated diabetes, hypertension and hyperlipidaemia should be treated Vitamin E Metformin Pioglitazone

No proven effective treatment

Gradual weight loss

10% over 6-12 months

Associated diabetes, hypertension and hyperlipidaemia should be treated

Vitamin E

Metformin

Pioglitazone

Summary asymptomatic in most cases obesity, diabetes mellitus, hypertension and hyperlipidaemia are frequent associated features increase plasma ALT the commonest liver function test abnormality NASH accounts for most cases of isolated increased plasma transaminase activity of otherwise unknown cause liver biopsy rarely needed long-term prognosis is favourable graduated weight loss is the best available treatment

asymptomatic in most cases

obesity, diabetes mellitus, hypertension and hyperlipidaemia are frequent associated features

increase plasma ALT the commonest liver function test abnormality

NASH accounts for most cases of isolated increased plasma transaminase activity of otherwise unknown cause

liver biopsy rarely needed

long-term prognosis is favourable

graduated weight loss is the best available treatment

 

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