1. ALCOHOLIC LIVER DISEASE

2. Alcohol is one of the most common causes of chronic liver disease worldwide,In the UK, a unit of alcohol contains 8 g of ethanol. A threshold of 14 units/week in women and 21 units/week in men is generally considered safe. The risk threshold for developing ALD is variable but begins at 30 g/day of ethanol. risk factors for ALD are: Drinking pattern. Liver damage is more likely to occur in continuous rather than intermittent, as this pattern gives the liver a chance to recover. so It is recommended that people should have at least two alcohol-free days each week. Alcohol type Beer, Wine, Vodka/rum/gin, Whisky/brandy unit = 8 g. Gender. The incidence of alcoholic liver disease is increasing in women. Genetics.. Nutrition. Obesity and nutritional deficiencies increases the incidence of liver-related mortality

3. Clinical features Alcohol is metabolised almost exclusively by the Liver, ALD has a wide clinical spectrum ranging from mild abnormalities of LFTs on biochemical testing to advanced cirrhosis. The liver is often enlarged in ALD,stigmata of chronic liver disease, such as palmar erythema, are more common in alcoholic cirrhosis than in cirrhosis of other aetiologies. Alcohol misuse may also cause damage of other organs. Three types of ALD are recognised but these overlap considerably, as do the pathological changes seen in the liver.

4. 1- Alcoholic fatty liver disease Alcoholic fatty liver disease (AFLD) usually presents with elevated transaminases in the absence of Hepatomegaly.It has a good prognosis and steatosis usually disappears after 3 months of abstinence. 2- Alcoholic hepatitis This presents with jaundice and hepatomegaly; complications of portal hypertension may also be present. It has a significantly worse Prognosis than AFLD. Cirrhosis often coexists; if not present, it is the Likely outcome if drinking continues. 3- Alcoholic cirrhosis Alcoholic cirrhosis often presents with a serious complication, such as variceal haemorrhage or ascites,

5. Investigations Investigations aim to establish 1-alcohol misuse, 2- to exclude alternative or additional coexistent causes of liver disease and 3-assess the severity of liver damage. The clinical history from patient, relatives and friends is important to establish alcohol misuse duration and severity. Biological markers, particularly macrocytosis in the absence of anaemia, may suggest and support a history of alcohol misuse. A raised GGT may be elevated, PT and bilirubin are used to assess prognosis

6. Management Cessation of alcohol consumption is the single most important treatment and prognostic factor. Life-long abstinence is the best advice. Abstinence is even effective at preventing progression, hepatic decompensation and death once cirrhosis is present. In the acute presentation of ALD it is important to identify and anticipate alcohol withdrawal and Wernicke’s encephalopathy, which need treating in parallel with the liver disease and any complications of cirrhosis. Nutrition Good nutrition is very important, and enteral feeding via a fine-bore nasogastric tube may be needed in severely ill patients. Corticosteroids These are of value in patients with severe alcoholic Hepatitis. Sepsis is the main side-effect of steroids, Pentoxifylline Liver transplantation

7. Non-alcoholic fatty liver disease Non-alcoholic fatty liver disease (NAFLD) represents 1- fatty infiltration (steatosis), 2- fat and inflammation (nonalcoholic steatohepatitis, NASH) and 3- cirrhosis, in the absence of excessive alcohol consumption, NASH is linked with progressive liver fibrosis, cirrhosis and liver cancer, as well as increased cardiovascular risk.

8. NAFLD is strongly associated with obesity, dyslipidaemia, insulin resistance and type 2 diabetes mellitus, and so may be considered to be the hepatic manifestation of the ‘metabolic syndrome’ Increasingly sedentary lifestyles and changing dietary patterns mean that the prevalence of obesity and insulin resistance has increased, making NAFLD the leading cause of liver dysfunction in the non-alcoholic, viral hepatitis-negative population in Europe and North America.

9. Whilst the majority of patients with the metabolic syndrome develop steatosis, only a minority exhibit NASH or fibrosis.

10. Clinical features NAFLD is frequently asymptomatic, although it may be associated with fatigue and mild right upper quadrant discomfort. It is commonly identified as an incidental biochemical abnormality during routine blood tests.Alternatively, patients with progressive NASH may present late in the natural history of the disease with complications of cirrhosis and portal hypertension, such as variceal haemorrhage, or HCC. The average age of NASH is 40–50 years (50–60 years for NASH–cirrhosis); Most patients with NAFLD have insulin resistance and exhibit features of the metabolic syndrome. NAFLD is also associated with polycystic ovary syndrome, obstructive sleep apnoea and small-bowel bacterial overgrowth.

11. Investigations Investigation of patients with suspected NAFLD should be directed first towards exclusion of excess alcohol consumption and other liver diseases (including viral, autoimmune and other metabolic causes), and then at confirming the presence of NAFLD, discriminating simple steatosis from NASH and determining the extent of any hepatic fibrosis that is present. So mainly we need LFTs and imaging studies

12. Management Non-pharmacological treatment Current treatment comprises lifestyle interventions to promote weight loss and improve insulin sensitivity through dietary changes and physical exercise. Sustained weight reduction of 7– 10% is associated with significant improvement in histological and biochemical NASH severity. Pharmacological treatment Treatment directed at coexisting metabolic disorders, such as dyslipidaemia and hypertension, should be given. Although use of HMG-CoA reductase inhibitors (statins) does not ameliorate NAFLD, there does not appear to be any increased risk of hepatotoxicity or other side-effects from these agents, and so they may be used to treat dyslipidaemia.S pecific insulin-sensitising agents, in particular glitazones, may help selected patients, and high-dose vitamin E.