Alcoholic liver disease

Alcoholic liver disease (ALD) is an umbrella term for liver conditions caused by significant and chronic alcohol abuse. It initially causes liver steatosis, which progresses to alcoholic hepatitis to cirrhosis unless alcohol consumption stops.

Almost all who abuse alcohol develop liver steatosis, which is reversible, but only a few progress to hepatitis and cirrhosis. Hepatitis C is often found in chronic alcoholics and leads to acceleration of alcoholic liver disease.

Excessive ethanol consumption causes more than 60% of chronic liver diseases in the Western countries and is the 5th leading cause of death. Alcoholic liver disease is a major cause of liver transplantation.

Diagnosis and evaluation

For diagnosis of alcoholic liver disease, it’s important to establish the diagnosis of alcohol abuse, in which case heteroanamnesis may be required. The following laboratory alterations are typical:

AST/ALT ratio > 2 (but both are elevated)
Macrocytic anaemia
Elevated GGT

Serum ethanol levels can be measured, but this only elevated in case of intake in the last hours. Phosphatidylethanol (PEth), a phospholipid which is only formed after alcohol consumption, is a marker of long-term alcohol intake. Carbohydrate-deficient transferrin (CDT) is another marker of long-term alcohol intake.

Liver fibrosis and cirrhosis

Cirrhosis is a chronic liver disease characterised by replacement of normal liver tissue by scar tissue and liver failure. It’s the irreversible end-stage of hepatitis and liver fibrosis and cause significant morbidity and mortality. There is continuous loss of functional liver tissue, which is initially compensated and asymptomatic as the remaining liver can compensate. However, acute insults precipitate decreases in liver function, causing hepatic decompensation and development of dramatic and life-threatening complications. Cirrhosis is also an important risk factor for hepatocellular carcinoma.

Diagnosis and evaluation

Diagnosis of cirrhosis can usually be made based on clinical features, ultrasound, and special non-invasive investigations like FibroScan, transient elastography (TE) and acoustic radiation force impulse (ARFI). Ultrasound shows a shrunk liver with nodular surface and loss of homogeneity.

Typical laboratory findings of cirrhosis include:

Elevated AST, ALT
Elevated INR – due to decreased production of coagulation factors
Hypoproteinaemia and hypoalbuminaemia
Thrombocytopaenia
Macrocytic anaemia
Hyperbilirubinaemia

Proprietary formulas like FIB-4, FibroTest, and Hepascore estimate the degree of fibrosis based on the age and sex as well as the level of certain parametres like thrombocyte count, ALT, AST, haptoglobin, bilirubin, and GGT. This may be useful to rule out liver fibrosis or to distinguish between severe and non-severe fibrosis.

Determination of the etiology is based on patient history as well as laboratory examination:

Viral hepatitis serology
Alpha-1 antitrypsin – for deficiency
Autoantibodies and hypergammaglobulinaemia – for autoimmune hepatitis
Iron studies – for haemochromatosis
Copper studies – for Wilson disease