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2.4.3 Alcoholic Steatohepatitis (ASH)
Presents with a marked increase in y-GT, accompanied by jaundice and an enlarged hyperreflective liver.
ASH occurs in a third of heavy drinkers and is usually already superimposed on alcoholic cirrhosis.
The symptoms and biochemistry are determined by the severity of the alcoholic static hepatitis. A severe form is characterized by:
- chachexia;
- icterus;
- leukocytosis and a low platelet count (also due to suppression by alcohol);
- a moderately increased amount of transaminases: about 100 IU/l;
- AST > ALT;
- very high y_GT, as well as Fe saturation and ferritin (differential diagnosis with primary hemochromatosis).
The prognosis is unfavorable if the Maddrey score is higher than 32. This is based on the prothrombin time (PT) and the amount of bilirubin. The patient can then evolve into acute or chronic liver failure.
Treatment consists of: stopping alcohol, preventing delirium tremens, administering vitamin B1 and providing sufficient calorie-rich food (enteral nutrition if necessary). If the Maddrey score is higher than or equal to 32, prednisolone must be administered for one month, to be stopped if the Lille score does not decrease after one week. This score is based on, among other things, the amount of bilirubin.
photo credit Hanna Lottritz
Binge drinking
Binge drinking
Excessive alcohol consumption and abuse may result in alcoholic liver disease (ALD), a major contributor of liver diseases and deaths [1,2]. Pathogenesis of ALD initiates with simple steatosis in a majority of drinkers and progresses to more severe pathologies including fibrosis, alcoholic hepatitis, and cirrhosis in a fraction of patients. In exceptional cases, ALD may progress to hepatocellular carcinoma [2]. Binge drinking is a form of alcohol abuse defined by consuming more than 5 drinks (males) or 4 drinks (females) in 2 h setting [3]. Around one out of three adults display high risk drinking pattern including binge drinking, but less attention has been given to liver injury induced by acute alcohol exposure despite the fact binge drinking is more common than chronic alcohol abuse [1]. At the physiological level, binge drinking induces glycogen depletion, acidosis, and hypoglycemia [4]. At the cellular level, binge drinking results in mitochondria damage, ablated insulin signaling, steatosis, and free radical generation [5–9]. Paradoxically, binge drinking induces autophagy as a cellular protective mechanism to selectively degrade damaged mitochondria (mitophagy) and lipid droplets (lipophagy), whereas suppression of autophagy by pharmacological inhibitors or small interfering RNAs exacerbates alcohol-induced hepatotoxicity and steatosis [10,11].
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