Binge drinking–induced liver injury

We read with interest the excellent article by Ioannou and colleagues demonstrating that diet may be an important determinant of liver disease, after adjusting for potential confounders including daily consumption of protein, carbohydrates, alcohol, fat, tea, and coffee; as well as sex, body mass index, etc.1 Alcohol consumption variable was categorized as none, 0 to 1, 1 to 2, and 2 drinks/day. In characterizing excessive alcohol consumers as those who consume 2 drinks/day, we may consider persons who drink alcohol chronically (alcoholics) or persons who occasionally drink higher amounts of alcohol (binge drinkers). Only 5% and 15% of persons suffering from cirrhosis or liver cancer, respectively, drank excessively.1 However, it would be prudent to divide them into occasional (binge) and chronic drinkers in further studies. The drastic increase in alcohol-induced liver injury and mortality rates is alarming.2 The binge drinking phenomenon that is now spreading throughout young populations worldwide is at least in part responsible for this drastic increase in liver injury.2 Binge drinking is characterized by the consumption of alcohol leading to intoxication (drinking to get drunk), often measured as having more than four (women) or five (men) number of drinks on one occasion.3 On more than 30% of occasions when men go out to drink, they consume binge amounts of alcohol.2 In the literature, alcohol binging has been described to increase the risk for numerous acute adverse health and social events including injuries, violence, suicide, acute myocardial infarction, etc.4 but liver consequences were often ignored. Most of experimental data concerning the impact of binge drinking on pathogenesis of the liver injury may not be completely extrapolated to humans, because most of the studies are based on animal models that do not completely mimic liver injury in humans (except a few studies describing oxidative stress involvement in pathogenesis of human liver lesions). 2,5 During the drinking session, binge drinkers often think they remain within the recommended safe weekly limits of alcohol consumption ( 168 g of alcohol or fewer than 21 units). 6 Furthermore, routine laboratory tests are not sensitive enough to detect harmful effects of single-occasion drinking on the liver, because pronounced changes are only measurable after very high and prolonged ethanol consumption.4 -Hexosaminidase, a very sensitive marker of harmful drinking to the liver, has been shown to increase in serum and urine after a single binge drinking session.3 Various mechanisms are responsible for alcohol-induced -hexosaminidase elevation: increase in lysosomal membrane permeability and leakage of the enzyme from lysosomes and subsequently from affected hepatocytes to the blood, delayed removal of -hexosaminidase by injured liver, and enhanced synthesis of the enzyme by activated reticuloendothelial cells.6 The impact of chronic alcohol consumption on liver tissue injury is well known and widely described by researchers. Less attention has been paid to binging-induced hepatoxicity, even though binge drinking is much more common than chronic alcoholism.4 The deleterious effect of binge drinking on the liver is an alarming public health issue that requires better prevention. Therefore, further studies focusing on binging-induced human liver injury seem to be warranted.