unclear reasons, only 30 to 35% of individuals with heavy and long-term
drinking develop alcoholic hepatitis, and less than 20% develop cirrhosis.
Women are at higher risk; for example, the risk of alcoholic cirrhosis increases
after 10 years of alcohol consumption at quantities of more than 60 to 80 g/
day in men, whereas in women, it can develop at quantities of only more than
20 g/day. Moreover, the peak incidence of alcoholic liver disease in women
is approximately a decade earlier than in men. The type of alcoholic beverage
consumed may not be as critical, but “spirits” and beer may be more hepatotoxic
than wine. African-American and Hispanic ethnic groups may be
predisposed to more significant alcoholic liver injury. Both obesity and protein-
calorie malnutrition, in which micronutrients and antioxidant capacity
are diminished, also are important predispositions.
Polymorphisms in genes associated with alcohol metabolism (alcohol and
aldehyde dehydrogenases and cytochrome P-450 enzymes) and dysregulated
cytokine production (e.g., TNF-α) may also influence genetic susceptibility.
In patients with other forms of chronic liver disease (e.g., viral hepatitis B or
C), concomitant alcohol consumption significantly aggravates liver injury