
Alcohol Volume 42, Issue 6, September 2008, Pages 513-518
Tumor necrosis factor-alpha (TNF-α) mediates alcohol-induced organ dysfunction, including alcoholic hepatitis. Variations in the TNF-α gene may underlie the individual predisposition to alcoholic liver disease. Measurement of serum TNF-α levels has become a routine in clinical practice.
The study was aimed at investigating the level of serum TNF-α levels in adults and analyzing its relationship with different levels of alcohol consumption, as well as the potential interaction between alcohol consumption and common TNF-α gene polymorphisms in relation to TNF-α levels and liver disease.
Serum TNF-α was measured in a random sample of 459 individuals from a general adult population and in 137 hospital-admitted alcoholics. Three common TNF-α gene polymorphisms (−238G>A, −308G>A, and −857C>T) were investigated in 419 of these individuals.
In the general adult population, the TNF-α levels were similar in alcohol abstainers and alcohol drinkers. Alcoholics admitted to the hospital showed the highest TNF-α levels, which were correlated with liver dysfunction. We found no evidence of an interaction between alcohol consumption and TNF-α gene polymorphisms in relation to TNF-α levels. Carriers of the TNF −238A allele tended to have a higher prevalence of advanced liver disease than −238G homozygotes, confirming previous reports.
In conclusion, light-to-moderate drinking had no significant effect on the levels of serum TNF-α levels. Serum TNF-α levels are elevated in alcoholics independently of common TNF gene polymorphisms.
Read Full Abstract
Request Reprint E-Mail: mearturo@usc.es
__________________________________________________________