Serum selenium levels and oxidative balance as differential markers in hepatic damage caused by alcohol.

Aims: Antioxidant system abnormalities have been associated with ethanol consumption. This study examines the effects of chronic ethanol consumption on oxidative balance, including selenium (Se) levels in alcoholic patients with or without liver disease, and if these measurements could be indicative of liver disease.

Main Methods: Serum Se levels, antioxidant enzymes' activities, malondialdehyde (MDA) and protein carbonyl (PC) were determined in three groups of patients: alcoholics without liver disease, alcoholics with liver disease, and non-alcoholics with liver disease; and in healthy volunteers.

[Alcoholic and non-alcoholic steatohepatitis: who is affected and what can we do for them?].

The most common causes of steatohepatitis are alcohol intake and metabolic disorders. Several methods based on biochemical determinations (carbohydrate deficient transferrin) and questionnaires (AUDIT, CAGE, MALE) are useful for detecting surreptitious alcohol intake. Although new non-invasive methods are under development, based both on lipidomics (Owl-Liver(®)) and on biochemical determinations and anthropometric parameters (NAFLD Fibrosis score) or imaging methods (DeMILI NASH-MRi(®)), none has been proposed as definitive and the gold standard continues to be liver biopsy.