Arylsulfatase (ASA) enzyme deficiency is associated with metachromatic leuk
odystrophy (MLD), which is a hereditary myelin metabolic disease. It has be
en proposed that in alcoholic subjects with abnormal ASA, the accumulation
of sulfatides may lead to demyelinization and generalized cerebral atrophy.
ASA may be diminished in subjects with alcoholic cirrhosis having encephal
opathic manifestations. This idea has not been previously proposed. Leukocy
te arylsulfatase A (ASA) activity was measured in 30 healthy male volunteer
s and 28 patients with alcohol-related cirrhosis. The patients were divided
into two groups: patients with alcohol-related cirrhosis with hepatic ence
phalopathy history and patients with alcoholic cirrhosis without history of
hepatic encephalopathy. Alcoholic cirrhotic patients with history of encep
halopathy showed 58.21% (40.95 nmol/mg protein/h) less enzymatic activity t
han a control group (98.00 nmol/mg protein/h), whereas the group without ,h
istory of encephalopathy showed an ASA value which was 38.2% (60.55 nmol/mg
protein/h) less than the control group. The results suggest that the low A
SA activity is a factor associated to the appearance of encephalopathy in p
atients with alcohol-related cirrhosis. (C) 2001 Wiley-Liss, Inc.