The
Wernicke-Korsakoff syndrome is a rare
neurological disorder which strikes primarily alcoholics and is caused, at least in part, by insufficient bioavailability of
thiamin. Because of the low cost of preventing this disease by adding
thiamin to alcoholic beverages relative to the cost of the
long-term care of patients with the chronic phase of the disease, there has been a need to determine the feasibility of this particular preventive strategy. Recent data demonstrating normal levels of erythrocyte
transketolase in patients presenting with
Wernicke's encephalopathy has led some to question the link between
thiamin deficiency, and the development of the syndrome, despite the fact that virtually all patients with
Wernicke's encephalopathy will respond favorably to parenteral
thiamin, and the evidence that rats deprived of
thiamin develop lesions that are characteristic of the disease.
Thiamin is nontoxic, is stable in alcoholic beverages, and is undetectable in beer to professional taste-testers at levels theoretically sufficient to guarantee adequate absorption. Although there is much inter-subject variability it appears that
thiamin at therapeutic concentrations can be absorbed by the jejunum in the presence of alcohol. Evidence that patients with the
Wernicke-Korsakoff syndrome have an altered
thiamin-requiring
isoenzyme and evidence that six patients with
Wernicke's encephalopathy failed to respond to oral
thiamin has caused some doubt as to whether the target population would be able to benefit from the measure. Other determinants of
thiamin utilization, such as
folate and
magnesium status, also may figure in the etiology of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)