Forty-six male alcoholics hospitalized with
polyneuropathy or intellectual impairment were studied after at least 2 wk of alcohol abstention. Neurological evaluation included neurophysiological examination of the sural nerve and tibial nerve, neurophysiological examinations, and CT-scanning of the brain. Alcohol and
vitamin intakes were quantified by the interview method.
Vitamin B-12 and
folate status included examinations of peripheral blood and bone marrow aspirate, plasma
vitamin B-12, plasma and erythrocyte
folate,
formiminoglutamic acid excretion test (
FiGlu),
methylmalonic acid excretion, and
deoxyuridine suppression test (dU) on
phytohemagglutinin-stimulated peripheral lymphocytes. The liver function was assessed by
galactose elimination capacity and plasma clearance of
antipyrine. There was no hematological sign of
folate or
vitamin B-12 deficiency. About 8% had low plasma
folate, while neither erythrocyte
folate nor plasma
vitamin B-12 were decreased. However, half of the patients had functional
folate deficiency as determined by abnormal
FiGlu or dU. Compared to the remaining patients, those with abnormal
FiGlu or dU had significantly more abnormal neurophysiological tests, and lower
folate intake. There was no correlation between
FiGlu or dU and the quantitative liver function tests. It is concluded that 1)
folate deficiency may contribute to the development of
alcoholic polyneuropathy, 2) the classical parameters for
folate deficiency (blood concentrations, peripheral blood, and bone marrow examinations) are not reliable in diagnosing
folate deficiency and 3) functional tests like
FiGlu and dU are necessary to diagnose
folate deficiency in alcoholics.