QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gimsing, P. Articles by Hippe, E. Search for Related Content PubMed PubMed Citation Articles by Gimsing, P. Articles by Hippe, E.

Vitamin B-12 and Folate Function in Chronic Alcoholic Men with Peripheral Neuropathy and Encephalopathy¹

Peter Gimsing², Bjørn Melgaard^*, Kjeld Andersen, Hendrik Vilstrup and Erik Hippe

^* Department of Internal Medicine and Hematology, Neurology, Department of Internal Medicine and Hematology, Clinical Neurophysiology, Gentofte Hospital, Faculty of Medicine, University of Copenhagen, DK 2900 Hellerup, Denmark Department of Internal Medicine and Hematology, Hepatology, Rigshospitalet, DK 2100 Copenhagen Ø Denmark

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.

KEY WORDS: • vitamin B-12 • folate • alcoholic neuropathy

¹ This study was supported by grants from the Danish Cancer Society (#78/42) and Danish Hospital Foundation for Medical Research. Region of Copenhagen, The Faroe Islands and Greenland (#82/22).

² To whom reprint requests should be addressed at: Strandøre 13, DK 2100, Copenhagen Ø, Denmark.

Manuscript received 7 April 1988. Revision accepted 7 November 1988.

This article has been cited by other articles:

				T. J. PETERS, J. KOTOWICZ, W. NYKA, W. KOZUBSKI, V. KUZNETSOV, F. VANDERBIST, S. DE NIET, D. MARCEREUIL, and M. COFFINER TREATMENT OF ALCOHOLIC POLYNEUROPATHY WITH VITAMIN B COMPLEX: A RANDOMISED CONTROLLED TRIAL Alcohol Alcohol., November 1, 2006; 41(6): 636 - 642. [Abstract] [Full Text] [PDF]