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Alcohol and Alcoholism Vol. 36, No. 2, pp. 180, 2001
© 2001 Medical Council on Alcoholism
LETTERS TO THE EDITORS
The value of oral thiamine: reply
Kent Institute of Medicine and Health Sciences, University of Kent at Canterbury, Canterbury, Kent CT2 7PD, UK
Received 2 October 2000; )
Dr Madden has drawn attention to two studies (Majumdar et al., 1981
; Baines et al., 1988), in which alcohol apparently did not reduce absorption of oral thiamine. Clearly, there appears to be some discrepancy between the results of these studies and others in which alcohol has been shown to reduce absorption of oral thiamine (see Thomson, 2000). It is somewhat outside my own field of expertise to speculate on the diverse possible reasons for these different findings. However, it would appear to be very significant that both the studies quoted by Dr Madden excluded malnourished subjects. Since the patients most at risk of Wernicke–Korsakoff syndrome are presumably those who are malnourished, and given that absorption of oral thiamine is apparently impaired by malnutrition in combination with alcohol misuse (Thomson, 2000), it would seem to me that there is still a very significant reason to be concerned at the probable inadequacy of oral thiamine in prophylaxis for Wernicke– Korsakoff syndrome.
Dr Madden also suggested that high doses of thiamine ‘ensured the passive absorption of thiamine that is not inhibited by alcohol’. It is not at all clear that there is any evidence for passive diffusion of thiamine across the bowel wall in human beings. Indeed, this process of transport seems to be saturated in such a way that further increases of oral dosage do not produce any greater absorption than a maximum of approximately 4.5 mg in normal subjects (Thomson, 2000).
Dr Madden clearly recognizes that parenteral replacement is essential in cases of an established (or probable) diagnosis of Wernicke's encephalopathy. However, if there is any value at all in providing thiamine supplementation for prophylaxis during alcohol detoxification, it is likely that thiamine replacement in these circumstances will also need to be relatively rapid. At a maximum replacement rate of 4.5 mg/oral dose (and this assumes that alcohol and malnutrition do not further impair absorption), it would seem unlikely that oral dosage would provide sufficient replenishment at a sufficient rate to address the increase in thiamine requirement associated with the metabolic demands of alcohol withdrawal.
It is of course true that injections of thiamine are associated with risk (albeit very low) and are inconvenient. However, this has to be weighed against the risks of not providing prophylaxis and the effectiveness of prophylaxis as offered. Taking into account all of these factors, it would seem to me that the balance lies heavily in favour of parenteral administration of thiamine for prophylaxis as well as for treatment.
REFERENCES
Baines, M., Blight, J. G. and Madden, J. S. (1988) Tissue thiamine levels of hospitalized alcoholics before and after oral or parenternal vitamins. Alcohol and Alcoholism 23, 49–52.
Majumdar, S. K., Shaw, G. K. and Thomson, A. D. (1981) Blood vitamin status in chronic alcoholics after a single dose of polyvitamin. A preliminary report. Postgraduate Medical Journal 57, 164–166.
Thomson, A. D. (2000) Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke–Korsakoff syndrome. Alcohol and Alcoholism 35 (Suppl. 1), 2–7.
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