File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Current progress toward the prevention of the wernicke-korsakoff syndrome

TitleCurrent progress toward the prevention of the wernicke-korsakoff syndrome
Authors
Issue Date1986
Citation
Alcohol and Alcoholism, 1986, v. 21, n. 4, p. 315-323 How to Cite?
AbstractThe 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.Although the prevention of the Wernicke-Korsakoff syndrome by the fortification of alcoholic beverages remains a theoretically attractive preventive strategy we conclude that there are some unanswered questions which may delay the implementation of the policy until more is known about the pathophysiology of the Wernicke-Korsakoff syndrome. © 1986 Medical Council on Alcoholism.
Persistent Identifierhttp://hdl.handle.net/10722/327482
ISSN
2023 Impact Factor: 2.1
2023 SCImago Journal Rankings: 0.752

 

DC FieldValueLanguage
dc.contributor.authorBishai, David M.-
dc.contributor.authorBozzetti, Louis P.-
dc.date.accessioned2023-03-31T05:31:40Z-
dc.date.available2023-03-31T05:31:40Z-
dc.date.issued1986-
dc.identifier.citationAlcohol and Alcoholism, 1986, v. 21, n. 4, p. 315-323-
dc.identifier.issn0735-0414-
dc.identifier.urihttp://hdl.handle.net/10722/327482-
dc.description.abstractThe 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.Although the prevention of the Wernicke-Korsakoff syndrome by the fortification of alcoholic beverages remains a theoretically attractive preventive strategy we conclude that there are some unanswered questions which may delay the implementation of the policy until more is known about the pathophysiology of the Wernicke-Korsakoff syndrome. © 1986 Medical Council on Alcoholism.-
dc.languageeng-
dc.relation.ispartofAlcohol and Alcoholism-
dc.titleCurrent progress toward the prevention of the wernicke-korsakoff syndrome-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid3814251-
dc.identifier.scopuseid_2-s2.0-0022914460-
dc.identifier.volume21-
dc.identifier.issue4-
dc.identifier.spage315-
dc.identifier.epage323-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats