Alcohol and Thiamine Metabolism

Hoyumpa, Anastacio M.

doi:10.1111/j.1530-0277.1983.tb05403.x

Cited by 33 publications

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“…The primary etiology of Wernicke–Korsakoff syndrome (WKS) is thiamine deficiency, and more than 90% of cases of WKS are reported in alcohol‐dependent patients (Thomson & Marshall, 2006a). Many alcohol‐dependent people suffer severe, prolonged nutritional deficiencies and alcohol acts to impair the absorption and utilization of thiamine in the brain (Hoyumpa, 1983; Pitel et al, 2011; Scalzo et al, 2014; Thomson & Marshall, 2006b). Dietary thiamine provides an essential coenzyme for diverse metabolic activities, perhaps most importantly for the energy (ATP) cycle in cells.…”

Section: Introductionmentioning

confidence: 99%

What is the optimum thiamine dose to treat or prevent Wernicke's encephalopathy or Wernicke–Korsakoff syndrome? Results of a randomized controlled trial

Dingwall

Delima

Binks

et al. 2022

Alcoholism Clin & Exp Res

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Background:The primary cause of Wernicke-Korsakoff syndrome (WKS) is thiamine deficiency, and more than 90% of cases are reported in alcohol-dependent patients.While observational studies show parenteral thiamine administration drastically reduced WKS-related mortality, relevant treatment trials have never been conducted to determine the optimum thiamine dose.Methods: Two double-blind, parallel groups, randomized controlled trials (RCTs) were conducted to determine the optimal thiamine dose required for (1) the prevention of Wernicke's encephalopathy (WE), the acute phase of WKS, in asymptomatic but "at-risk" alcohol misuse patients (Study 1) and (2) the treatment of WE in symptomatic alcohol misuse patients (Study 2). Each study had a dosage regimen comprising three parenteral thiamine doses that were allocated at a ratio of 1:1:1. Study 1: Asymptomatic At-Risk patients (N = 393) received either 100 mg daily, 100 mg thrice daily, or 300 mg thrice daily, for 3 days. Study 2: Symptomatic patients (N = 127) received either 100 mg thrice daily, 300 mg thrice daily, or 500 mg thrice daily, for 5 days. Cognitive function was the primary outcome, assessed using the Rowland Universal Dementia Assessment Scale, two Cogstate subtests, and an adapted Story Memory Recall test. Secondary analyses examined differences in neurological function (ataxia, oculomotor abnormalities, and confusion) at follow-up.Results: No significant differences were observed between any of the dosage conditions for either Study 1 or Study 2 on cognition or neurological functioning. This real-world study found that having a clinically unwell target population with high comorbidity and multiple presentations, coupled with challenges in cross-cultural assessment is likely to complicate RCT findings. Conclusions:The results of this study showed no clear benefit of high dose thiamine over intermediate or lower doses of thiamine, over the time intervals examined, for the treatment and prevention of cognitive and neurological abnormalities related to WKS.

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Section: Introductionmentioning

confidence: 99%

What is the optimum thiamine dose to treat or prevent Wernicke's encephalopathy or Wernicke–Korsakoff syndrome? Results of a randomized controlled trial

Dingwall

Delima

Binks

et al. 2022

Alcoholism Clin & Exp Res

View full text Add to dashboard Cite

show abstract

“…In affluent countries where adequate thiamine is usually received through dietary intake, thiamine deficiency is commonly associated with alcohol dependence [1]. Poor dietary patterns, along with the impact of alcohol consumption on absorption, storage, activation and excretion of thiamine are thought to be the mechanisms for thiamine deficiency among alcohol‐dependent individuals [2,3]. Australia introduced thiamine supplementation to flour in 1991, and a recent study demonstrated elevated thiamine concentrations among a sample of Australians with alcohol use disorders [4].…”

Section: Introductionmentioning

confidence: 99%