Evidence map›Paper›PMID 28225048›Full record

ReviewEuropean journal of clinical nutrition2017

Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity: how poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease.

L M P Fernandes, F R Bezerra, M C Monteiro, M L Silva, F R de Oliveira, R R Lima, E A Fontes-Júnior, C S F Maia

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of clinical nutrition, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 86 citations in OpenAlex.

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  6. Antemortem radiologic and histopathologic presentation of Marchiafava-Bignami disease.Journal of neuropathology and experimental neurology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

L M P FernandesPrograma de Pós-Graduação em Ciências Farmacêuticas, Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, Pará, Brazil.
F R BezerraPrograma de Pós-Graduação em Ciências Farmacêuticas, Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, Pará, Brazil.
M C MonteiroPrograma de Pós-Graduação em Ciências Farmacêuticas, Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, Pará, Brazil.
M L SilvaLaboratório de Farmacologia da Inflamação e do Comportamento, Faculdade de Farmácia, Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, Pará, Brazil.
F R de OliveiraPrograma de Pós-graduação em Neurociências e Biologia Celular, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Pará, Brazil.
R R LimaPrograma de Pós-graduação em Neurociências e Biologia Celular, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Pará, Brazil.
E A Fontes-JúniorPrograma de Pós-Graduação em Ciências Farmacêuticas, Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, Pará, Brazil.
C S F MaiaPrograma de Pós-Graduação em Ciências Farmacêuticas, Instituto de Ciências da Saúde, Universidade Federal do Pará, Belém, Pará, Brazil.
Universidade Federal do Pará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ethanol is an important risk factor for the occurrence of several brain disorders that depend on the amount, period and frequency of its consumption. Chronic use of ethanol often leads to the development of neurodegenerative syndromes, which cause morphological and functional impairments such as foetal alcohol syndrome in newborns exposed to ethanol during pregnancy, Wernicke-Korsakoff Syndrome and, more rarely, Marchiafava-Bignami disease (MBD). MBD is characterized by primary degeneration of the corpus callosum, without inflammation and is associated with oxidative stress and hypovitaminosis, as well as altered mental status, to mention dementia, seizures, depression and so on. This review discusses MBD and poor nutrition as a risk factor for the development of such alcoholic syndrome, with focus on diagnosis, pathogenic aspects, signs and symptoms, as well as therapeutic perspectives. On the basis of the inclusion/exclusion criteria adopted, the performed search in scientific databases (Pubmed, Scielo and Google Scholar) resulted in 100 studies that are being presented and discussed in the present work. Review, case-control and cohort studies on alcoholism-associated hypovitaminosis, oxidative stress, MBD and ethanol metabolism pathways were admitted as relevant. We highlight that MBD is a poorly described, diagnosed, insidious and progressive condition, for which evidence suggests a synergism between ethanol-induced neurotoxic effects and hypovitaminosis B. Present treatment consists of vitamin B1(thiamine) supplementation. Nonetheless, other strategies such as the inclusion of antidepressants or steroidal anti-inflammatories as add-on therapies have been employed as an attempt to improve the damage. Indeed, both the diagnosis and treatment are difficult, and death occurs within few years.

Indexed as

Alcohol DrinkingAlcoholismEthanolMarchiafava-Bignami DiseaseNeurotoxicity SyndromesOxidative StressThiamineThiamine DeficiencyVitamin B ComplexEthanolThiamineVitamin B Complex

Identifiers

PMID28225048
OpenAlexW2590126026

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.