Metabolic failure due to thiamine deficiency during critical illness.

PURPOSE OF REVIEW: Thiamine is a crucial component in cellular energy metabolism, serving as a cofactor for multiple enzymatic processes and also having a role in regulating neuronal and neuromuscular transmission. Also it exerts antioxidant proprieties. The objective of this review is to consolidate and assess the most recent research concerning the consequences of insufficient thiamine levels for critically ill patients and to examine thiamine-related interventions. RECENT FINDINGS: Recent studies have unveiled a noteworthy association between thiamine deficiency and unfavorable consequences, such as heightened morbidity and fatality rates. The aforementioned deficiency exhibits a significant presence in medical situations such as starvation and alcohol use disorder, but also in patients during critical illness. Thiamine deficiency can have significant metabolic implications resulting in compromised energy generation and organ dysfunction, warranting prompt recognition and management. SUMMARY: Thiamine deficiency may not be recognized in critical care. Timely identification and management are imperative to mitigate adverse outcomes and improve patient prognosis. Thiamine may offer benefits for specific patient groups at higher risk of deficiency. Future studies should focus to establish optimal dosing, timing, and monitoring strategies on understanding the pathophysiological changes associated with thiamine deficiency in ICU patients and clarify its role in improving clinical outcomes.

Thiamine deficiency contributes to synapse and neural circuit defects

BACKGROUND: The previous studies have demonstrated the reduction of thiamine diphosphate is specific to Alzheimer's disease (AD) and causal factor of brain glucose hypometabolism, which is considered as a neurodegenerative index of AD and closely correlates with the degree of cognitive impairment. The reduction of thiamine diphosphate may contribute to the dysfunction of synapses and neural circuits, finally leading to cognitive decline. RESULTS: To demonstrate this hypothesis, we established abnormalities in the glucose metabolism utilizing thiamine deficiency in vitro and in vivo, and we found dramatically reduced dendrite spine density. We further detected lowered excitatory neurotransmission and impaired hippocampal long-term potentiation, which are induced by TPK RNAi in vitro. Importantly, via treatment with benfotiamine, Aß induced spines density decrease was considerably ameliorated. CONCLUSIONS: These results revealed that thiamine deficiency contributed to synaptic dysfunction which strongly related to AD pathogenesis. Our results provide new insights into pathogenesis of synaptic and neuronal dysfunction in AD.

Síndrome de Wernicke-Korsakoff y resonancia magnética / No disponible

El diagnóstico de encefalopatía deWernicke (EW) esclínico. En algunas ocasiones este no es realizado deforma precoz, llegando a desarrollar un síndrome deWernicke-Korsakoff. En la actualidad la realización deuna resonancia magnética (RM) cerebral puede confirmareste diagnóstico.Se presenta un caso de síndrome deWernicke-Korsakoffen paciente alcohólico, confirmado a través de lasimágenes encontradas mediante RM cerebral(AU)

The diagnosis of Wernicke encephalopathy (EW) isclinical. Some times this is not done early, developing aWernicke-Korsakoff syndrome. At present the MagneticResonance (MR) brain can confirm this diagnosis.We report a case of Wernicke-Korsakoff syndromein alcoholic patient, confirmed by the images found byMR brain(AU)

Deficiência aguda de tiamina: efeitos no crescimento e resposta quimioterápica de um fibro-histiocitoma maligno de rato / Acute thiamine deficiency: effects on growth and response chemotherapy of a malignant fibrohistocytoma of rat

Os objetivos do presente trabalho foram estdar os efeitos da deficiência aguda de tiamina no crescimento e na resposta quimiterápica de um fibro-histiocitoma maligno no rato. Para tanto, ratos foram inoculados por via subcutânea com suspensäo de células tumorais e divididos em quadro grupos, de 10 animais cada: DCT - alimentados com dieta sem tiamina; TGT - alimentados com dieta controle; e TVC - alimentados com dieta controle e tratados com SVC. Os animais tratados com SVC (DVC e TVC) apresentaram diminuiçäo de volume tumoral quando comparados com os näo tratados (DCT e TCT). Entretanto, näo houve alteraçäo no volume tumoral de animais carentes em tiamina tratados (DVC) em relaçäo àqueles tratados e com dieta controle (DCT). Estes dados indicam que a deficiência aguda de tiamina per se näo altera o cresciento do FHM como também näo modifica a resposta de tumor frente à quimioterapia com SVC.