Hypothesis on cellular ATP depletion and adenosine release as causes of heart failure and vasodilatation in cardiovascular beriberi
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Cited by (27)
The Key to a Boy's Heart Is Through His Intestine
2020, GastroenterologyOxidative stress in sepsis: Pathophysiological implications justifying antioxidant co-therapy
2017, BurnsCitation Excerpt :However, in a study with septic patients, it was observed that oxidative stress was positively associated with mortality, but thiamine deficiency was not associated with oxidative stress [144]. Therefore, in clinical practice, it is not yet fully confirmed if thiamine deficiency can negatively affect patient survival by predisposing them to stronger oxidative stress, although it possibly impairs energy metabolism and ATP synthesis, similar to that observed in patients suffering from the beriberi syndrome [145,146]. In the literature, studies with experimental animals either injected with LPS and/or peptidoglycan or that underwent the CLP procedure to induce sepsis, mainly for rats and mice, are very common.
Are brain and heart tissue prone to the development of thiamine deficiency?
2013, AlcoholCitation Excerpt :From animal studies it is known that thiamine deficiency is complicated by loss of food intake and weight loss (Klooster et al., 2008). A patient with alcohol abuse may be able to develop a more severe state of thiamine deficiency than in a patient without alcohol abuse (Bakker & Leunissen, 1995). It is therefore important to investigate the prevalence of thiamine deficiency and the effectiveness of thiamine supplementation in other disease states than classical Wernicke–Korsakoff syndrome.
Shoshin beriberi mimicking a high-risk non-ST-segment elevation acute coronary syndrome with cardiogenic shock: When the arteries are not guilty
2011, Journal of Emergency MedicineCitation Excerpt :Thiamine deficiency causes a severe reduction of pyruvate dehydrogenase activity, subsequently preventing conversion of its substrate pyruvate into acethyl-CoA. This decrease in acetyl-CoA produces a deficiency of reduced nicotinamide adenine dinucleotide, resulting in a fall in cellular ATP (14). The accumulation of pyruvate and lactate thereby causes intense vasodilatation due to peripheral arteriovenous shunts in the skeletal musculature, with a resulting drop in systemic vascular resistance and increase in venous return (15).
Non-specific hyperamylasemia in shosin beri-beri
2003, Resuscitation
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