Objective: Refeeding syndrome can occur in several contexts of relative malnutrition in which an overaggressive nutritional support is started. The consequences are life threatening with multiorgan impairment, and severe electrolyte imbalances. During refeeding, glucose-involved insulin secretion causes abrupt reverse of lipolysis and a switch from catabolism to anabolism. This creates a sudden cellular demand for electrolytes (phosphate, potassium, and magnesium) necessary for synthesis of adenosine triphosphate, glucose transport, and other synthesis reactions, resulting in decreased serum levels. Laboratory findings and multiorgan impairment similar to refeeding syndrome also are observed in acute thiamine deficiency. The aim of this study was to determine whether thiamine deficiency was responsible for the electrolyte imbalance caused by tubular electrolyte losses.
Methods: We describe two patients with leukemia who developed acute thiamine deficiency with an electrolyte pattern suggestive of refeeding syndrome, severe lactic acidosis, and evidence of proximal renal tubular dysfunction.
Results: A single thiamine administration led to rapid resolution of the tubular dysfunction and normalization of acidosis and electrolyte imbalance. This demonstrated that thiamine deficiency was responsible for the electrolyte imbalance, caused by tubular electrolyte losses.
Conclusions: Our study indicates that, despite sharing many laboratory similarities, refeeding syndrome and acute thiamine deficiency should be viewed as separate entities in which the electrolyte abnormalities reported in cases of refeeding syndrome with thiamine deficiency and refractory lactic acidosis may be due to renal tubular losses instead of a shifting from extracellular to intracellular compartments. In oncologic and malnourished patients, individuals at particular risk for developing refeeding syndrome, in the presence of these biochemical abnormalities, acute thiamine deficiency should be suspected and treated because it promptly responds to thiamine administration.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.nut.2014.02.019 | DOI Listing |
Eur J Intern Med
January 2025
Universidade Católica Portuguesa, Católica Medical School, Sintra, Portugal.
Cognitive impairments are frequently observed in patients with Alcohol Use Disorder (AUD). Thiamine deficiency is often found in AUD patients and has been suggested as a possible cause of cognitive impairments. While thiamine deficiency is not consistently present in all AUD patients with cognitive deficits, thiamine is traditionally prescribed to patients with AUD to treat or prevent cognitive impairment.
View Article and Find Full Text PDFJ Small Anim Pract
January 2025
The Department of Small Animal DiagnosticImaging, Queen Mother Hospital for Animals, Hatfield, UK.
Palliat Support Care
January 2025
Department of Psycho-Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Objectives: Wernicke encephalopathy (WE) is an acute neuropsychiatric disorder caused by thiamine deficiency. The classical triad of symptoms for WE include mental status changes, ataxia, and ophthalmoplegia. In contrast, more uncommon symptoms include hallucinations.
View Article and Find Full Text PDFJ Clin Med
January 2025
Department of Emergency Medicine, Henry Ford Health, Detroit, MI 48202, USA.
: Wernicke's encephalopathy can occur in oncology patients independent of alcohol use, likely resulting from poor dietary thiamine intake. High metabolic demands, such as those in acute illnesses seen in the emergency department (ED), can exacerbate thiamine deficiency. In this study, our objective was to assess the incidence of thiamine deficiency in ED oncology patients, which could lead to Wernicke's encephalopathy or other thiamine deficiency disorders if left untreated.
View Article and Find Full Text PDFPediatr Neurol
December 2024
University of Alabama, Birmingham, Children's of Alabama, Birmingham, Alabama.
Wernicke encephalopathy is a well-described neurological complication of thiamine deficiency that is classically characterized by a triad of mental confusion, ophthalmoplegia, and gait ataxia. Although most commonly linked to alcoholism and thiamine deficiency in adults, it can present in pediatric patients. Wernicke encephalopathy presenting as dysnatremias is not well described.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!