Thiamin is a water-soluble vitamin also known as vitamin B1. Its biologically active form, thiamin pyrophosphate (TPP), is a cofactor in macronutrient metabolism. In addition to its coenzyme roles, TPP plays a role in nerve structure and function as well as brain metabolism. Signs and symptoms of thiamin deficiency (TD) include lactic acidosis, peripheral neuropathy, ataxia, and ocular changes (eg, nystagmus). More advanced symptoms include confabulation and memory loss and/or psychosis, resulting in Wernicke's encephalopathy and/or Wernicke's Korsakoff syndrome, respectively. The nutrition support clinician should be aware of patients who may be at risk for TD. Risk factors include those patients with malnutrition due to 1 or more nutrition-related etiologies: decreased nutrient intake, increased nutrient losses, or impaired nutrient absorption. Clinical scenarios such as unexplained heart failure or lactic acidosis, renal failure with dialysis, alcoholism, starvation, hyperemesis gravidarum, or bariatric surgery may increase the risk for TD. Patients who are critically ill and require nutrition support may also be at risk for TD, especially those who are given intravenous dextrose void of thiamin repletion. Furthermore, understanding thiamin's role as a potential therapeutic agent for diabetes, some inborn errors of metabolism, and neurodegenerative diseases warrants further research. This tutorial describes the absorption, digestion, and metabolism of thiamin. Issues pertaining to thiamin in clinical practice will be described, and evidence-based practice suggestions for the prevention and treatment of TD will be discussed.
Keywords: adult; life cycle; nutrition; nutrition assessment; research and diseases; vitamins.
© 2015 American Society for Parenteral and Enteral Nutrition.