Thiamine as a metabolic resuscitator in septic shock: one size does not fit all

Thiamine is an essential component of cellular metabolism, and the lack of this vitamin can result in life-threatening biochemical damage (1). Specifically, thiamine is a cofactor in oxidative decarboxylation in three mitochondrial complexes (pyruvate, α-ketoglutarate and α-keto acids). In addition, this vitamin is also a cofactor of transketolase, an enzyme involved in the tricarboxylic acid cycle (2,3). Therefore, thiamine deficiency can lead to the onset of anaerobic metabolism, associated with severe lactic acidosis. The classical clinical presentations of thiamine deficiency are Wernicke-Korsakoff encephalopathy; peripheral neuropathy, muscle weakness and anorexia (dry beriberi), high-output heart failure (wet beriberi), and beriberi associated with shock (Shoshin beriberi) (4-6).