From the Guidelines
Thiamine (Vitamin B1) plays a crucial role in the recovery of lactic acidosis-related liver failure by serving as an essential cofactor for several key enzymes involved in cellular energy metabolism, and its administration is recommended at a dose of 100-300 mg/day IV for 3-4 days in patients admitted to emergency or intensive care, as stated in the espen micronutrient guideline 1.
Key Points
- Thiamine is essential for the pyruvate dehydrogenase complex, which converts pyruvate to acetyl-CoA instead of lactic acid, thereby reducing lactate levels and supporting liver recovery.
- Thiamine deficiency is common in patients with liver disease, alcoholism, and malnutrition, which are risk factors for developing lactic acidosis.
- Prompt thiamine administration can rapidly improve metabolic function and prevent progression to more severe conditions like Wernicke's encephalopathy, particularly in alcoholic liver disease.
- The recommended dose of thiamine is 100-300 mg/day IV for 3-4 days, as stated in the espen micronutrient guideline 1, which has a grade of recommendation B and a strong consensus of 80%.
Clinical Considerations
- Thiamine supplementation is crucial in patients with liver disease, especially those with a history of alcoholism or malnutrition, to prevent thiamine deficiency and related complications.
- Thiamine administration should be considered in patients with lactic acidosis and liver dysfunction, as it can help restore proper energy metabolism pathways and support liver recovery.
- The espen guideline on clinical nutrition in liver disease 1 and the easl clinical practice guidelines on nutrition in chronic liver disease 1 provide additional guidance on nutrition and micronutrient supplementation in patients with liver disease, but the most recent and highest quality study, the espen micronutrient guideline 1, should be prioritized.
From the Research
Role of Thiamine in Recovery of Lactic Acidosis-Related Liver Failure
- Thiamine plays a critical role in energy metabolism, and its deficiency can lead to lactic acidosis, especially in patients receiving total parenteral nutrition 2, 3, 4, 5, 6.
- Thiamine deficiency can cause mitochondrial dysfunction, leading to impaired clearance of lactic acid and resulting in lactic acidosis 2, 4.
- Administration of thiamine has been shown to rapidly reverse severe lactic acidosis in critically ill patients, improving clinical and metabolic conditions 3, 4, 5, 6.
- Thiamine supplementation is essential for patients receiving total parenteral nutrition, and its deficiency should be considered in the differential diagnosis of lactic acidosis 2, 3, 4, 5, 6.
- The resolution of lactic acidosis after thiamine administration has been observed in various cases, including patients with liver failure and those undergoing liver transplantation 2, 3.
- Thiamine deficiency can be prevented by integrating thiamine supplementation into parenteral nutrition and other forms of nutrition support 4, 5, 6.