Thiamine and lactic acidosis

The approach to a lactic acidosis involves separating it into two possible classes, termed type A or type B. Type A is classified as lactic acidosis secondary to tissue hypoperfusion. This is usually not a mystery, and the patient has signs of end-organ damage, tissue hypoxia and hypotension. Type B lactic acidosis is felt to be from some derangement in metabolism of lactate, including:


1. Drugs - metformin use, HIV medications (through mitochondrial dysfunction)

2. Alcohol - decrease gluconeogenesis

3. Malignancy - suspected to be secondary to increased cell turnover, though the mechanism is somewhat unclear, this is more often seen in leukemia/lymphoma

4. Type-D-lactate- present in patients with short gut syndrome, bowel bacteria (usually lactobacillis) produce D-lactate which is absorbed but cannot be metabolised by endogenous LDH leading to accumulation.

5. Liver dysfunction

Today we discussed a patient that had an elevated lactate of unclear cause. The patient was treated with thiamine with rapid improvement, which raises nutritional deficiency as a potential contributor to type B lactic acidosis.

Thiamine (vitamin B1) is a water soluble molecule that is required for aerobic metabolism. It acts as a cofactor for several enzymes present in the glycolysis pathway. Thiamine deficiency prevents pyruvate from converting into Acetyl-CoA, which is the entry point into the Krebs cycle, which is responsible for ATP production and NADH which is utilized in the electron transport chain. As a result, pyruvate accumulates and is metabolized into lactate resulting in acidosis.

Thiamine deficiency can occur quickly. Because it is water soluble it is not readily stored in fat and levels lowering the total body amounts. It is estimated that thiamine deficiency can develop as quickly as four weeks in poor nutritional intake. In cases of thiamine deficiency lactate production has been seen as early as 1-3 weeks. Risk factors for thiamine deficicency include, poor nutritional intake, folate deficiency, alcohol use, malabsorption, TPN and renal disease (specifically dialysis/peritoneal dialysis).

So next time you see a lactic acidosis in the absence of tissue hypoperfusion, consider vitamin B1 deficiency.