Related Experiment Video
Updated: Jul 11, 2026
09:28
One-step Metabolomics: Carbohydrates, Organic and Amino Acids Quantified in a Single Procedure
Published on: June 26, 2010
Metabolic acidosis and thiamine deficiency
1Division of Endocrinology, Metabolism, and Nutrition, Mayo Clinic Rochester, MN 55905, USA.
Mayo Clinic Proceedings
|March 25, 1999
Summary
Thiamine deficiency in patients receiving parenteral nutrition can cause lactic acidosis. Supplementing thiamine resolves the condition, highlighting its critical role in glucose metabolism and preventing severe complications.
Area of Science:
- Biochemistry
- Clinical Medicine
- Nutritional Science
Background:
- Parenteral nutrition (PN) is a life-sustaining therapy for individuals unable to absorb nutrients orally.
- Nutrient deficiencies can arise from inadequate PN formulations, impacting patient health.
- Thiamine (vitamin B1) is a crucial cofactor in carbohydrate metabolism.
Observation:
- A 19-year-old patient on home parenteral nutrition developed lactic acidosis.
- Investigation revealed the absence of multivitamins, specifically thiamine, in her PN formula.
- The patient showed significant clinical improvement and resolution of acidosis after thiamine administration.
Findings:
- Thiamine deficiency is a direct cause of lactic acidosis in patients receiving PN.
- Thiamine is essential for normal glucose metabolism; its absence impairs this process.
- Lactic acidosis due to thiamine deficiency should be considered in the differential diagnosis for patients on PN.
Implications:
- Healthcare providers must ensure adequate thiamine supplementation in all parenteral nutrition regimens.
- Recent shortages of intravenous multivitamins have exacerbated thiamine deficiency cases and associated fatalities.
- Routine monitoring for vitamin levels and prompt supplementation are crucial for patients on long-term PN.
Related Concept Videos
01:30Vitamins
Vitamins, derived from the Latin word for life, are essential organic substances required in small quantities for optimal growth and overall well-being. Unlike other organic nutrients, vitamins don't act as sources of energy or building materials but rather facilitate these nutrients' utilization by the body. Vitamins are predominantly coenzymes, assisting enzymes in specific chemical actions, like the oxidation of glucose for energy involving B vitamins. Most vitamins are not produced in our...
01:20Inborn Errors of Metabolism
Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
01:24Diagnosing Acidosis and Alkalosis
Diagnosing acid-base imbalances involves systematically analyzing arterial blood samples, focusing on three key measurements: pH, bicarbonate (HCO3−) concentration, and carbon dioxide partial pressure (PCO2). This analysis follows a four-step process that helps identify the imbalance's underlying cause and nature.
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2 and HCO3− values are examined to...
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2 and HCO3− values are examined to...
01:25Diabetic Ketoacidosis l: Introduction
DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
01:22Diabetic Ketoacidosis ll: Pathophysiology
Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...