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Published on: September 18, 2013
Severe Lactic Acidosis Caused by Thiamine Deficiency in a Child with Relapsing Acute Lymphoblastic Leukemia: A Case
Francesco Baldo1, Enrico Drago2, Daniela Nisticò3
1Institute for Maternal and Child Health IRCCS Burlo Garofolo, 34137 Trieste, Italy.
Insights
Thiamine deficiency can cause lactic acidosis, even in well-nourished patients. Early thiamine administration is crucial for managing this rare but serious condition in hospitalized children.
Area of Science:
- Biochemistry
- Pediatrics
- Critical Care Medicine
Background:
- Lactic acidosis is a critical condition resulting from lactic acid imbalance.
- Thiamine deficiency is a rare cause of lactic acidosis, particularly in non-malnourished populations.
- Acute lymphoblastic leukemia (ALL) treatment can involve complications like pancreatitis and ileus.
Observation:
- A 5-year-old boy with relapsed ALL developed severe lactic acidosis, hypoglycemia, and liver injury during chemotherapy.
- Despite fluid infusion and continuous venovenous hemodiafiltration (CVVHDF), lactic acidosis persisted.
- Symptoms improved significantly after parenteral nutrition and thiamine administration.
Findings:
- The patient's lactic acidosis and hypoglycemia resolved with thiamine supplementation, suggesting mitochondrial dysfunction due to thiamine deficiency.
- This case highlights an uncommon etiology of lactic acidosis in a critically ill pediatric patient.
- Thiamine deficiency should be considered in prolonged critical illness with unexplained lactic acidosis.
Implications:
- Early recognition and management of thiamine deficiency can prevent severe metabolic derangements in critically ill patients.
- This case underscores the importance of considering vitamin deficiencies in complex pediatric critical care scenarios.
- Investigating thiamine levels may be warranted in patients with persistent lactic acidosis unresponsive to standard treatments.
Abstract:
Lactic acidosis is characterized by an excessive production of lactic acid or by its impaired clearance. Thiamine deficiency is an uncommon cause of lactic acidosis, especially in countries where malnutrition is rare. We describe the case of a 5-year-old boy who presented with a central nervous system relapse of acute lymphoblastic leukemia. During the chemotherapy regimen, the patient developed drug-induced pancreatitis with paralytic ileus requiring prolonged glucosaline solution infusion. In the following days, severe lactic acidosis (pH 7.0, lactates 253 mg/dL, HCO3- 8 mmol/L) was detected, associated with hypoglycemia (42 mg/dL) and laboratory signs of acute liver injury. Due to the persistent hypoglycemia, the dextrose infusion was gradually increased. Lactates, however, continued to raise, so continuous venovenous hemodiafiltration was started. While lactates initially decreased, 12 h after CVVHDF suspension, they started to raise again. Assuming that it could have been caused by mitochondrial dysfunction due to vitamin deficiency after prolonged fasting and feeding difficulties, parenteral nutrition and thiamine were administered, resulting in a progressive reduction in lactates, with the normalization of pH during the next few hours. In the presence of acute and progressive lactic acidosis in a long-term hospitalized patient, thiamine deficiency should be carefully considered and managed as early as possible.
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