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case_report·pediatrics, oncology, hematology, nutrition, micronutrients·PMC10605394

Severe Lactic Acidosis Caused by Thiamine Deficiency in a Child with Relapsing Acute Lymphoblastic Leukemia: A Case Report

Children · 8 authors, 6 centres

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TL;DR

This is a case report of a 5-year-old boy with relapsing leukemia who developed severe lactic acidosis during chemotherapy, which was ultimately attributed to thiamine deficiency. The patient's condition improved significantly after thiamine supplementation.

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The paper describes a 5-year-old boy with central nervous system relapse of acute lymphoblastic leukemia who developed drug-induced pancreatitis and paralytic ileus, leading to prolonged glucosaline infusion. He subsequently developed severe lactic acidosis (pH 7.0, lactates 253 mg/dL) with hypoglycemia and liver injury. Initial management with dextrose and continuous venovenous hemodiafiltration (CVVHDF) provided only temporary improvement. Thiamine deficiency was suspected, and parenteral nutrition with thiamine was administered, resulting in rapid normalization of lactates and pH. The authors conclude that thiamine deficiency is an important, treatable cause of lactic acidosis in long-term hospitalized pediatric oncology patients.

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case_report

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pediatrics

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ORIGINAL PAPER

PMC10605394

Severe Lactic Acidosis Caused by Thiamine Deficiency in a Child with Relapsing Acute Lymphoblastic Leukemia: A Case Report

Children

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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.

CITATION EXPORT

Francesco Baldo, Enrico Drago, Daniela Nisticò et al.. Severe Lactic Acidosis Caused by Thiamine Deficiency in a Child with Relapsing Acute Lymphoblastic Leukemia: A Case Report. Children. (2023). https://doi.org/10.3390/children10101602

AUTHORS

8 · 6 CENTRES

Francesco Baldo, Enrico Drago, Daniela Nisticò, Silvia Buratti, Michaela Calvillo, Concetta Micalizzi, Maria Cristina Schiaffino, Mohamad Maghnie

1Institute for Maternal and Child Health IRCCS Burlo Garofolo, 34137 Trieste, Italy
2Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, 16147 Genoa, Italy
3Department of Medicine, Surgery and Health Sciences, University of Trieste, 34127 Trieste, Italy
4Neonatal and Pediatric Intensive Care Unit, IRCCS Giannina Gaslini, 16147 Genoa, Italy
5Hematology Unit, IRCCS Giannina Gaslini, 16147 Genoa, Italy; [email protected] (M.C.);
6Pediatric Clinic and Endocrinology Unit, IRCCS Giannina Gaslini, 16147 Genoa, Italy

EDITOR / REVIEWER

Pierluigi Marzuillo