Amoxicillin-induced hemolytic anemia in a child with glucose 6-phosphate isomerase deficiency

Francesca Rossi1, Simona Ruggiero, Mariapina Gallo

  • 1Department of Paediatrics, Second University of Naples, Naples, Italy.

Insights

Amoxicillin caused nonimmune hemolytic anemia in a child with glucose-6-phosphate isomerase (GPI) deficiency. This case highlights how genetic enzyme deficiencies can trigger drug reactions, leading to acute hemolysis.

Area of Science:

  • Pediatric Hematology
  • Pharmacogenomics
  • Biochemistry

Background:

  • Glucose-6-phosphate isomerase (GPI) deficiency is a rare genetic disorder.
  • GPI deficiency typically presents as well-compensated chronic hemolytic anemia.
  • Drug administration can exacerbate underlying enzyme deficiencies, leading to acute hemolytic crises.

Observation:

  • A 3-year-old boy with known GPI deficiency developed acute hemolytic anemia within 24 hours of amoxicillin administration.
  • The patient exhibited a significant drop in hemoglobin, elevated reticulocyte count, and darkened urine.
  • Direct and indirect Coombs tests were negative, ruling out immune-mediated hemolysis.

Findings:

  • This case represents the first documented instance of amoxicillin-induced nonimmune hemolytic anemia in a child with GPI deficiency.
  • The mechanism is proposed to involve amoxicillin-induced oxidative stress overwhelming the impaired free radical scavenging system in GPI-deficient red blood cells.
  • The Naranjo probability score indicated a probable link between amoxicillin and the observed hemolytic anemia.

Implications:

  • This finding underscores the critical role of genetic enzyme deficiencies in drug sensitivity reactions.
  • It suggests that patients with GPI deficiency may be at increased risk for nonimmune hemolytic anemia when treated with certain drugs like amoxicillin.
  • Further research into drug metabolism and genetic predispositions is warranted to prevent adverse drug events.
Abstract

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