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Published on: February 7, 2013
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.
Objective:
To describe the first case of amoxicillin-induced nonimmune hemolytic anemia in a child with glucose-6-phosphate isomerase (GPI) deficiency.
Case Summary:
A 3-year-old boy with GPI deficiency was admitted for upper respiratory tract infection and fever. The patient was treated with a standard dose of amoxicillin (50 mg/kg/day). On hospital admission, the child had a chronic moderately low hemoglobin level (8.6 g/dL), but within 24 hours of the first amoxicillin dose, the hemoglobin level markedly decreased (5.8 g/dL), the reticulocyte level increased (58%), and the urine darkened. Results of the direct and indirect Coomb's tests were negative and the acute hemolytic phase ended spontaneously 8 days after amoxicillin withdrawal (hemoglobin 9.5 g/dL, reticulocytes 22%).
Discussion:
All previous cases of amoxicillin-induced hemolytic anemia have been attributed to an immune mechanism. Given the absence of anti-reticulocyte antibodies (Coomb's test), we suggest that the amoxicillin-induced hemolytic anemia in our patient occurred via a nonimmune mechanism favored by the child's GPI deficiency. Based on a MEDLINE search, we believe this to be the first report of amoxicillin-induced nonimmune hemolytic anemia in a child with GPI deficiency. GPI deficiency has been associated with well-compensated chronic hemolytic anemia that can become clinically relevant consequent to the administration of drugs. GPI deficiency can lead to impairment of the system that removes free radicals generated by amoxicillin, thereby resulting in oxidation of hemoglobin and destabilization of red cell membranes, with acute hemolysis and severe hemoglobinuria. The Naranjo probability score was consistent with a probable relationship between the hemolytic anemia and amoxicillin therapy.
Conclusions:
This report reinforces the hypothesis that a drug-sensitivity reaction is closely related to a genetically transmitted enzyme deficiency.
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