Amoxicillin-Induced Hemolytic Anemia in a Child with Glucose 6-Phosphate Isomerase Deficiency

Ruggiero, Simona; Gallo, Mariapina; Simeone, Gelsomina; Miceli, Sofia; Matarese, Rosaria; Nobili, Brúno

doi:10.1345/aph.1p030

Cited by 12 publications

(12 citation statements)

References 11 publications

(5 reference statements)

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“…The only reported case of amoxicillin-associate hemolytic anemia occurred a patient with G6PD isomerase deficiency receiving 50mg/kg/ day, and no cases have been reported in patients with G6PDD. [1] Although generally safe for patients with G6PDD, acetaminophen has numerous potential mechanisms that may predispose susceptible individuals to oxidative stressors. It is well established that acetaminophen, through its toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQI), causes oxidative hepatocellular damage after depletion of glutathione (GSH).…”

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confidence: 99%

Hemolytic crisis following acetaminophen overdose in a patient with G6PD deficiency

Rickner

Cao

Simpson

2016

Clinical Toxicology

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confidence: 99%

Hemolytic crisis following acetaminophen overdose in a patient with G6PD deficiency

Rickner

Cao

Simpson

2016

Clinical Toxicology

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“…Lack of NADPH can be a cause of destabilization of the erythrocyte membrane, lysis, and the onset of chronic hemolytic anemia. Lack of reducing agents such as NADPH and GSH in the presence of GPI deficiency may be the cause of a hemolytic crisis due to exogenous oxidants such as infections or drugs (Rossi et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…- Rossi et al (2010) reported on nonimmune hemolytic anemia caused by amoxicillin in a child with a GPI deficiency. Decreasing the content of reducing equivalents in case of deficiency of this enzyme can lead to impairment of the system that removes free radicals generated by antibiotics, thereby resulting in perioxidative damage to hemoglobin, red blood cell enzymes, and soluble constituents, thereby leading to hemolytic crisis.…”

Section: Discussionmentioning

confidence: 99%

“…However, in many cases, the decline in the activity of the enzyme seems to be clearly not enough to disrupt the normal metabolism. In hemolytic anemia associated with enzymopathy, the activity of other key enzymes and the metabolites' content may exceed the normal level up to several times, be-cause of the high reticulocytosis (Rossi et al, 2010, Warang et al, 2012Mojzikova et al, 2018;Fermo et al, 2019). It is known that young erythrocytes, formed in conditions of intense erythropoiesis, are unstable and age rapidly, especially in the presence of unstable enzymes (Mairbäurl, 2018).…”

Section: Introductionmentioning

confidence: 99%

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In silico study of peculiarities of metabolism of erythrocytes with glucosephosphate isomerase deficiency

Dotsenko

2019

Regul. Mech. Biosyst.

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Glucose phosphate isomerase (GPI) deficiency, the third most common cause of hereditary nonspherocytic hemolytic anemia, is associated with the mutation of the GPI gene. The results of the GPI deficiency are premature aging of erythrocytes, macrocytosis, reticulocytosis, minor splenomegaly, hyperbilirubinemia and hyperferritinemia, and hemolytic crisis under the influence of exogenous oxidants such as infections or drugs. Regarding the the lack of GPI correction drugs, the theoretical substantiation of supportive therapy based on system biology approaches that would allow the analysis of the relationships between numerical metabolic processes in a cell would be beneficial. The stoichiometric model of erythrocytes’ steady state metabolism, including the pathways of Embden-Meyerhof and pentose phosphate (PPP), purine metabolism cycles and glutathione synthesis, has been developed. To predict the redistribution of metabolic flows in erythrocytes under conditions of GPI deficiency, we used the flux balance analysis (FBA). In this approach, calculations of the elementary flux modes (EFMs) and the control-effective flux (CEF) have been performed. Using the CEF evaluation approach, effective profiles of enzymatic reactions depending on the degree of enzyme deficiency were obtained. It has been shown that these relationships can be the basis for future experimental studies. Analysis of the profiles of enzymatic reactions of metabolic networks suggests that erythrocytes are capable of metabolizing other substrates that contribute to overcoming the effects of energy stress in the case of enzymopathies. So, it is shown that erythrocytes can effectively use SAM and adenosine as alternative energy sources. It has been established that the GPI enzymopathy results in a decrease in the flow through the glycolysis and pentose phosphate pathway, resulting in a decrease in the content of such reducing agents as NADPH and GSH, ATP. The processes of the GSH synthesis from amino acids in the cell are shown to be suppressed. Decreased content of NADPH and GSH cause the premature aging of erythrocytes. The target therapeutic approaches that influence the behaviour of the metabolic network of erythrocytes are discussed.

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“…In this condition, the erythrocyte membrane loses its stabilization and a chronic non-spherocytic anemia develops. In case of exposure to oxidants including viral infections or antibiotherapy, acute hemolytic attacks may be observed as a result of decreased synthesis of antioxidant substances (5). Hydrops fetalis may even be observed, when the disease has a severe course (6).…”

Section: Discussionmentioning

confidence: 99%

An infant with chronic hemolytic anemia

2014

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A 7-month old male patient was referred to our clinic because of mild anemia and icteric sclerae. The patient had a history of intensive phototherapy which was applied for three days because of neonatal jaundice which developed on the second day of life. In the follow-up performed in the external center where the delivery took place, moderate reticulocytosis, increased indirect bilirubin and decreased haptoglobulin which suggested chronic hemolysis were found. In the familial history, it was learned that the parents were third degree relatives. A history of chronic jaundice and anemia was present in the patient's aunt's daughter who was one year old. On physical examination, the conjunctivae were slightly pale, the sclerae were icteric; the spleen was nonpalpable and percussion of the Traube's space was found to be normal. The neuromotor development of the patient was appropriate for age. The necessary laboratory tests were performed.

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Amoxicillin-Induced Hemolytic Anemia in a Child with Glucose 6-Phosphate Isomerase Deficiency

Abstract: This report reinforces the hypothesis that a drug-sensitivity reaction is closely related to a genetically transmitted enzyme deficiency.

Cited by 12 publications

References 11 publications

Hemolytic crisis following acetaminophen overdose in a patient with G6PD deficiency

Hemolytic crisis following acetaminophen overdose in a patient with G6PD deficiency

In silico study of peculiarities of metabolism of erythrocytes with glucosephosphate isomerase deficiency

An infant with chronic hemolytic anemia

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