Hemolytic crisis following acetaminophen overdose in a patient with G6PD deficiency

Rickner, Shannon S.; Cao, Dazhe; Simpson, Serge Emile

doi:10.1080/15563650.2016.1222415

Cited by 9 publications

(5 citation statements)

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“…7 In S.S. Rickner et al case report, the patient presented jaundice at the time of admission and also the patient developed hepatotoxicity thirty-three hour post ingestion in addition to a haemoglobin decline of 5g/dl in four days despite resolving hepatotoxicity. 10 Our case report had a similar finding to the previous case reports. A number of factors favours acetaminophen as the probable cause of haemolysis such as evidence from previous case reports and the other drugs (Chlorpheniramine maleate, Phenylephrine, Sodium Citrate) that the patient taken have not been reported to cause haemolysis in G6PD deficient patients.…”

Section: Discussionsupporting

confidence: 90%

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A Case Report of Haemolysis in a G6PD Deficient Child due to Acetaminophen Overdose Resulted from Parental Unawareness

Panachiyil¹,

Babu²,

Juny³

et al. 2019

JYP

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Although acetaminophen is considered a low-risk analgesic and antipyretic drug in Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency patients, cases of haemolysis following acetaminophen overdose have been published in the literature. An eleven-month-old boy was admitted to the paediatrics department of the hospital with the complaints of haematuria and yellowish discolouration of the eyes since one day. He had been previously diagnosed as G6PD deficiency. Unknowingly the mother of the child simultaneously given three different brands of acetaminophen prescribed by different paediatricians at various times resulted in an overdose of acetaminophen. On admission, the child had haemoglobin of 4 g/dl. The laboratory results were suggestive of haemolytic process. Direct Coombs test was negative. Acetaminophen overdose was the most likely cause of the haemolysis. The child was managed conservatively and no further episodes of haematuria was observed. Naranjo and WHO causality assessments were done, indicating a probable relationship between the patient's symptoms and the use of acetaminophen. Acetaminophen overdose induced haemolysis due to G6PD deficiency is an unusual complication which is generally reported in children. The majority of G6PD deficient individuals remains asymptomatic until a trigger (during certain infections or fava beans or certain drugs) induces haemolysis. We document a case report of acetaminophen overdose induced haemolysis in a baby with G6PD deficiency and conclude that there is a need for parental education about the drugs that can trigger haemolysis in G6PD deficient children and also about the different brands of the same drug available in the market.This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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Section: Discussionsupporting

confidence: 90%

“…1 There are several case reports of haemolysis as a potential complication after acetaminophen overdose in G6PD deficient individuals. [6][7][8][9][10] We report a case of haemolysis attributed to acetaminophen overdose in a patient with known G6PD deficiency.…”

Section: Introductionmentioning

confidence: 98%

A Case Report of Haemolysis in a G6PD Deficient Child due to Acetaminophen Overdose Resulted from Parental Unawareness

Panachiyil¹,

Babu²,

Juny³

et al. 2019

JYP

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“…Several mechanisms could explain the increase of unconjugated bilirubin after acetaminophen overdose. Hemolysis is not a classical complication of acetaminophen overdose except in some patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency [ 3 ]. It was also advocated that acetaminophen might impair the uptake of bilirubin from the blood by the liver, either by competing with bilirubin for the binding sites on the liver cell membrane or in the cytoplasm or by damaging the uptake mechanism [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Unconjugated Hyperbilirubinemia in Acetaminophen-Related Acute Liver Failure

Philippart,

Mesland,

Haufroid

et al. 2024

Am J Case Rep

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Patient: Male, 52-year-old Final Diagnosis: Fatal hepatic failure after acetaminophen overdose Symptoms: Hepatic failure Clinical Procedure: — Specialty: Gastroenterology and Hepatology Objective: Unusual clinical course Background: In the absence of liver transplantation, the natural history of acetaminophen-induced liver failure is characterized by a progressive increase of liver function tests, including bilirubin mainly as its conjugated form. The presence of high levels of unconjugated bilirubin is more unusual; its etiology is unclear and its prognostic factor has been poorly investigated. Case Report: A 52-year-old man with a history of chronic analgesics, alcohol, and illicit drug abuse developed acute liver failure in relationship with the ingestion of largely supra-therapeutic doses of acetaminophen over the days preceding admission. The patient received the classical N-acetylcysteine treatment regimen for acetaminophen overdose. Clinical course was characterized by a progressive worsening of the neurological condition, evolving to grade IV encephalopathy. Coagulation disorders persisted, with factor V level <10%. He fulfilled the criteria for liver transplantation, but this option was rejected after a careful psychiatric evaluation. Laboratory investigations revealed a progressive increase in serum unconjugated bilirubin until his death. As evidence for hemolysis was lacking, acquired deficit in bilirubin glucuronidation appeared likely and diagnosis of Gilbert’s syndrome was excluded. Conclusions: After the exclusion of other causes of high unconjugated bilirubin levels, the progressive increase in unconju-gated bilirubin can reflect a persistent defect in bilirubin conjugation in relationship with liver centrilobular injury, but the relationship with acetaminophen-glucuronidation is not known and there are insufficient data to affirm that the ratio unconjugated/conjugated bilirubin could be used as a prognostic factor.

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“…It has been reported that an APAP overdose in glucose-6-phosphate dehydrogenase-deficient individuals causes hemolytic anemia (Rickner et al, 2017). Glucose-6-phosphate dehydrogenase is a critical enzyme in the redox metabolism of RBCs, which enables RBCs to counterbalance the oxidative stress triggered by several drugs, such as APAP.…”

Section: Discussionmentioning

confidence: 99%

Preexisting diabetes mellitus had no effect on the no-observed-adverse-effect-level of acetaminophen in rats

et al. 2020

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Information on the safety of chemical substances in patients with various preexisting conditions remains limited. Acetaminophen was added to the basal diet at 0, 80, 253, 800, 2530, or 8000 ppm and administered to type 2 diabetes mellitus rats (GK/Jcl) and the control male rats (Wistar) for 13 weeks. Both strains treated with 8000 ppm acetaminophen (561.4 and 567.7 mg/kg body weight/ day, GK/Jcl and Wistar rats, respectively) showed decreased levels of red blood cell counts, blood urea nitrogen, creatinine, and total bilirubin compared to those of non-treated rats. Treatment with 8000 ppm of acetaminophen reduced the blood glucose and hemoglobin A1c levels of GK/Jcl rats. An increase in the relative weights of the kidneys and liver, and a decrease in the weight of the salivary glands were observed in both GK/Jcl and Wistar rats treated with 8000 ppm acetaminophen relative to those of nontreated control rats. Microscopically, both strains treated with 2530 (174.3 and 164.2 mg/kg body weight/ day, GK/Jcl and Wistar rats, respectively) or 8000 ppm acetaminophen showed hepatocellular hypertrophy and degenerative lesions in the salivary glands, whereas similar lesions were not observed in nontreated rats. In conclusion, the no-observed-adverse-effect-level of acetaminophen was 800 ppm in both diabetic and control rats.

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Hemolytic crisis following acetaminophen overdose in a patient with G6PD deficiency

Cited by 9 publications

References 5 publications

A Case Report of Haemolysis in a G6PD Deficient Child due to Acetaminophen Overdose Resulted from Parental Unawareness

A Case Report of Haemolysis in a G6PD Deficient Child due to Acetaminophen Overdose Resulted from Parental Unawareness

Unconjugated Hyperbilirubinemia in Acetaminophen-Related Acute Liver Failure

Preexisting diabetes mellitus had no effect on the no-observed-adverse-effect-level of acetaminophen in rats

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