Hemolytic jaundice induced by pharmacological dose ascorbic acid in glucose-6-phosphate dehydrogenase deficiency

Abstract

Rationale:Hemolysis induced by high dose ascorbic acid (AA) in patients with G6PD deficiency has been reported, but is rare. To our knowledge, this is the first reported case of a male with G6PD deficiency, coexpressed with cholecystolithiasis and cholecystitis, who developed extreme hemolysis and hyperbilirubinemia after receiving pharmacological doses ascorbic acid infusion.Patient concerns:A 27-year-old man history with glucose-6-phosphate dehydrogenase deficiency was admitted to our hospital because of cholecystolithiasis and cholecystitis. He appeared with scleral jaundice and very deep colored urine after receiving pharmacological doses ascorbic acid infusion.Diagnoses:Clinical findings when combined with his medical history and various laboratory results confirmed the diagnosis as hemolysis and hyperbilirubinemia induced by ascorbic acid.Interventions:The patient was treated with steroids, hepatoprotective drugs, and folic acid in addition avoidance of agents with known hemolysis risk (such as vitamin C).Outcomes:As a result, the patient's symptoms from hemolytic jaundice improved, hemoglobin remained stable, and the patient was discharged 11 days later.Lessons:Clinicians should bear in mind the possibility that vitamin C exposure may result in hemolysis in patients with G6PD deficiency, especially in those with known severe disease.

Influence of Vitamin C on Antioxidant Capacity of In Vitro Perfused Porcine Kidneys

“…We assume that the effect of vitamin C on the RBCs is one of the main effects which might contribute to improved kidney function during in vitro kidney perfusion, especially as a counterpart to the impaired microcirculation in I/R-settings, but the exact mechanisms have to be further elucidated. A possible negative effect of vitamin C is hemolysis, which was shown in glucose-6-phosphate dehydrogenase (G6DP)-deficient patients [34], however, we did not detect increased hemolysis in comparison to the control group.…”

The prevalence of glucose-6-phosphate dehydrogenase deficiency in the Cape Verdean population in the context of malaria elimination

“…These results are consistent with results from a preliminary study in the country in 2010 [36], and similary to the reports from other studies conducted in other African countries, as Mauritania [37], Uganda [38], Mozambique [39] Senegal [40,41] and Gambia [42]. The high G6PDd prevalence in the African or Afro-descendant population as shown by several studies [39][40][41][42][43] may reflect the population's exposure to malaria endemicity or ethnicity related [8][9][10][11][12][13][14][15][16]. However, our results do not allow drawing any conclusions of this nature since almost all the participants of this study were of Cape Verdean citizenship and no ethnic classification was made.…”

“…The schizontocidal treatment for non-falciparum malaria is done with the AL or Artesunate + Amodiaquine, following the WHO guidelines [7]. Nevertheless, this use of primaquine is carried out regardless the knowledge of the frequency of the Glucose-6-phosphate-dehydrogenase (G6PD) deficiency among the target population, which endangers all the patients harbouring this deficiency with the risk of haemolysis [8][9][10][11][12].…”

The impact of using primaquine without prior G6PD testing: a case series describing the obstacles to the medical management of haemolysis

“…The second case, presented with an elevated methaemoglobin 19 , a nearly normal haematocrit and normal reticulocyte count indicating that the bulk of haemolysis occurred after primaquine had been stopped. Administration of Vitamin C, which has been shown to cause haemolysis in G6PD deficient subjects 13, 14, 20 might have contributed to continued haemolysis. This patient also demonstrated reduced reticulocyte production, which may have been caused by iron deficiency or a concomitant haemoglobinopathy 21 .…”