Detection of Occult Glomerular Dysfunction in Glucose Six Phosphate Dehydrogenase Deficiency Anemia

Hakeem, Gehan Abdel; Naem, Emad; Swelam, Salwa; Fotoh, Laila Aboul; Mazary, Abdel Azeem Al; Fadeil, Ashraf Abdel; Hafez, Asmaa Abdel

doi:10.4084/mjhid.2016.038

Cited by 12 publications

(7 citation statements)

References 27 publications

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“…Renal impairment is well described in favism and drug-induced acute hemolytic anemia and is usually reversible [38, 39]. The pathogenesis is incompletely defined but appears to be related to increased renal cellular uptake of free Hb that is converted to heme, resulting in oxidant damage to the tubules and glomeruli [40].…”

Section: Discussionmentioning

confidence: 99%

“…Most of our patients had normal creatinine concentrations, but 2 G6PD − patients developed stage 1 acute kidney injury [26], which resolved without intervention. Reversible renal impairment was also seen in 30 Egyptian children aged 5 months to 7.5 years with acute hemolytic anemia (due to favism in 25), whose median estimated glomerular filtration rate increased from 73.6 mL/minute/1.73 m 2 (range, 41.25‒125 mL/minute/1.73 m 2 ) to 89.6 mL/minute/1.73 m 2 (range, 82.5‒475 mL/minute/1.73 m 2 ) 1 month after hemolysis [39].…”

Section: Discussionmentioning

confidence: 99%

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Hemolytic Dynamics of Weekly Primaquine Antirelapse Therapy Among Cambodians With Acute Plasmodium vivax Malaria With or Without Glucose-6-Phosphate Dehydrogenase Deficiency

Taylor

Kheng

Muth

et al. 2019

The Journal of Infectious Diseases

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Background Hemoglobin (Hb) data are limited in Southeast Asian glucose-6-phosphate dehydrogenase (G6PD) deficient (G6PD−) patients treated weekly with the World Health Organization–recommended primaquine regimen (ie, 0.75 mg/kg/week for 8 weeks [PQ 0.75]). Methods We treated Cambodians who had acute Plasmodium vivax infection with PQ0.75 and a 3-day course of dihydroartemisinin/piperaquine and determined the Hb level, reticulocyte count, G6PD genotype, and Hb type. Results Seventy-five patients (male sex, 63) aged 5–63 years (median, 24 years) were enrolled. Eighteen were G6PD deficient (including 17 with G6PD Viangchan) and 57 were not G6PD deficient; 26 had HbE (of whom 25 were heterozygous), and 6 had α-/β-thalassemia. Mean Hb concentrations at baseline (ie, day 0) were similar between G6PD deficient and G6PD normal patients (12.9 g/dL [range, 9‒16.3 g/dL] and 13.26 g/dL [range, 9.6‒16 g/dL], respectively; P = .46). G6PD deficiency (P = <.001), higher Hb concentration at baseline (P = <.001), higher parasitemia level at baseline (P = .02), and thalassemia (P = .027) influenced the initial decrease in Hb level, calculated as the nadir level minus the baseline level (range, −5.8–0 g/dL; mean, −1.88 g/dL). By day 14, the mean difference from the day 7 level (calculated as the day 14 level minus the day 7 level) was 0.03 g/dL (range, −0.25‒0.32 g/dL). Reticulocyte counts decreased from days 1 to 3, peaking on day 7 (in the G6PD normal group) and day 14 (in the G6PD deficient group); reticulocytemia at baseline (P = .001), G6PD deficiency (P = <.001), and female sex (P = .034) correlated with higher counts. One symptomatic, G6PD-deficient, anemic male patient was transfused on day 4. Conclusions The first PQ0.75 exposure was associated with the greatest decrease in Hb level and 1 blood transfusion, followed by clinically insignificant decreases in Hb levels. PQ0.75 requires monitoring during the week after treatment. Safer antirelapse regimens are needed in Southeast Asia. Clinical Trials Registration ACTRN12613000003774.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hemolytic Dynamics of Weekly Primaquine Antirelapse Therapy Among Cambodians With Acute Plasmodium vivax Malaria With or Without Glucose-6-Phosphate Dehydrogenase Deficiency

Taylor

Kheng

Muth

et al. 2019

The Journal of Infectious Diseases

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“…Severe cases of G6PD deficiency can cause damage to the kidneys and liver, but the mechanism underlying the liver damage is poorly understood. 4 , 6 …”

Section: Discussionmentioning

confidence: 99%

Liver Failure in Neonates With G6PD Deficiency

Shah

Gopalareddy

2022

ACG Case Rep J

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a commonly inherited enzyme defect that can present with hemolysis, hyperbilirubinemia, and jaundice and may cause kidney and liver dysfunction. G6PD deficiency may serve as a cofactor for chronic liver disease; however, an association with liver failure is not well described. We present the cases of 2 neonates with G6PD deficiency and progressive liver failure resistant to treatment with ursodiol that eventually required liver transplantation. Our cases underscore the importance of monitoring liver function in jaundiced neonates with underlying G6PD deficiency and demonstrate the potential precipitation of liver disease by G6PD deficiency.

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“…pneumonia, typhoid fever), drugs [e.g. the 8-aminoquinolines, primaquine (PQ) and tafenoquine (TQ)], and fava beans [ 3 , 4 , 5 , 6 , 7 , 8 ] are well established causes of oxidant-related acute haemolysis (AH) that may necessitate a blood transfusion [ 7 , 9 , 10 , 11 , 12 ] and be complicated by acute kidney injury[ 10 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Dynamics of G6PD activity in patients receiving weekly primaquine for therapy of Plasmodium vivax malaria

et al. 2021

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Background Acute Plasmodium vivax malaria is associated with haemolysis, bone marrow suppression, reticulocytopenia, and post-treatment reticulocytosis leading to haemoglobin recovery. Little is known how malaria affects glucose-6-phosphate dehydrogenase (G6PD) activity and whether changes in activity when patients present may lead qualitative tests, like the fluorescent spot test (FST), to misdiagnose G6PD deficient (G6PDd) patients as G6PD normal (G6PDn). Giving primaquine or tafenoquine to such patients could result in severe haemolysis. Methods We investigated the G6PD genotype, G6PD enzyme activity over time and the baseline FST phenotype in Cambodians with acute P. vivax malaria treated with 3-day dihydroartemisinin piperaquine and weekly primaquine, 0·75 mg/kg x8 doses. Results Of 75 recruited patients (males 63), aged 5–63 years (median 24), 15 were G6PDd males (14 Viangchan, 1 Canton), 3 were G6PD Viangchan heterozygous females, and 57 were G6PDn; 6 patients had α/β-thalassaemia and 26 had HbE. Median (range) Day0 G6PD activities were 0·85 U/g Hb (0·10–1·36) and 11·4 U/g Hb (6·67–16·78) in G6PDd and G6PDn patients, respectively, rising significantly to 1·45 (0·36–5·54, p<0.01) and 12·0 (8·1–17·4, p = 0.04) U/g Hb on Day7, then falling to ~Day0 values by Day56. Day0 G6PD activity did not correlate (p = 0.28) with the Day0 reticulocyte counts but both correlated over time. The FST diagnosed correctly 17/18 G6PDd patients, misclassifying one heterozygous female as G6PDn. Conclusions In Cambodia, acute P. vivax malaria did not elevate G6PD activities in our small sample of G6PDd patients to levels that would result in a false normal qualitative test. Low G6PDd enzyme activity at disease presentation increases upon parasite clearance, parallel to reticulocytosis. More work is needed in G6PDd heterozygous females to ascertain the effect of P. vivax on their G6PD activities. Trial registration The trial was registered (ACTRN12613000003774) with the Australia New Zealand Clinical trials (https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363399&isReview=true).

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Detection of Occult Glomerular Dysfunction in Glucose Six Phosphate Dehydrogenase Deficiency Anemia

Cited by 12 publications

References 27 publications

Hemolytic Dynamics of Weekly Primaquine Antirelapse Therapy Among Cambodians With Acute Plasmodium vivax Malaria With or Without Glucose-6-Phosphate Dehydrogenase Deficiency

Hemolytic Dynamics of Weekly Primaquine Antirelapse Therapy Among Cambodians With Acute Plasmodium vivax Malaria With or Without Glucose-6-Phosphate Dehydrogenase Deficiency

Liver Failure in Neonates With G6PD Deficiency

Dynamics of G6PD activity in patients receiving weekly primaquine for therapy of Plasmodium vivax malaria

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