Glucose‐6‐phosphate dehydrogenase deficiency induced haemolysis in a woman with newly diagnosed diabetes after normalisation of hyperglycaemia

ALjishi, F.; Al-Darwish, Mohammed

doi:10.1111/dme.13385

Cited by 7 publications

(4 citation statements)

References 21 publications

(60 reference statements)

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“…When treated with DKA, during insulin infusion, rapid correction of prolonged hyperglycaemia may increased the inability of the red blood cells to produce NADPH. This leads to an imbalance in the consumption and production of NADPH [ 25 ]. In addition, hyperglycaemia increased the production of reactive oxygen species (ROS) in the form of superoxide [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

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Glucose-6-Phosphate dehydrogenase deficiency associated hemolysis in a cohort of new onset type 1 diabetes children in Guangdong province, China

Jiang

Zhang

et al. 2022

Diabetol Metab Syndr

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Background Glucose-6-phosphate dehydrogenase (G6PD) deficiency is one of the most common human genetic abnormalities, with a high prevalence in Guangdong, China. The purpose of this study was to explore the characteristics of newly diagnosed type 1 diabetes (T1D) patients with G6PD deficiency in a cohort of Chinese children and to investigate the relationship between the diabetic ketoacidosis (DKA) and hemolysis due to G6PD deficiency in these patients. Methods A total of 503 newly diagnosed T1D children aged 6 months–18 years were collected and their G6PD enzyme activity were measured. Fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and G6PD gene were analysed. The pH, HCO3, and plasma osmotic pressure between DKA patients with and without hemolysis at the presentation were compared. Results In the present study, G6PD deficiency accounted for 5.3% of newly diagnosed T1D children. There were no significant differences in FPG/HbA1c and HbA1c levels between T1D children alone and T1D children with G6PD deficiency. Hemolysis appeared in five of the twenty-two DKA patients with G6PD deficiency. Two patients had fever at onset and were given ibuprofen and cefazolin. The other three patients did not have infection or ingestion of hemolytic drugs. There were no significant difference in pH, HCO3, and osmotic pressure between the children with DKA with and without hemolysis at the presentation. The hemolysis occurred between 2 and 7 days after admission and the hyperglycaemia had been corrected by the time hemolysis occurs. Four G6PD gene mutations were found in the diabetes with G6PD deficiency patients: c.1376G > T, c.1388G > A, c.95A > G, and c.871G > A, all of which were genes with high frequency of G6PD deficiency in Guangdong Province. No correlation between genotype and hemolysis was found. Conclusion In the present study, we found the frequency of G6PD deficiency among newly diagnosed T1D children was similar to that of the general population. However, DKA children with G6PD deficiency are prone to occur hemolytic anemia, and these hemolysis usually occurs when DKA is corrected and blood glucose is in homeostatic state, which is easy to be ignored. To reduce the risk of this complication, especially in areas with high incidence of G6PD deficiency, screening for G6PD activity in people with newly diagnosed diabetes should be considered.

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Section: Discussionmentioning

confidence: 99%

“…In addition, hyperglycaemia increased the production of reactive oxygen species (ROS) in the form of superoxide [ 26 ]. These reactive oxygen species can destroy and deform the erythrocyte membrane, which leads to erythrocytes to be fragile and prone to lysis [ 25 ]. So, it is important to avoid the rapid decline in glucose availability.…”

Section: Discussionmentioning

confidence: 99%

Glucose-6-Phosphate dehydrogenase deficiency associated hemolysis in a cohort of new onset type 1 diabetes children in Guangdong province, China

Jiang

Zhang

et al. 2022

Diabetol Metab Syndr

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“…Gradual plasma glucose correction to avoid rapid decrease in glucose availability for red blood cells is likely to reduce the occurrence of hemolysis in G6PD-deficient patients [13]. Also, screening of G6PD enzyme activity should be considered in patients newly diagnosed with diabetes, especially in boys, considering the ethnic origin of the patient, to reduce the risk of hemolysis.…”

Section: Discussionmentioning

confidence: 99%

Manifestation of glucose-6-phosphate dehydrogenase deficiency in the wake of new-onset type 1 diabetes mellitus: a case report

Govindarajan

Zamir

Bagewadi³

et al. 2022

J Med Case Reports

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Background Diabetes mellitus is the most common metabolic disease globally, while glucose-6-phosphate dehydrogenase deficiency, an X-linked inherited disorder, is the most common erythrocyte enzyme defect. The association between the two in children has been infrequently reported. Case presentation We report the case of a 10-year-old boy of Iraqi descent who presented to our emergency department with new-onset type 1 diabetes mellitus without Diabetic Keto Acidosis. He was treated with subcutaneous insulin and discharged. Eleven days after hospitalization, he was found to be jaundiced during his home visit. Hence, he was referred to the pediatric unit, and his hemoglobin had declined from 130 g/L at the previous admission to 81 g/L. Blood tests revealed low haptoglobin, and his peripheral blood film showed anisocytosis, polychromasia, and occasional red cell fragments suggestive of acute hemolysis. His glucose-6-phosphate dehydrogenase activity was very low, and his subsequent genetic tests confirmed Mediterranean-type glucose-6-phosphate dehydrogenase deficiency. Conclusion Glucose-6-phosphate dehydrogenase deficiency in people with diabetes mellitus has been underreported in the literature so far, and screening of glucose-6-phosphate dehydrogenase deficiency should be considered on diagnosis of diabetes mellitus, especially in boys of African, Mediterranean, or Asian descent.

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“…In G6PD deficiency, the severity of hemolysis is variable, and this hemolysis resolves when the normal metabolic balance is restored ( 3 ). It has been reported that severe hemolytic anemia due to G6PD deficiency may develop in newly diagnosed diabetes, especially during the correction of hyperglycemia, but this is very rare ( 4 , 5 ).…”

Section: Introductionmentioning

confidence: 99%

Hemolytic Anemia due to Glucose 6 Phosphate Dehydrogenase Deficiency Triggered by Type 1 Diabetes Mellitus

Orman,

Çetinkaya,

Öner

et al. 2023

Jcrpe

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Glucose 6 phosphate dehydrogenase (G6PD) is expressed in all tissues and is necessary to maintain oxidant stress capacity of cells. G6PD deficiency is the most common enzymopathy in humans and is among the important causes of hemolytic anemia. It has been reported that severe hemolytic anemia due to G6PD deficiency may develop in newly diagnosed diabetes, especially during the correction of hyperglycemia. To date, nine cases have been published. Genetic analysis was not performed for G6PD deficiency in these published patients. We present a case of hemolytic anemia due to G6PD deficiency secondary to newly diagnosed type 1 diabetes mellitus. Genetic testing was performed for the index patient and revealed a previously reported missense pathogenic variant (c.653C>T; p.Ser218Phe) in the G6PD gene.

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Glucose‐6‐phosphate dehydrogenase deficiency induced haemolysis in a woman with newly diagnosed diabetes after normalisation of hyperglycaemia

Cited by 7 publications

References 21 publications

Glucose-6-Phosphate dehydrogenase deficiency associated hemolysis in a cohort of new onset type 1 diabetes children in Guangdong province, China

Glucose-6-Phosphate dehydrogenase deficiency associated hemolysis in a cohort of new onset type 1 diabetes children in Guangdong province, China

Manifestation of glucose-6-phosphate dehydrogenase deficiency in the wake of new-onset type 1 diabetes mellitus: a case report

Hemolytic Anemia due to Glucose 6 Phosphate Dehydrogenase Deficiency Triggered by Type 1 Diabetes Mellitus

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