Glusoce-6-phosphate dehydrogenase- History and diagnosis

Gautam, Keyoor

doi:10.3126/jpn.v6i12.16260

Cited by 10 publications

(8 citation statements)

References 3 publications

(5 reference statements)

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“…Most of the G6PD have neither anemia nor evidence of increased RBC destruction, nor an alteration in blood morphology, although a modest shortening of RBC survival can be demonstrated by isotopic techniques. However, episodes of acute hemolysis with hemolytic anemia may be triggered by medications, certain foods, and acute illnesses, especially infection [17]. In present study, the G6PD deficiency was higher in mild anemia followed by moderate and than severe anemia which might be due to lack of the history taking that triggers acute hemolytic attack in G6PD deficiency cases.…”

Section: Discussionmentioning

confidence: 56%

Glucose 6 phosphate dehydrogenase deficiency and hemoglobinopathy in South Western Region Nepal: a boon or burden

Gautam

Gaire²,

Manandhar³

et al. 2019

BMC Res Notes

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ObjectivesThe study was carried out to optimize the phenotypic method to characterize the sickle cell trait (SCT), sickle cell anemia (SCA), and β-thalassemia (β-TT) suspected sample from tharu community of South Western province-5, Nepal. SCT and SCA were further evaluated by genotypic method employing amplification refractory mutation system (ARMS PCR). Moreover, Glucose 6 phosphate dehydrogenase (G6PD) was estimated in those hemoglobinopathy to observe its prevalence. The accurate and reliable method can play an important role in reduction of morbidity and mortality rate.ResultsThe 100 suspected cases were subjected to phenotypic method adopting cellulose acetate electrophoresis and genotypic method using ARMS PCR which portraits (5%) SCA positive test showing HBS/HBS, (38%) SCT positive trait HBA/HBS and (36%) cases normal HBA/HBA. β-TT (21%) cases were confirmed by electropherogram. G6PD deficiency was observed in (40%) of SCA, (18.4%) of SCT, (4.8%) of β-TT and (2.8%) in normal cases. Increased G6PD were developed only in SCT (5.3%) and β-TT (4.8%). The study highlighted sickle cell disorder (SCD) and β-TT as the most common hemoglobinopathy coexisting with G6PD deficiency. Though hemoglobinopathy sometime could be protective in malaria but G6PD deficiency can cause massive hemolysis which may exacerbate the condition.

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Section: Discussionmentioning

confidence: 56%

Glucose 6 phosphate dehydrogenase deficiency and hemoglobinopathy in South Western Region Nepal: a boon or burden

Gautam

Gaire²,

Manandhar³

et al. 2019

BMC Res Notes

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show abstract

“…The clinical course of SCD, including the degree of anemia was not milder in G6PD deficiency than in G6PD normal patients but could not be proved to be significantly more severe [16].G6PD don't have neither anemia nor evidence of increased RBC destruction, nor an alteration in blood morphology, although a modest shortening of RBC survival can be demonstrated by isotopic techniques. However, episodes of acute hemolysis with hemolytic anemia may be triggered by medications, certain foods, and acute illnesses, especially infection [17].…”

Section: Discussionmentioning

confidence: 99%

Glucose 6 Phosphate Dehydrogenase Deficiency and Hemoglobinopathy in South Western Region Nepal: A Boon or Burden

Gautam

Gaire²,

Manandhar³

et al. 2019

Preprint

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Objectives: The study was carried out to optimize the phenotypic method to characterize the sickle cell trait (SCT), sickle cell anaemia (SCA) and β-thalassemia (β-TT) suspected sample from tharu community of South Western province-5, Nepal. SCT and SCA were further evaluated by genotypic method employing amplification refractory mutation system (ARMS PCR). Moreover, Glucose 6 Phosphate Dehydrogenase (G6PD) was estimated in those hemoglobinopathy to observe its prevalence. The accurate and reliable method can play an important role in reduction of morbidity and mortality rate. Results: The 100 suspected cases were subjected to phenotypic method adopting cellulose acetate electrophoresis and genotypic metod using ARMS PCR which portraits (5%) SCA positive test showing HBS/HBS, (38%) SCT positive trait HBA/HBS and (36%) cases normal HBA/HBA. β-TT (21%) cases were confirmed by electropherogram. G6PD deficiency was observed in (40%) of SCA, (18.4%) of SCT, (4.8%) of β-TT and (2.8%) in normal cases. Increased G6PD were developed only in SCT (5.3 %) and β-TT (4.8%). The study highlighted sickle cell disorder (SCD) and β-TT as the most common hemoglobinopathy coexisting with G6PD deficiency. Though hemoglobinopathy sometime could be protective in malaria but G6PD deficiency can cause massive hemolysis which may exacerbate the condition.

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“…Not only primaquine but a large spectrum of drugs can induce hemolysis in G6PD deficient individuals [6]. Ingestion of fava beans (Vicia faba) has been associated with hemolytic anemia in G6PD deficient individuals since a very ancient period of time [7].…”

Section: Introductionmentioning

confidence: 99%

Qualitative and quantitative assay of glucose 6 phosphate dehydrogenase in patients attending tertiary care center

2020

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Objectives: The study was carried out with the aim to find out the frequency of Glucose 6 phosphate dehydrogenase (G6PD) deficiency among the patients attending the hospital and to rationalize the qualitative methemoglobin reduction test in reference to the quantitative spectrophotometric assay. Timely screening of the patients for G6PD with appropriate screening method can play an important role in preventing hemolytic crisis that arises from therapeutic use of oxidative drugs like primaquine. Result: The frequency of G6PD deficient cases was 3% by both of the employed tests. The mean ± SD of G6PD activity in the patients under study was 15.34 ± 4.7 IU/g Hb in males and 16.01 ± 3.74 IU/g Hb in females. G6PD activity was positively associated with reticulocyte count (r = 0.289, p value = 0.004) and negatively with mean corpuscular hemoglobin concentration (r = −0.220, p-value = 0.028). The correlation of red blood corpuscular count and G6PD was statistically significant (p-value = 0.048).

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Glusoce-6-phosphate dehydrogenase- History and diagnosis

Cited by 10 publications

References 3 publications

Glucose 6 phosphate dehydrogenase deficiency and hemoglobinopathy in South Western Region Nepal: a boon or burden

Glucose 6 phosphate dehydrogenase deficiency and hemoglobinopathy in South Western Region Nepal: a boon or burden

Glucose 6 Phosphate Dehydrogenase Deficiency and Hemoglobinopathy in South Western Region Nepal: A Boon or Burden

Qualitative and quantitative assay of glucose 6 phosphate dehydrogenase in patients attending tertiary care center

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