Enhanced Erythrocyte Apoptosis in Sickle Cell Anemia, Thalassemia and Glucose-6-Phosphate Dehydrogenase Deficiency

2002 ◽  
Vol 12 (5-6) ◽  
pp. 365-372 ◽  
Author(s):  
Karl Lang ◽  
Benjamin Roll ◽  
Svetlana Myssina ◽  
Markus Schittenhelm ◽  
Hans-Gerhard Scheel-Walter ◽  
...  
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase

Clinical and Biochemical Interactions of Glucose-6-Phosphate Dehydrogenase Deficiency and Sickle-Cell Anemia

1972 ◽  
Vol 287 (5) ◽  
pp. 213-217 ◽  
Author(s):  
Sergio Piomelli ◽  
Carl A. Reindorf ◽  
Mohamed T. Arzanian ◽  
Laurence M. Corash
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Glucose 6-phosphate dehydrogenase deficiency and sickle cell anemia: frequency and features of the association in an African community

Blood ◽  
1975 ◽  
Vol 46 (4) ◽  
pp. 591-597 ◽  
Author(s):  
U Bienzle ◽  
O Sodeinde ◽  
CE Effiong ◽  
L Luzzatto
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Clinical Course ◽  
Normal Subjects ◽  
Starch Gel Electrophoresis ◽  
African Community ◽  
Starch Gel ◽  
Male Patients ◽  
Glucose 6 Phosphate Dehydrogenase

Abstract The glucose 6-phosphate dehydrogenase (G6PD) genotype was determined in 100 male patients with homozygous sickle cell anemia (SS) by a combination of quantitative assay, cytochemical testing, and starch-gel electrophoresis. Of the 100 patients tested, 16 were found to be G6PD deficient (GdA-), AND 84 G6PD normal (22GsA and 62 GdB). This distribution of G6PD genotypes did not differ significantly from that observed in the general population. The level of G6PD activity in GdA- SS patients was nearly always higher than in G6PD-deficient subjects who did not have an associated hemolytic state, but it was nearly always lower than in G6PD-normal subjects. The clinical course of sickle cell disease, including the degree of anemia, was not milder in GdA- than in G6PD-normal patients but could not be proved to be significantly more severe. It was concluded that in this community the incidence of G6PD deficiency in sickle cell anemia was not greater than would be expected by chance, and there was no evidence that the coexistence of the GdA- gene in SS patients ameliorated their disease.

Glucose 6 phosphate dehydrogenase deficiency is not associated with cerebrovascular disease in children with sickle cell anemia

Blood ◽  
2009 ◽  
Vol 114 (3) ◽  
pp. 742-743 ◽  
Author(s):  
David C. Rees ◽  
Christopher Lambert ◽  
Elaine Cooper ◽  
Jack Bartram ◽  
David Goss ◽  
...  
Keyword(s):  
Cerebrovascular Disease ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Glucose 6-phosphate dehydrogenase deficiency and sickle cell anemia: frequency and features of the association in an African community

Blood ◽  
1975 ◽  
Vol 46 (4) ◽  
pp. 591-597
Author(s):  
U Bienzle ◽  
O Sodeinde ◽  
CE Effiong ◽  
L Luzzatto
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Clinical Course ◽  
Normal Subjects ◽  
Starch Gel Electrophoresis ◽  
African Community ◽  
Starch Gel ◽  
Male Patients ◽  
Glucose 6 Phosphate Dehydrogenase

The glucose 6-phosphate dehydrogenase (G6PD) genotype was determined in 100 male patients with homozygous sickle cell anemia (SS) by a combination of quantitative assay, cytochemical testing, and starch-gel electrophoresis. Of the 100 patients tested, 16 were found to be G6PD deficient (GdA-), AND 84 G6PD normal (22GsA and 62 GdB). This distribution of G6PD genotypes did not differ significantly from that observed in the general population. The level of G6PD activity in GdA- SS patients was nearly always higher than in G6PD-deficient subjects who did not have an associated hemolytic state, but it was nearly always lower than in G6PD-normal subjects. The clinical course of sickle cell disease, including the degree of anemia, was not milder in GdA- than in G6PD-normal patients but could not be proved to be significantly more severe. It was concluded that in this community the incidence of G6PD deficiency in sickle cell anemia was not greater than would be expected by chance, and there was no evidence that the coexistence of the GdA- gene in SS patients ameliorated their disease.

Glucose-6-Phosphate Dehydrogenase Deficiency in Brazilian Children With Sickle Cell Anemia is not Associated With Clinical Ischemic Stroke or High-Risk Transcranial Doppler

2016 ◽  
Vol 63 (6) ◽  
pp. 1046-1049 ◽  
Author(s):  
André Rolim Belisário ◽  
Rahyssa Rodrigues Sales ◽  
Nayara Evelin Toledo ◽  
Cibele Velloso-Rodrigues ◽  
Célia Maria Silva ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
High Risk ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Transcranial Doppler ◽  
Dehydrogenase Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Brazilian Children
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