2nd Edition of Public Health World Conference (PHWC) 2026

Abstract

Background: Glucose 6 phosphate dehydrogenase (G6PD) deficiency and sickle cell disease (SCD) are inherited red blood cell disorders associated with oxidative stress and hemolysis. The coinheritance of these conditions may influence the hematological profile and clinical outcomes in the affected individuals. This study aimed to determine the prevalence of G6PD deficiency among SCD patients and to evaluate its association with hematological and biochemical parameters.

Method:A cross-sectional study was conducted among 79 patients with confirmed SCD attending the Hematology Department at King Fahad Hospital, Almadinah between November 2024 and November 2025. G6PD enzyme activity was measured using a quantitative UV kinetic method. Statistical analysis included the Mann-Whitney U test, Fisher’s exact test, and Spearman correlation analysis. Bonferroni correction was applied only for the correlation analysis to adjust for multiple correlations, with the adjusted statistical significance defined as p=0.003.

Results:G6PD deficiency was identified in 10 of 79 patients (12.7%). G6PD-deficient patients were significantly younger than non-deficient patients (median age:22 vs. 28.5; p=0.01). No statistically significant differences were observed between G6PD-deficient and non-deficient groups in hematological or biochemical parameters. However, non-deficient patients demonstrated a higher frequency of Vaso-occlusive crisis (p=0.04). After Bonferroni correction, significant positive correlations were observed between G6PD activity and hemoglobin (r=0.33, p<0.0001), RBC count (r=0.24, p=0.001) and hematocrit (r=0.37, p<0.0001). No significant associations were identified between G6PD activity and biochemical markers of hemolysis, including LDH and total bilirubin.

Conclusion:The prevalence of G6PD deficiency among SCD patients was 12.7%. G6PD activity showed significant positive associations with erythrocyte-related parameters but not with hemolysis markers. These findings suggest a potential role of G6PD activity in maintaining erythrocyte integrity in SCD patients. Larger studies are recommended to further clarify the clinical implications of G6PD deficiency in sickle cell disease.