000			04244nam a22003137a 4500
001			CUHAS/BM/1001023/T/20
003			CUHAS/BM/1001023/T/20
005			20240305194007.0
008			231101b |||||||| |||| 00| 0 eng d
028			_bPhone: +255 28 298 3384
028			_b Fax: +255 28 298 3386
028			_b Email: vc@bugando.ac.tz
028			_bWebsite: www.bugando.ac.tz
035			_aCUHAS/BM/1001023/T/20
040			_bEnglish _cDDC
041			_aEnglish
041			_aKiswahili
100			_a Esther Germiah Mwenda _dCUHAS/BM/1001023/T/20
245			_aPrevalence of Glucose 6 Phosphate Dehydrogenase Deficiency, Degree of Anaemia among Sickle Cell Disease Patients Attending Clinic at Bugando Medical Centre Mwanza, Tanzania.
260			_aMwanza, Tanzania: _bCatholic University of Health and Allied Sciences [CUHAS – Bugando] : _c©2023
300			_a45 Pages
300			_aIncludes References and Appendicies
520			_aAbstract: Background: Glucose-6-phosphate dehydrogenase (G6PD) is the cytoplasmic enzyme that is essential for an erythrocyte’s capacity to withstand oxidative stress, the deficiency of this enzyme leads to a buildup of free radical and insoluble hemoglobin within the cell. Precipitated hemoglobin is disruptive to the structure and function of the RBCs membrane and leads to increase membrane permeability, osmotic fragility, and cell rigidity. The compromised integrity of the RBCs membrane results in both intravascular hemolysis and rapid removal of this cell within the splenic pump. Sickle cell disease (SCD) is the most common inherited disorder which occurs when both parents have either sickle cell disease (two sickle cell genes) or sickle cell trait (one sickle gene). Both G6PD deficiency and SCD are prevalent in malaria-endemic regions, controversy however persists as to whether G6PD is commoner in SCD subjects since the occurrence of enzyme deficient state with a chronic hemolytic disorder like SCD could potential predisposes to fetal hemolytic episodes. There is however a dearth of pediatric studies on this subject. Objectives: To determine the prevalence of Glucose-6-phosphate dehydrogenase (G6PD) deficiency, degree of anemia among sickle cell disease patients at BMC, Mwanza Tanzania. Methodology: This cross-sectional study was conducted in the Department of Hematology and blood transfusion of Bugando Medical Centre, Mwanza Tanzania among the sickle cell disease confirmed patients. Screening test for G6PD activity and degree of anemia by hemoglobin concentration. Blood samples of not less than 6ml volume was collected in disodium ethylenediaminetetraacetic acid (EDTA) coated anticoagulant venipuncture vacuum tube Then G6PD qualitative screening test was performed where hemoglobin (red color) is oxidized to methemoglobin which is (brown in color) by sodium nitrate. Their redox dye, methylene blue activates the pentose phosphate pathway resulting in the enzymatic conversion of methemoglobin back to hemoglobin in blood with normal G6PD activity, in G6PD deficiency cells there is no enzymatic conversion to hemoglobin due to this blood sample retaining brown color. Results: This study revealed that 21.25% (n=51) of patients with sickle cell disease were G6PD deficiency positive. The results indicate notable presence of this deficiency within the study population.This study has also found that patients with SCD with moderate to severe anemia were more likely to have G6PD deficiency, this is due to co-existence of two hemolytic disease. We also found that the degree of hemolysis, lower MCV, MCHC and high reticulocytes were more likely to be seen in patients with the two pathologies. Conclusion: This study places the prevalence of G6PD-deficiency among sickle cell disease patient at 21.5% which indicates a significant of G6PD-deficieny among SCD patient. There was also significant difference between the RBC indices of G6PD-normal and G6PD-deficincy participant. This implies that G6PD-deficeincy may increase the severity of anemia in SCD patient.
600			_xPathology
600			_xHematology
600			_xMedical Laboratory Sciences
700			_aErius Tebuka
942			_2ddc _cCR
999			_c22968 _d22968