Simpore J, Ilboudo D, Damintoti K, Sawadogo L, Maria E, Binet S, Nitiema H, Ouedraogo P, Pignatelli S, Nikiema JB.
Pak J Biol Sci. 2007 Feb 1 ;10(3):409-14. PMID : 19069510
[PubMed - indexed for MEDLINE]
Where malaria is endemic, there is an unexpected association between haemoglobinopathies and glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. Their coexistence in a patient with sickle cell disease (SCD) can lead to hemolytic anemia, hemoglobinuria, sepsis, renal failure and vaso-occlusive attacks (VOA). The aim of this research was to determine the impact of G-6-PD deficiency in SCD patients. That is why, we screened haemoglobinopathies and G-6-PD deficiency in 7 villages and at 10 primary schools in Kadiogo Province, Burkina Faso. Hemoglobin electrophoresis was performed on blood from 18,383 people. From these results, we chose 342 subjects for a hemogram and the measure of the G-6-PD activity. The results were analyzed with Epilnfo-6 and Spss-10. Statistical significance was set at p < 0.05. We found a prevalence of 28.9% of Sickle Cell Trait (SCT), 1.3% of Major Sickle Cell Syndromes (MSCS), 12.3% of G-6-PD deficiency among women and 20.5% among men. We did not detect a statistically significant difference for counts of erythrocytes (p = 0.773), leucocytes (p = 0.227) and reticulocytes (0.292) ; hemoglobin levels (p = 0.998) ; annual vasoocclusive attacks (p = 0.869) between persons with SCD having a G-6-PD deficiency and those with normal G-6-PD activity. According to this study, G-6-PD deficiency does not seem to increase the severity of SCD. However, these patients should know their G-6-PD genotype in order to avoid consuming oxidative drugs that might provoke oxidative stress.