Of the 1998 randomly selected individuals, 1429 (71.5%) DBS samples were genotyped and merged to the database, of which 53.5% were from females. G6PD*A (A376G) was the only genotype detected. No sample was positive for either G6PD*A- (G202A) or Mediterranean (C563T) variants. The prevalence of G6PD*A (A376G) was 8.9% [95% confidence interval (CI) 6.7-11.2] ranging from 12.2% in the Southern Nations, Nationalities and Peoples' (95% CI 5.7-18.7) to none in Dire Dawa/Harari Region.
CONCLUSION:
The common G6PD*A- (G202A) or Mediterranean (C563T) variants were not observed in this nationwide study. The observed G6PD*A (A376G) mutation has little or no clinical significance. These findings supported the adoption of primaquine for P. falciparum transmission interruption and radical cure of P. vivax in Ethiopia. As the presence of other clinically important, less common variants cannot be ruled out, the implementation of radical cure will be accompanied by active haematological and adverse events monitoring in Ethiopia.
The absence of clinical significant G6DP deficiency is a good news for implementing the national eradication plan of malaria in Ethiopia. However, it is wise to follow patients for any possible hematologic complications.
I will summarize based on the studies cited @Meyer. There is limited knowledge about the prevalence of G6PD deficiency in Ethiopia. One study detected only G6PD*A variant and found a prevalence of 8.99%, another study observed a low overall prevalence of 1.4% but detected another variant, G6PD*A-. This suggests geographical variation in the prevalence of G6PD deficiency in Ethiopia. Highest prevalence was observed in the southern region; regional prevalence were; 5.73% in Amhara, 9.4% in Gambella and 9,48% in Oromia. Yet another study found a high genetic diversity [14%] across the population studied. So far studies suggest that the distribution of G6PD deficiency in Ethiopia differs from region to region. More robust studies are needed to establish the prevalence of clinically significant G6PD deficiency which will inform malaria elimination programme in Ethiopia.
It’s enough to enact screening programs before antimalarial MDA... having tribal/ community predisposition screening would identify the areas that need to be the focus of medical supplies
My experience- i worked in a pediatric hospital in rural Sudan and there seemed to be some strong racial patterns- migrants from north sudan had strong sickel cell anemia while migrants from the east (Ethiopia) predominantly had G6PD... with many traditional foods containing nuts, the disease was immediately apparent. Most kids (from both diseases) had related parents- explaining the tribal predilections. Because the health system is pretty weak diagnosis was only done after presentation.
The literature- central Africa and East Africa have been described to have (super!) high rates of G6PD (https://scholar.google.com/scholar?hl=en&as_sdt=0,5&as_vis=1&q=g6pd+and+antimalarial+east+africa#d=gs_qabs&u=%23p%3Dyiapegv-4voJ) which many are considering an ethical issue for Antimalarial MDA. I.e. is it worth the mass hemolysis?
My opinion- regional screening should be done to assess a) locality prevalence of g6pd rather than national rates because of the tribal risk b) cost effectiveness analysis of how much antimalarials would cost the country since way more G6PD management kits would be needed
thats just my personal scope though... hope it helps!
The results of some support the limited historical evidence of low G6PD deficiency prevalence in Ethiopia. The A376G (A)mutation observed is a mild deficiency causing around 85% of thenormal enzymatic activity with little clinical significance. The more severe G6PD deficiencyallelic types, G202A (A-) and C563T (Mediterranean), common in Africa were not observed, supporting the safe use of primaquine especially the single low dose for falciparum in Ethiopia.
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