We screened 423 patients referred to our laboratory after hemolysis triggered by 
fava beans ingestion, neonatal jaundice or drug hemolysis. Others were 
asymptomatic but belonged to a family with a history of G6PD deficiency. The 
determination of enzymatic activity using spectrophotometric method, revealed 
293 deficient (143 males and 150 females). The molecular analysis was performed 
by a combination of PCR-RFLP and DNA sequencing to characterize the mutations 
causing G6PD deficiency. 14 different genotypes have been identified : G6PD A(-) 
(376A>G;202G>A) (46.07%) and G6PD Med (33.10%) were the most common variants 
followed by G6PD Santamaria (5.80%), G6PD Kaiping (3.75%), the association 
[c.1311T and IVS11 93c] (3.75%), G6PD Chatham (2.04%), G6PD Aures (1.70%), G6PD 
A(-) Betica (0.68%), the association [ 376G;c.1311T;IVS11 93c] (0.68%), G6PD 
Malaga, G6PD Canton and G6PD Abeno respectively (0.34%). Two novel missense 
mutations were identified (c.920A>C: p.307Gln>Pro and c.968T>C: p.323 Leu>Pro). 
We designated these two class III variants as G6PD Tunis and G6PD Nefza. A 
mechanism which could account for the defective activity is discussed.