Sixty-five of 3261 (2%) Saudi neonates were found to be severely G6PD-
deficient during a cord blood screening programme conducted from April
to December, 1992. However, at the time of molecular studies, the blo
od samples were available from only 20 randomly selected children, age
d from 1 to 6 years. DNA analyses showed that seven (three boys, four
girls) of these 20 (35%) had G6PD Aures (nt 143 T --> C), a variant as
sociated with favism which was recently reported in an Algerian. Twelv
e carried the G6PD Mediterranean (563 T) mutation, and in one child th
e mutation remained unidentified. The medical records of these childre
n showed that all who had G6PD Aures, including a premature baby, were
jaundiced during the Ist week of life, but only six full-term infants
had moderate-to-severe hyperbilirubinaemia. Two of seven babies had s
eizures and one of these two developed kernicterus, in spite of timely
blood transfusion.