**5.6. Neonatal jaundice**

One of the most threatening consequences of G6PD deficiency is neonatal jaundice (Beutler, 1994). Jaundice in babies with G6PD enzyme deficiency could be mild or severe enough to cause kernicterus, a spastic type of cerebral palsy, and may even cause death (Luzzatto, 1993). In addition, infants with G6PD deficiency, hyperbilirubinemia is more remarkable than anemia. It facilitates this because of the inadequate physiological conjugation in liver in the neonatal period (Moskaug*, et al.*, 2004). G6PD Aˉ, G6PD mediterrian, G6PD Canton variants are known as types that cause kernicterus and hyperbilirubinemia (Luzzatto, 2001). Clinically, the jaundice, the level of G6PD in the normal physiological jaundice in newborns occur on the same days, or a little earlier, but it takes as long as 2-3 weeks (Tan, 1981, Luzzatto, 2001). There are two major differences between jaundice due to incompatibility of blood groups and jaundice due to G6PD deficiency. First, the presence of jaundice in G6PD deficiency is very rare during childbirth and usually it begins in the second or third day. Second, according to anemia, jaundice is more pronounced and it is encountered with severe anemia very rarely in the absence of the enzyme (Luzzatto, 1993, Luzzatto, 2001).
