الفهرس 
Bilrubin induced neurological dysfunctionOnly 14 pages are availabe for public view
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Abstract
Glucose-6-Phosphate Dehydrogenase (G6PD)
deficiency is the most common human enzyme defect, affects
more than 400 million people worldwide, most commonly
males due to X-Linked heritability (Luzzatto et al., 2020) .
Glucose-6-Phosphate Dehydrogenase (G6PD)
deficiency is an X-Linked recessive disorder with varied
clinical presentations including neonatal jaundice, hemolysis,
acute icterus after exposure to chemicals and drugs, anemia,
acute jaundice following consumption of fava beans
(favism), and also congenital chronic non-spherocytic
hemolytic anemia (Richardson and O’Malley, 2020) .
Neonatal jaundice is the earliest manifestation of
G6PD deficiency, and the most critical sign for early
diagnosis of this genetic disorder (Roper et al., 2020) .
The incidences of G6PD deficiency in icteric
newborns in numerous studies were found to be from 3.5% to
40% (Kasemy et al., 2020) .
Two Egyptian studies, one at Cairo University and
another at Menoufia University found that the prevalence of
G6PD deficiency among jaundiced neonates was 14.9% and
Introduction
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8.9% respectively (Elella et al., 2017; M Abo El Fotoh and
Rizk, 2016) .
The American Academy of Pediatrics (AAP)
recognizes G6PD deficiency as a major risk factor for the
development of sever neonatal hyperbilirubinemia, and
recommends that treatments such as phototherapy and
exchange transfusion, occur at lower total bilirubin levels in
infants with G6PD deficiency than in those without (Sinha et
al., 2017) .
Around 5% of neonates with G6PD deficiency will
develop jaundice after the first 24 hours of life (in contrast to
fetal erythroblastosis), and their serum indirect bilirubin
reaches a peak at days 3 to 5, often more than 20mg/dl.
When jaundice becomes apparent from the end of first week,
its peak may be delayed up to the 2 nd week. Early diagnosis
of deficiency of G6PD is quit important, because this
disorder may cause sever hemolysis and anemia in the
newborn, if undiagnosed (Elella et al., 2017) .
World Health Organization (WHO) data suggest that
the global infant mortality due to G6PD- associated neonatal
jaundice is in the range of 0.7ــ 1.6 per 1000 of all birth.
Infants, who survive the acute hyperbilirubinemia, may
develop sever athetoid cerebral palsy, auditory dysfunction,
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intellectual and other handicaps associated with chronic
bilirubin encephalopathy (M Abo El Fotoh and Rizk, 2016) .
Neonatal screening programs coupled with parental
and medical caretaker education may be successful in
limiting the severity of disease (Luzzatto et al., 2020)