Manifestations of Gastrointestinal Disease in the Child

Gastrointestinal Disease in the Child 727
TABLE 12.
Causes of unconjugated hyperbilirubinemia in the neonate
Increased bilirubin production
Hemolytic disease
Blood group incompatibility (Rh, ABO, minor groups)
Membrane defects (spherocytosis, elliptocytosis, infantile pyknocytosis)
Enzyme deficits (G6-PD, hexokinase, pyruvate kinase)
Drugs (oxytocin, vitamin K)
Increased breakdown
Infection
Hematoma, swallowed maternal blood
Increased RBC mass
Polycythemia (maternal diabetes, delayed cord clamp, small for gestational age, altitude)
Decreased bilirubin metabolism
Reduced uptake
Portacaval shunt, hypoxia, sepsis, acidosis, congenital heart disease
Decreased conjugation
Crigler-Najjar type I, II
Gilbert’s syndrome
Lucey-Driscoll syndrome
Hypothyroidism
Panhypopituitarism
Altered enterohepatic circulation
Breastfeeding
Free fatty acids, steroids, breast milk -glucuronidase
Intestinal hypomotility
Retained meconium
Reduced intestinal flora
Newborn, antibiotic use
caused by immune-mediated or inherited red cell membrane defects, and less
frequently hemoglobinopathies.
Unconjugated bilirubin concentration will be affected by any condition
which reduces the clearance of bilirubin from the liver. These are primarily
inherited conditions resulting in defects in uridine glucuronyl transferase
(UGT) the enzyme which conjugates bilirubin. These conditions include
Crigler-Najjar syndrome types I and II and Gilbert Syndrome which are
discussed in more detail in Chapter 13. The Lucey-Driscoll syndrome is a
transient form of acquired reduction in UGT which is likely caused by an
unidentified maternal serum factor.
Congenital hypothyroidism and panhypopituitarism may also result in an
unconjugated hyperbilirubinemia by unknown mechanisms.