Causes, Significance and Pathophysiological Rationale of Hyperbilirubinemia

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Causes, Significance and Pathophysiological Rationale of Hyperbilirubinemia

Hyperbilirubinemia or excessive bilirubin is the main cause of jaundice. Bilirubin is responsible for the yellow color in jaundice is a normal pigment that is released from red blood cells breakdown. Jaundice is caused by a problem from any of bilirubin’s three phases. Before bilirubin is produced, unconjugated jaundice may be present due to increased bilirubin that is caused by hemolytic anemia and reabsorption of a large hematoma (Demet Cabar, Aydin, & Gullu, 2014). During bilirubin production, some jaundice causes include viruses like Chronic Hepatitis B and C, Hepatitis A, and Epstein-Barr virus infection. Other causes include rare genetic metabolic defects, alcohol, autoimmune disorders, and medicines like chlorpromazine, penicillin, oral contraceptives, acetaminophen and estrogenic or anabolic steroids.

According to Demet Cabar, Aydin, and Gullu (2014), hyperbilirubinemia is found in both adults and children. Jaundice is common in infants because they have a high level of red blood cells which breakdown and are frequently replaced. The baby’s liver is not fully developed making it less effective in processing bilirubin and discharging it from the blood, making their bilirubin twice as high as in adults. Hyperbilirubinemia is clinically significant as it is associated with high mortality especially in toddlers. The condition also significantly increases the likelihood of common duct stones in clients with acute cholecystitis.

Neonatal physiologic jaundice results from the simultaneous occurrence of two phenomena. Production of bilirubin is elevated due to increased fetal erythrocyte breakdown resulting to shortened fetal erythrocytes lifespan and higher erythrocyte mass in neonates (Ip, Glicken, Kulig, O’Brien, & Sege, 2002). The excretory heparin capacity is low in concentration due to the low binding protein ligandin in hepatocytes and due to the low glucuronyl transferase activity that is responsible for binding bilirubin to glucuronic acid making it water soluble. Bilirubin is an end product of the heme produced by the reticuloendothelial system formed through oxidation-reduction reactions. In the liver, bilirubin is transported in to the liver cells where it combines with ligandin.

References

Demet Cabar, H., Aydin, A., & Gullu, U. (2014). Care in neonatal jaundice. International Journal Of Academic Research, 6(3), 8-14. http://dx.doi.org/10.7813/2075-4124.2014/6-3/a.2

Ip, S., Glicken, S., Kulig, J., O’Brien, R., & Sege, R. (2002). Management of neonatal hyperbilirubinemia. Evidence report/technology assessment (Summary), (65), 1.

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