Background Jaundice is a common condition that requires medical attention in newborns worldwide. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin. In many infants, unconjugated hyperbilirubinemia reflects a normal transitional phenomenon. In some cases, however, serum bilirubin levels may rise excessively, which can be cause for concern because unconjugated bilirubin is neurotoxic and can cause death in newborns, and lifelong neurologic sequelae in infants who survive—including hearing loss (Christensen and Yaish, 2015). This issue of CSI examined the prevalence of neonatal jaundice in Nigeria, where it is a major cause of hearing loss for a long period of time. Audiological data collected from the International Hearing Center (the Center) over a period of 15 years shows that 265 patients with different degree of hearing loss were affected by neonatal jaundice Biochemically, hyperbilirubinamia is the major cause of neonatal jaundice, but it could be mitigated by the use of some drugs (phenobarbitols, dexamethasone, and clofibrates) that causes the production of uridine diphospate glucoronyl transferase (UDPGT), an enzyme that helps to convert the bilirubin to water soluble bilirubin (conjugated bilirubin). This is because if unconjugated bilirubin is not converted, it could pass through the brain barrier membrane and cause neurotoxicity which results in auditory nerve damage thereby giving rise to hearing loss. Instead of these drugs, patients are normally given antibiotics that have little or no action on the enzyme UDPGT conversion of unconjugated bilirubin to conjugated water soluble bilirubin. Introduction Jaundice in infants is caused by the accumulation of unconjugated bilirubin. This normally reflects as the yellow coloration of the skin and sclera in newborns. Unconjugated bilirubin is neurotoxic and can lead to death in newborns or lifelong neurologic sequelae. Neonatal physiologic jaundice results from simultaneous occurrence of the following two phenomena: Bilirubin production is elevated because of increased breakdown of fetal erythrocytes. This is the result of the shortened lifespan of fetal erythrocytes and the higher erythrocyte mass in neonates. Hepatic excretory capacity is low both because of low concentrations of the binding protein ligandin in the hepatocytes and because of low activity of glucuronyl transferase, the enzyme responsible for binding bilirubin to glucuronic acid, thus making bilirubin water soluble (conjugation). This content is an exclusive benefit for American Academy of Audiology members. If you're a member, log in and you'll get immediate access. Member Login If you're not yet a member, you'll be interested to know that joining not only gives you access to top-notch resources like this one, but also invitations to member-only events, inclusion in the member directory, participation in professional forums, and access to patient resources, tools, and continuing education. Join today!