Unbound<unk>  (Bf) levels can be used to predict the risk of neurodevelopmental handicaps within infants. Unconjugated hyperbilirubinemia in a newborn can lead to accumulation of<unk>  in certain<unk> ain regions (particularly the basal nuclei) with consequent irreversible damage to these areas manifesting as various neurological deficits, seizures, abnormal reflexes and eye movements. This type of neurological injury is known as kernicterus. The spectrum of clinical effect is called<unk>  encephalopathy. The neurotoxicity of neonatal hyperbilirubinemia manifests because the blood–brain barrier has yet to develop fully, and<unk>  can freely pass into the<unk> ain interstitium, whereas more developed individuals with increased<unk>  in the blood are protected. Aside from specific chronic medical conditions that may lead to hyperbilirubinemia, neonates in general are at increased risk since they lack the intestinal bacteria that facilitate the<unk> eakdown and excretion of conjugated<unk>  in the feces (this is largely why the feces of a neonate are paler than those of an adult). Instead the conjugated<unk>  is converted back into the unconjugated form by the enzyme β-glucuronidase (in the gut, this enzyme is located in the<unk> ush border of the lining intestinal cells) and a large proportion is reabsorbed through the enterohepatic circulation. In addition, recent studies point towards high total<unk>  levels as a cause for gallstones regardless of gender or age.
Bilirubin
Lumirubin
Bile acid
Uric acid
Lipoprotein
Blood protein
Hemoglobin
Alanine transaminase