Bilirubin is a natural pigment that can indicate liver disease in adults, but is common in infants. It is released when red blood cells break down and is eliminated through the liver. High levels can cause jaundice and brain damage in infants, but in adults, moderately elevated levels are usually not harmful. Causes of high levels include Gilbert’s syndrome, antipsychotic drugs, and liver disease.
Elevated bilirubin levels could be a symptom of liver disease in adults or older children, but can be common in infants. Bilirubin is a naturally occurring organic molecule that appears in bile, blood, urine, and body fluids due to the breakdown of red blood cells. It is classified as a pigment having multiple conjugated double bonds which absorb particular wavelengths of light resulting in colored molecules. The yellow-green of high bilirubin levels gives bruises, jaundiced children, urine and bile their characteristic color. Similar to the pigments used by plants to perceive light or by some algae to capture light energy, bilirubin consists of an open chain of four five-membered pyrolic rings containing nitrogen.
The heme portion of hemoglobin, the molecule that carries oxygen in blood, consists of a large ring, called the porphyrin ring, made up of four smaller pyrolic rings. At the center of the large ring lies an atom of iron. Its state of ionization determines the degree of attraction towards oxygen molecules. Upon red blood cell death, the porphyrin ring is broken, the iron recovered for recycling, and the remaining open-chain bilirubin molecule is released into the surrounding environment. It is a waste product to be eliminated.
The bilirubin released in its unconjugated form is not soluble in water but is bound to albumin, the predominant plasma protein, for transport to the liver where it is conjugated with glucuronic acid. Most of this conjugated form is concentrated in the bile and released in the small intestine. A small amount may pass in the urine. The presence of increased bilirubin in the urine in its conjugated and unconjugated forms serves as an indicator of possible liver damage or disease.
The blood detoxification activity of the liver is one of the last to be fully functional in newborns, because their mothers’ digestive systems did this job for them. Within two to five days after birth, a newborn’s liver must take over the filtration of the blood. Meanwhile, the baby may experience high bilirubin counts to the point that the whites of the eyes and skin have a yellow tint. This is concerning as the blood brain barrier is not fully established in the infant and high bilirubin levels can leave deposits in the brain and cause neuronal defects. Phototherapy in which the child is exposed to natural or artificial light sources for specified periods of time causes the isomerization of the photosensitive bilirubin molecule, a change of its geometric configuration, into a water-soluble form and elimination from the body in the urine.
In adults, moderately increased bilirubin levels are usually not harmful. Ten to 10 percent of the population is thought to have Gilbert’s syndrome, which causes less activity in the enzyme that conjugates bilirubin. Other causes of high bilirubin levels include the use of antipsychotic drugs and chemotherapy. Severely elevated bilirubin levels are associated with bile duct blockage, cirrhosis, or other liver disease.
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