Causes of Jaundice and Hyperbilirubinemia

Jaundice is a disorder in which a person's skin, whites of the eyes and mucous membranes look yellow. The yellow coloration is produced by excess bilirubin in the body, a condition known as hyperbilirubinemia. Bilrubin is a yellow pigment produced from the breakdown of hemoglobin from red blood cells. When a person suffers from hyperbilirubinemia, some of the excess bilirubin may be deposited in the skin, producing jaundice.

Hemoglobin is a red protein that carries inhaled oxygen around the body inside the red blood cells and distributes it to the cells. When red blood cells die and are destroyed, their hemoglobin is converted into a green substance called biliverdin. Biliverdin is then changed into a fat-soluble form of bilirubin called unconjugated bilirubin. The liver changes unconjugated bilirubin into a water-soluble substance called conjugated bilirubin.

The liver produces bile, a liquid which emulsifies fats in the small intestine, helping them to be digested. The liver sends conjugated bilirubin into the bile and then sends the bile to the gall bladder. The gall bladder stores the bile until fat is eaten, and then delivers it to the small intestine through the bile duct. As the bile travels through the intestine, bacteria act on the bilirubinin. Eventually a brown substance called stercobilin is formed, which gives feces its color. The stercobilin leaves the body with the feces.

Excess bilirubin can build up if too many red blood cells are broken down, if the liver is infected or damaged or if the ducts (tubes) that transport bile from the liver to the gall bladder or from the gall bladder to the small intestine are blocked.

In a condition called hemolytic anemia a large number of red blood cells are destroyed. The body may not be able to process all the bilirubin that is made, causing jaundice to develop. Hemolytic anemia can result from a number of causes, including malaria and sickle cell anemia. In sickle cell anemia, which is an inherited disease, the red blood cells are shaped like the letter C instead of being disc shaped like normal red blood cells. The abnormal red blood cells don’t live for long, and die after ten to twenty days. Normal red blood cells live for about one hundred and twenty days.

Some people are unable to make an enzyme called glucose-6-phosphate dehydrogenase, or G6PD, due to a genetic problem. Without this enzyme the red blood cells are easily ruptured when exposed to certain substances. Substances which may destroy red blood cells in G6PD deficient people include some anti-malarial drugs, such as chloroquine, sulfa drugs and naphthalene, a pesticide often found in moth balls. Fava beans, also known as broad beans, may be another cause of red blood cell destruction in some people. In this case the G6PD deficiency is known as favism.

Hepatitis is inflammation of the liver. As a result of this inflammation some liver cells may be destroyed. This can hinder the liver’s ability to convert unconjugated bilirubin into conjugated bilirubin and excrete the bilirubin into bile. A liver damaged by alcohol and toxins may also have trouble dealing with bilirubin. Cirrhosis of the liver will interfere with the liver’s ability to process bilirubin since in cirrhosis scar tissue replaces liver cells.

Gilbert’s syndrome is a hereditary disorder which causes an increase in bilirubin due to a decreased activity of the liver enzyme which produces conjugated bilirubin from unconjugated bilirubin. Mild and temporary jaundice may appear at times, especially during periods of body stress.

Non-steroidal anti-inflammatory drugs (NSAID’s), including aspirin and ibuprofen, can interfere with liver function and may cause jaundice if they are taken at high doses.

Blocked bile ducts can cause hyperbilirubinemia, since the bile is unable to reach the small intestine. The accumulating bilirubin collects in the tissues. Bile ducts may be blocked by gallstones, inflammation or tumors. The stool will be pale, since the bilirubin doesn’t enter the intestine and can’t be converted into stercobilin.

About sixty percent of newborn babies develop jaundice shortly after birth. The yellow color develops during the first week of the baby’s life. It appears in the head first and then spreads down the body. In a newborn baby many red blood cells are broken down as fetal hemoglobin is replaced with adult hemoglobin. The liver of a very young baby is often not developed enough to remove all the bilirubin from the body. Neonatal jaundice usually disappears without treatment. If it lasts for a long time, however, the baby will need treatment to lower the bilirubin level. Unconjugated bilirubin, the type that predominates in a newborn baby, is more dangerous than conjugated bilirubin, since the unconjugated form is fat-soluble and can enter the brain through the baby’s immature blood-brain barrier, where it may cause a type of brain damage called kernicterus. Phototherapy has been found to lower a baby’s bilirubin level. Blue light causes bilirubin to be converted to biliverdin, which is water-soluble and does not cause kernicterus.

Jaundice itself is not a serious condition, but it indicates that the body’s bilirubin level is too high. This may be a temporary increase and may be easily reversed, or it may be due to a serious problem in the body.