Linda Crampton is a writer and teacher with a first-class honors degree in biology. She often writes about the scientific basis of disease.
What Is Jaundice?
Jaundice is a disorder in which a person's skin, sclera, and mucous membranes in the mouth look yellow. The yellow coloration is produced by excess bilirubin in the body, a condition known as hyperbilirubinemia. It's important that the cause of the high bilirubin level and the yellow color that results is investigated by a doctor.
Bilirubin is a yellow pigment produced from the breakdown of the hemoglobin in dead red blood cells. Hemoglobin is the pigment that gives the red blood cells their color and transports oxygen. Old red blood cells die every day in our bodies and are replaced by new cells made in the red bone marrow. The breakdown of the hemoglobin in the dead cells causes bilirubin to be produced on a daily basis.
In a healthy person, the bilirubin is eliminated from the body. If the chemical collects in the body instead of being removed, there is likely a problem somewhere in the system that produces, processes, and gets rid of bilirubin. This problem may be minor and temporary or it may be more serious.
Hemoglobin Function and Bilirubin Production
Hemoglobin is a protein as well as a pigment. It carries inhaled oxygen around the body and distributes it to the body's cells. The cells use the oxygen to produce energy from nutrients.
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 substance called unconjugated bilirubin. The liver changes unconjugated bilirubin into a water-soluble substance called conjugated bilirubin. Both chemicals are yellow.
How Is Bilirubin Removed From the Body?
The liver produces bile, a liquid that emulsifies fats in the small intestine, helping them to be digested. The liver sends conjugated bilirubin into the bile. It then sends the liquid to the gallbladder. The gallbladder 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. First, a colorless substance called urobilinogen is made. Bacteria then convert some of the urobilinogen into a brown substance called stercobilin, which gives feces its color. The stercobilin leaves the body with the feces.
Urobilinogen also passes through the lining of the intestine and enters the bloodstream. The bloodstream transports the chemical to the kidneys. Some of the urobilinogen is converted to urobilin, the yellow pigment in urine. The kidneys send urobilinogen and urobilin into the urine, enabling the chemicals to leave the body during urination.
Another yellow pigment called urochrome is also present in urine. Some reference sources say that urobilin and urochrome are alternate names for the same substance. Others say that they are slightly different substances and that some of the urobilin is converted to urochrome.
Possible Causes of Hyperbilirubinemia
Excess bilirubin can build up in the following situations. Other causes of jaundice exist, but the ones listed below are some of the most common ones and are the ones that I will discuss in this article. The causes are:
- too many red blood cells are broken down
- the liver is infected or damaged
- the ducts (tubes) that transport bile from the liver to the gall bladder are blocked
- the ducts that transport bile from the gall bladder to the small intestine are blocked
- Gilbert's syndrome
Red blood cells look like pink discs under a microscope. The blood sample shown above was taken from someone with autoimmune hemolytic anemia. Some of the red blood cells have burst, producing white centers and misshapen cells. (The larger cells with a stained nucleus are white blood cells.)
In a condition called hemolytic anemia, a large number of red blood cells are destroyed. The body may not be able to process all of the bilirubin that is made, causing jaundice to develop.
Hemolytic anemia can result from a number of causes, including malaria and sickle cell anemia. The malaria parasite infects and destroys red blood cells. 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 10 to 20 days. Normal red blood cells live for around 120 days.
In some cases, hemolytic anemia is an autoimmune condition. In this condition, antibodies in the immune system mistakenly attack the red blood cells, causing them to break open. The disorder is rare, but it's unpleasant for the people who experience it.
G6PD Enzyme Deficiency
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 or conditions. Factors which lead to the destruction of red blood cells in G6PD deficient people include a variety of medications and serious infections.
Fava beans, also known as broad beans, may be another cause of red blood cell destruction in some people with G6PD deficiency. This body’s response to the beans is known as favism. In sensitive people, chemicals in the beans trigger a chain of processes that lead to the destruction of red blood cells. Not all people with G6PD deficiency have favism, however.
Hepatitis is inflammation of the liver. It can be caused by a viral infection, exposure to certain toxins, specific medicines if they are used inappropriately, trauma to the liver, or fat buildup inside the liver. It can also be caused by an autoimmune condition in which the body's immune system mistakenly attacks the liver.
As a result of the inflammation in hepatitis, some liver cells may be destroyed. This can hinder the organ’s ability to convert unconjugated bilirubin into conjugated bilirubin and then send the bilirubin into bile. As a result, jaundice may develop.
Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen, and naproxen, can interfere with liver function and may cause jaundice if they are taken at high doses for a long period of time. Large doses of acetaminophen can also cause the disorder.
Cirrhosis of the Liver
Alcohol is a special problem for the liver. Chronic alcohol consumption can not only cause inflammation in the liver but also cause the development of a potentially serious disorder known as cirrhosis. In cirrhosis, fibrous and scar tissue replace liver cells. This interferes with the liver's ability to process bilirubin and may result in jaundice.
Cirrhosis sometimes develops in people who don't drink alcohol. In a condition known as non-alcoholic fatty liver disease, or NAFLD, fat collects in the liver. A healthy liver may contain a small amount of fat, but in NAFLD an excessive amount in deposited. Obesity, diabetes, and a high cholesterol or triglyceride (fat) level in the blood are risk factors for NAFLD. Sometimes, though, the condition develops with no apparent cause.
NAFLD may not be serious and may not cause any symptoms. Severe cases can cause liver inflammation and swelling, however. In this case, the disorder is known as NASH, or non-alcoholic steatohepatitis. The fat deposits may be accompanied by the formation of scar tissue, or cirrhosis. A decreased ability to process bilirubin and the production of jaundice may be one result of the disease.
Jaundice and Blocked Bile Ducts
A blocked bile duct may cause hyperbilirubinemia. The bile that is released from the gall bladder or the liver may be unable to reach the small intestine due to the blockage. The bilirubin from the accumulating bile may then collect in the tissues, producing jaundice.
Bile ducts may be blocked by gallstones, inflammation accompanied by swollen tissues, or tumors. Someone with blocked bile ducts often has pale feces, since the bilirubin doesn’t enter the intestine and can’t be converted into stercobilin.
The Liver and Its Ducts
Gilbert’s syndrome is a hereditary disorder. Someone with this syndrome experiences a slight increase in bilirubin due to a decreased activity of the liver enzyme that produces conjugated bilirubin from the unconjugated form. The enzyme deficiency causes the level of unconjugated bilirubin to rise.
Gilbert's syndrome is a fairly common condition that generally doesn't require any treatment, though this decision is up to a doctor. The jaundice that develops is mild and temporary. Certain triggers tend to produce this transitory jaundice. These include stress, fatigue, strenuous exercise, dehydration, and fasting. Some people with Gilbert's syndrome develop jaundice when they're ill or, in the case of females, during menstruation.
What Is Neonatal or Newborn Jaundice?
Several types of jaundice can develop in newborn babies. These conditions are collectively known as neonatal or newborn jaundice.
The most common type of neonatal jaundice is called physiological or physiologic jaundice. About sixty percent of newborn babies develop this condition shortly after birth. The percentage rises to around eighty percent if the babies are premature. The yellow color develops during the first week of the baby’s life. It appears in the head first and may then spread down the body.
The cycle of red blood cell destruction and production typically occurs at an accelerated rate in the first ten to fourteen days after birth. Physiological jaundice develops when the liver of a very young baby isn't developed enough to remove all the bilirubin produced from the hemoglobin breakdown in its body.
Breast Milk Jaundice
A few babies develop jaundice due to being breast fed. The condition begins after the first week of life. The reason for the condition isn't completely understood, but it's thought that there may be a chemical in the milk that blocks the breakdown of bilirubin in the baby's body. The condition doesn't necessarily mean that a women needs to stop feeding her baby. As always, a doctor's advice should be sought in relation to the jaundice.
Breast Feeding Jaundice
If a baby doesn't obtain enough fluids from milk due to a feeding problem, the bilirubin in his or body may become too concentrated. This may result in jaundice. Health professionals can help a woman find a solution to this problem.
Neonatal Jaundice and Treatment With Blue Light
A Common Treatment for Neonatal Jaundice
Neonatal jaundice is usually a temporary condition and may disappear without treatment. A newborn baby should be monitored closely and a doctor consulted if jaundice appears, however. If jaundice lasts for a long time or if it's severe, the baby may need treatment to lower the bilirubin level. Unconjugated bilirubin, the type that predominates in a newborn baby, is more dangerous than conjugated bilirubin. 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—the use of light to treat a disease—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. The treatment with blue light may take place in a hospital or with a special light-emitting mat at home.
Taking Care of the Liver
Some conditions that cause hyperbilirubinemia and jaundice, such as inherited disorders, can't be avoided. In these cases, the focus of medical treatment is the management of the disorder. The chance of developing other conditions can be reduced by changing the diet or lifestyle, however.
Since the liver is the site of many problems that can increase the bilirubin level, it's important that we take care of the organ. Reducing or eliminating alcohol consumption, following a healthy diet, and getting regular exercise are useful strategies to improve and maintain the health of the liver and the entire body.
- Jaundice in adults from the Merck Manual
- Diseases associated with hyperbilirubinemia from the University of Utah
- Facts about hemolytic anemia from the National Heart, Lung, and Blood Institute
- G6PD information from Cedars-Sinai Medical Center
- Drug-induced hepatitis information from John Hopkins Medicine
- Non-alcoholic fatty liver disease from the National Health Service
- Information about cirrhosis of the liver from WebMD
- Gilbert's syndrome information from the Mayo Clinic
- Newborn jaundice from the National Institutes of Health
- Facts about infant jaundice from the Mayo Clinic
This content is accurate and true to the best of the author’s knowledge and does not substitute for diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed health professional. Drugs, supplements, and natural remedies may have dangerous side effects. If pregnant or nursing, consult with a qualified provider on an individual basis. Seek immediate help if you are experiencing a medical emergency.
© 2010 Linda Crampton
Linda Crampton (author) from British Columbia, Canada on December 13, 2011:
Hi, healthwriterbob! Thank you very much for the comment.
healthwriterbob from United States on December 13, 2011:
I enjoyed your article. I particularly liked the way that you discussed the formation and transformation of bilirubin followed by its elimination from the body in the bile.
Linda Crampton (author) from British Columbia, Canada on November 02, 2011:
Thank you for the comment, Journey*. I'm glad that you found the hub informative. Hyperbilirubinemia and jaundice are interesting subjects to research.
Nyesha Pagnou MPH from USA on November 02, 2011:
This is very interesting, informative and well detailed. Thanks for sharing.
Linda Crampton (author) from British Columbia, Canada on February 24, 2011:
Thank you very much for the vote, daydreamer13. I find jaundice an interesting topic too.
daydreamer13 on February 24, 2011:
I know a lot of babies who had jaundice right after birth. This is all very interesting. Voted up!