Red blood cells have a finite lifespan of approximately 3 months in the bloodstream. Once removed from the circulation, the liver and spleen break down the red blood cells, releasing unconjugated bilirubin. Liver cells process unconjugated bilirubin into conjugated bilirubin, which is then incorporated into the bile. Conditions that increase the rate of red blood cell breakdown or interfere with bilirubin conjugation commonly cause elevations in the blood level of unconjugated bilirubin.
Gilbert's Syndrome
Gilbert's syndrome is an inherited disorder in which a genetic mutation leads to a decreased rate of conversion of unconjugated to conjugated bilirubin. The slowed conversion caused an increased level of unconjugated bilirubin in the blood, or unconjugated hyperbilirubinemia.
Gilbert's syndrome frequently causes no symptoms. Some people may develop jaundice, a yellowing of the skin and whites of the eyes, due to increased levels of blood bilirubin. A small percentage of those affected by Gilbert's syndrome experience poor appetite, abdominal pain and mild fatigue. Approximately 3 to 7 percent of the population in the United States is affected by Gilbert's syndrome, reports the University of Pittsburgh Medical Center.
Sickle Cell Anemia
Sickle cell anemia is an inherited abnormality of the red blood cells. A distortion of the oxygen-carrying hemoglobin in people with sickle cell anemia causes misshapen red blood cells, explains the National Heart, Lung and Blood Institute. The liver and spleen remove the abnormally shaped red blood cell from the circulation at a rapid rate, leading to chronic anemia.
The increased rate of red blood cell destruction associated with sickle cell anemia presents the liver with a chronic overload of unconjugated bilirubin, which builds up in the bloodstream. People with sickle cell anemia characteristically exhibit a persistently elevated level of unconjugated bilirubin.
Erythroblastosis Fetalis
Erythroblastosis fetalis is a serious condition caused by blood type incompatibility between a pregnant woman and her baby. Antibodies from the mother's bloodstream cross into the baby's bloodstream, leading to destruction of the baby's red blood cells, explains The Merck Manual for Healthcare Professionals.
At birth, babies with erythroblastosis fetalis present with anemia and an elevated unconjugated bilirubin level, caused by red blood cell destruction while in the womb. Other symptoms include jaundice, liver and spleen enlargement and tissue swelling. Complete replacement of the circulating blood pool, or exchange transfusion, may be required in babies with severe disease.
Extensive Bruising
As noted in a National Library of Medicine MedlinePlus entry, large areas of tissue bruising, such as sustained in a traumatic accident, may cause a transient elevation in unconjugated bilirubin. Increased red blood cell breakdown caused by a large volume of blood in the bruised tissues temporarily overwhelms the liver's capacity to process bilirubin. With resolution of the bruises, the liver catches up with the temporary bilirubin overload and unconjugated bilirubin levels return to normal.
References
- University of Pittsburgh Medical Center: Gilbert's Syndrome
- National Heart, Lung and Blood Institute: Sickle Cell Anemia
- The Merck Manual for Healthcare Professionals: Erythroblastosis Fetalis
- MedlinePlus: Bilirubin--Blood
- "Harrison’s Principles of Internal Medicine, 16th Edition"; Dennis L. Kasper, M.D., et al., (eds.); 2004
