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Gilbert's (zheel-BAYRS) syndrome is a common, harmless liver condition in which the liver doesn't properly process bilirubin. Bilirubin is produced by the breakdown of red blood cells. If you have Gilbert's syndrome — also known as constitutional hepatic dysfunction and familial nonhemolytic jaundice — you're born with the condition as a ...
Gilbert’s syndrome is an inherited liver condition in which your liver can’t fully process a compound called bilirubin. Your liver breaks down old red blood cells into compounds, including ...
Gilbert syndrome is a common disorder that's passed through families. When you have it, too much of a waste product called bilirubin builds up in your blood.It can make your skin and eyes look ...
Gilbert's syndrome is a phenotypic effect, mostly clearly associated with increased blood bilirubin levels, but also sometimes characterized by mild jaundice due to increased unconjugated bilirubin, that arises from several different genotypic variants of the gene for the enzyme responsible for changing bilirubin to the conjugated form.
Gilbert syndrome is a relatively mild condition characterized by periods of elevated levels of a toxic substance called bilirubin in the blood (hyperbilirubinemia). ). Bilirubin, which has an orange-yellow tint, is produced when red blood cells are br
Gilbert Syndrome is a common, harmless genetic condition in which a liver enzyme essential to the disposal of bilirubin (the chemical that results from the normal breakdown of hemoglobin from red blood cells) is abnormal.
Kernicterus is a bilirubin-induced brain dysfunction. The term was coined in 1904 by Schmorl. Bilirubin is a naturally occurring substance in the body of humans and many other animals, but it is neurotoxic when its concentration in the blood is too high, a condition known as hyperbilirubinemia. Hyperbilirubinemia may cause bilirubin to accumulate in the grey matter of the central nervous system, potentially causing irreversible neurological damage. Depending on the level of exposure, the effects range from clinically unnoticeable to severe brain damage and even death. When hyperbilirubinemia increases past a mild level, it leads to jaundice, raising the risk of progressing to kernicterus. When this happens in adults, it is usually because of liver problems. Newborns are especially vulnerable to hyperbilirubinemia-induced neurological damage, because in the earliest days of life, the still-developing liver is heavily exercised by the breakdown of fetal hemoglobin as it is replaced with adult hemoglobin and the blood brain barrier is not as developed.
In medicine, bilirubinuria is an abnormality in which conjugated bilirubin is detected in the urine. The term "biliuria" is very similar, but more general. It refers to the presence of any bile pigment in the urine. Conjugated bilirubin is detected in urine at bilirubinemia of approximately 30-34 mmol/l or 20 mg/dL. In this concentration of conjugated bilirubin in the blood appears yellowness of the mucous membranes and sclera.
Gilbert's syndrome (GS) is a mild liver disorder in which the liver does not properly process bilirubin. Many people never have symptoms. Occasionally a slight yellowish color of the skin or whites of the eyes may occur. Other possible symptoms include feeling tired, weakness, and abdominal pain. Gilbert's syndrome is due to a mutation in the UGT1A1 gene which results in decreased activity of the bilirubin uridine diphosphate glucuronosyltransferase enzyme. It is typically inherited in an autosomal recessive pattern and occasionally in an autosomal dominant pattern depending on the type of mutation. Episodes of jaundice may be triggered by stress such as exercise, menstruation, or not eating. Diagnosis is based on higher levels of unconjugated bilirubin in the blood without either signs of other liver problems or red blood cell breakdown. Typically no treatment is needed. If jaundice is significant phenobarbital may be used. Gilbert's syndrome affects about 5% of people in the United States. Males are more often diagnosed than females. It is often not noticed until late childhood to early adulthood. The condition was first described in 1901 by Augustin Nicolas Gilbert.