Jaundice, also known as icterus, is a yellowish or greenish pigmentation of the skin and whites of the eyes due to high bilirubin levels.[2][5] It is commonly associated with itchiness.[1] The feces may be pale and the urine dark.[3] Jaundice in babies occurs in over half in the first week following birth and does not pose a serious threat in most.[2][5] If bilirubin levels in babies are very high for too long, a type of brain damage, known as kernicterus, may occur.[6]

Causes of jaundice vary from non-serious to potentially fatal.[7] Levels of bilirubin in blood are normally below 1.0 mg/dL (17 µmol/L) and levels over 2–3 mg/dL (34-51 µmol/L) typically results in jaundice.[8][3] High bilirubin is divided into two types: unconjugated (indirect) and conjugated (direct).[7] Conjugated bilirubin can be confirmed by finding bilirubin in the urine.[9] Other conditions that can cause yellowish skin but are not jaundice include carotenemia from eating large amounts of certain foods and medications like rifampin.[3]

High unconjugated bilirubin may be due to excess red blood cell breakdown, large bruises, genetic conditions such as Gilbert's syndrome, not eating for a prolonged period of time, newborn jaundice, or thyroid problems.[3][7] High conjugated bilirubin may be due to liver diseases such as cirrhosis or hepatitis, infections, medications, or blockage of the bile duct.[3] In the developed world, the cause is more often blockage of the bile duct or medications while in the developing world, it is more often infections such as viral hepatitis, leptospirosis, schistosomiasis, or malaria.[3] Blockage of the bile duct may occur due to gallstones, cancer, or pancreatitis.[3] Medical imaging such as ultrasound is useful for detecting bile duct blockage.[9]

Treatment of jaundice is typically determined by the underlying cause.[4] If a bile duct blockage is present, surgery is typically required; otherwise, management is medical.[4] Medical management may involve treating infectious causes and stopping medication that could be contributing.[4] Among newborns, depending on age and prematurity, a bilirubin greater than 4–21 mg/dL (68-360 µmol/L) may be treated with phototherapy or exchanged transfusion.[8] The itchiness may be helped by draining the gallbladder or ursodeoxycholic acid.[1] The word jaundice is from the French jaunisse, meaning "yellow disease".[10]

Other namesIcterus
Jaundice of the skin caused by pancreatic cancer
  • /ˈdʒɔːndɪs/
SpecialtyGastroenterology, hepatology, general surgery
SymptomsYellowish coloration of skin and whites of the eyes, pruritis[1][2]
CausesHigh bilirubin levels[2]
Diagnostic methodBlood bilirubin, liver panel[2]
Differential diagnosisCarotenemia, taking rifampin[3]
TreatmentBased on the underlying cause[4]

Signs and symptoms

4-year-old boy with jaundiced (yellowish) scleras that later proved to be a manifestation of hemolytic anemia due to G6PD deficiency following fava bean consumption.

The main sign of jaundice is a yellowish discoloration of the white area of the eye and the skin. Urine is dark in colour.[11] Slight increases in serum bilirubin are best detected by examining the sclerae, which have a particular affinity for bilirubin due to their high elastin content. The presence of scleral icterus indicates a serum bilirubin of at least 3 mg/dL. The conjunctiva of the eye are one of the first tissues to change color as bilirubin levels rise in jaundice. This is sometimes referred to as scleral icterus. The sclera themselves are not "icteric" (stained with bile pigment), however, but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly termed conjunctival icterus. The term "icterus" itself is sometimes incorrectly used to refer to jaundice that is noted in the sclera of the eyes; its more common and more correct meaning is entirely synonymous with jaundice, however.[12][13]


Hyperbilirubinemia, more precisely hyperbilirubinemia due to the unconjugated fraction, may cause bilirubin to accumulate in the gray matter of the central nervous system, potentially causing irreversible neurological damage leading to a condition known as kernicterus. Depending on the level of exposure, the effects range from unnoticeable to severe brain damage and even death. Newborns are especially vulnerable to hyperbilirubinemia-induced neurological damage and therefore must be carefully monitored for alterations in their serum bilirubin levels.

Differential diagnosis

Types of jaundice

When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

Category Definition
Pre-hepatic/hemolytic The pathology is occurring prior to the liver due to either:

A. Intrinsic defects in RB cells B. Extrinsic causes external to RB cells

Hepatic/hepatocellular The pathology is located within the liver caused due to disease of parenchymal cells of liver.
Post-hepatic/cholestatic The pathology is located after the conjugation of bilirubin in the liver caused due to obstruction of biliary passage.[14]


Pre-hepaticular jaundice is caused by anything that causes an increased rate of hemolysis (breakdown of red blood cells). Unconjugated bilirubin comes from the breakdown of the heme pigment found in red blood cells' hemoglobin. The increased breakdown of red blood cells leads to an increase in the amount of unconjugated bilirubin present in the blood and deposition of this unconjugated bilirubin into various tissues can lead to a jaundiced appearance. In tropical countries, severe malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia, pyruvate kinase deficiency, and glucose-6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic-uremic syndrome, can also lead to coloration.

In jaundice secondary to hemolysis, the increased production of bilirubin leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble, so, the combination of increased urine-urobilinogen with no bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.

Laboratory findings include:

  • Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed).
  • Serum: increased unconjugated bilirubin.
  • Kernicterus is associated with increased unconjugated bilirubin not carried by albumin. Newborns are especially vulnerable to this due to increased permeability of the blood–brain barrier.


Bilirubin pigment in cholestatic liver 40X
Microscopy of cholestatic liver showing bilirubin pigment, H&E stain

Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug-induced hepatitis and alcoholic liver disease. Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood. Other causes include primary biliary cirrhosis leading to an increase in plasma conjugated bilirubin because there is impairment of excretion of conjugated bilirubin into the bile. The blood contains an abnormally raised amount of conjugated bilirubin and bile salts, which are excreted in the urine. Jaundice seen in the newborn, known as neonatal jaundice, is common in newborns[15] as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age. Rat fever (leptospirosis) can also cause hepatic jaundice. In hepatic jaundice, there is invariably cholestasis. Defects in bilirubin metabolism also leads to jaundice, as in Gilbert's syndrome (a genetic disorder of bilirubin metabolism that can result in mild jaundice, which is found in about 5% of the population) and Crigler–Najjar syndrome, Type I and II.

Laboratory findings depend on the cause of jaundice.

  • Urine: Conjugated bilirubin present, urobilinogen > 2 units but variable (except in children). Kernicterus is a condition not associated with increased conjugated bilirubin.
  • Plasma protein show characteristic changes.
  • Plasma albumin level is low but plasma globulins are raised due to an increased formation of antibodies.

Bilirubin transport across the hepatocyte may be impaired at any point between the uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin into biliary canaliculi. In addition, swelling of cells and oedema due to inflammation cause mechanical obstruction of intrahepatic biliary tree. Hence in hepatocellular jaundice, concentration of both unconjugated and conjugated bilirubin rises in the blood. In hepatocellular disease, there is usually interference in all major steps of bilirubin metabolism—uptake, conjugation and excretion. Excretion is the rate-limiting step, however, and usually impaired to the greatest extent. As a result, conjugated hyperbilirubinaemia predominates.[16]

The unconjugated bilirubin still enters the liver cells and becomes conjugated in the usual way. This conjugated bilirubin is then returned to the blood, probably by rupture of the congested bile canaliculi and direct emptying of the bile into the lymph leaving the liver. Thus, most of the bilirubin in the plasma becomes the conjugated type rather than the unconjugated type, and this conjugated bilirubin, which did not go to intestine to become urobilinogen, gives the urine the dark color.[17]


Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile containing conjugated bilirubin in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" can live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, cholangiocarcinoma, pancreatitis, cholestasis of pregnancy, and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome (gallstone impaction in the cystic duct or gallbladder neck, with the enlarged gallbladder squeezing on the common hepatic duct).

In complete obstruction of the bile duct, no urobilinogen is found in the urine, since bilirubin has no access to the intestine and it is in the intestine that bilirubin gets converted to urobilinogen by microorganisms, with the urobilinogen later being partially reabsorbed from the intestine into the general circulation, and then excreted into the urine. In this case, presence of bilirubin (conjugated) in the urine without urine-urobilinogen suggests obstructive jaundice, either intra-hepatic or post-hepatic.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments. They can, however, occur in many intra-hepatic illnesses and are therefore not a reliable clinical feature to distinguish obstruction from hepatic causes of jaundice.[18]

Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus" because of the direct and indirect effects of pruritogens in bile such as bile salts.[19]

No single test can differentiate between various classifications of jaundice. A combination of liver function tests is essential to arrive at a diagnosis.

Diagnostic tests[20]
Function test Pre-hepatic jaundice Hepatic jaundice Post-hepatic jaundice
Total bilirubin Normal / increased Increased
Conjugated bilirubin Normal Increased
Unconjugated bilirubin Normal / increased Increased Normal
Urobilinogen Normal / increased Decreased Decreased / negative
Urine color Normal[21] Dark (urobilinogen + conjugated bilirubin) Dark (conjugated bilirubin)
Stool color Brown Slightly pale Pale
Alkaline phosphatase levels Normal Increased
Alanine transferase and aspartate transferase levels Increased
Conjugated bilirubin in urine Not present Present
Large spleen Present Present Absent


Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Typical causes for neonatal jaundice include normal physiologic jaundice, jaundice due to formula supplementation,[22] and hemolytic disorders that include hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, pyruvate kinase deficiency, ABO/Rh blood type autoantibodies, or infantile pyknocytosis. Serum bilirubin normally drops to a low level without any intervention required. In cases where bilirubin rises higher, a brain-damaging condition known as kernicterus can occur, leading to significant disability.[23] This condition has been rising in recent years due to less time spent outdoors. A Bili light is often the tool used for early treatment, which often consists of exposing the baby to intensive phototherapy. Sunbathing is effective treatment,[24][25] and has the advantage of ultra-violet-B, which promotes Vitamin D production.[26] Bilirubin count is lowered through bowel movements and urination, so frequent and effective feedings are especially important.[27]

Differential diagnosis

Yellow discoloration of the skin, especially on the palms and the soles, but not of the sclera or inside the mouth is due to carotenemia—a harmless condition.[28]


Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occur at some point along the normal physiological pathway of the metabolism of bilirubin in blood.

When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. As each red blood cell traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this. Cellular contents, including hemoglobin, are subsequently released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice. Two reactions then take place with the heme molecule. The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron and carbon monoxide. The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is "unconjugated," "free" or "indirect" bilirubin. Approximately 4 mg of bilirubin per kg of blood is produced each day.[29] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. Approximately twenty percent comes from other heme sources, however, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.[29]

Hepatic events

The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water-soluble. The reaction is catalyzed by the enzyme UDP-glucuronyl transferase.

This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of feces and urine, respectively.


It is unclear how common jaundice is among adults.[30]

Diagnostic approach

Biliary tract dilation due to obstruction as seen on CAT scan
Biliary tract dilation due to obstruction

Most patients presenting with jaundice will have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel will include blood levels of enzymes found primarily from the liver, such as the aminotransferases (ALT, AST), and alkaline phosphatase (ALP); bilirubin (which causes the jaundice); and protein levels, specifically, total protein and albumin. Other primary lab tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT).

Some bone and heart disorders can lead to an increase in ALP and the aminotransferases, so the first step in differentiating these from liver problems is to compare the levels of GGT, which will only be elevated in liver-specific conditions. The second step is distinguishing from biliary (cholestatic) or liver (hepatic) causes of jaundice and altered laboratory results. The former typically indicates a surgical response, while the latter typically leans toward a medical response. ALP and GGT levels will typically rise with one pattern while aspartate aminotransferase (AST) and alanine aminotransferase (ALT) rise in a separate pattern. If the ALP (10–45 IU/L) and GGT (18–85) levels rise proportionately about as high as the AST (12–38 IU/L) and ALT (10–45 IU/L) levels, this indicates a cholestatic problem. On the other hand, if the AST and ALT rise is significantly higher than the ALP and GGT rise, this indicates an hepatic problem. Finally, distinguishing between hepatic causes of jaundice, comparing levels of AST and ALT can prove useful. AST levels will typically be higher than ALT. This remains the case in most hepatic disorders except for hepatitis (viral or hepatotoxic). Alcoholic liver damage may see fairly normal ALT levels, with AST 10x higher than ALT. On the other hand, if ALT is higher than AST, this is indicative of hepatitis. Levels of ALT and AST are not well correlated to the extent of liver damage, although rapid drops in these levels from very high levels can indicate severe necrosis. Low levels of albumin tend to indicate a chronic condition, while it is normal in hepatitis and cholestasis.

Lab results for liver panels are frequently compared by the magnitude of their differences, not the pure number, as well as by their ratios. The AST:ALT ratio can be a good indicator of whether the disorder is alcoholic liver damage (above 10), some other form of liver damage (above 1), or hepatitis (less than 1). Bilirubin levels greater than 10x normal could indicate neoplastic or intrahepatic cholestasis. Levels lower than this tend to indicate hepatocellular causes. AST levels greater than 15x tends to indicate acute hepatocellular damage. Less than this tend to indicate obstructive causes. ALP levels greater than 5x normal tend to indicate obstruction, while levels greater than 10x normal can indicate drug (toxic) induced cholestatic hepatitis or Cytomegalovirus. Both of these conditions can also have ALT and AST greater than 20× normal. GGT levels greater than 10x normal typically indicate cholestasis. Levels 5–10× tend to indicate viral hepatitis. Levels less than 5× normal tend to indicate drug toxicity. Acute hepatitis will typically have ALT and AST levels rising 20–30× normal (above 1000), and may remain significantly elevated for several weeks. Acetaminophen toxicity can result in ALT and AST levels greater than 50x normal.


Jaundice comes from the French jaune, meaning yellow, jaunisse meaning "yellow disease". The medical term for it is icterus, from the Greek word ίκτερος; adjectival form, icteric.[12]


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  19. ^ Bassari R, Koea JB (2015). "Jaundice associated pruritis: A review of pathophysiology and treatment". World J. Gastroenterol. 21 (5): 1404–13. doi:10.3748/wjg.v21.i5.1404. PMC 4316083. PMID 25663760.
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External links

External resources
  • The dictionary definition of jaundice at Wiktionary
  • Media related to Jaundice at Wikimedia Commons

Athetosis is a symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue. Movements typical of athetosis are sometimes called athetoid movements. Lesions to the brain are most often the direct cause of the symptoms, particularly to the

corpus striatum. This symptom does not occur alone and is often accompanied by the symptoms of cerebral palsy, as it is often a result of this disease. Treatments for athetosis are not very effective, and in most cases are simply aimed at managing the uncontrollable movement, rather than the cause itself.

Bile duct

A bile duct is any of a number of long tube-like structures that carry bile, and is present in most vertebrates.

Bile, required for the digestion of food, is secreted by the liver into passages that carry bile toward the hepatic duct, which joins with the cystic duct (carrying bile to and from the gallbladder) to form the common bile duct, which opens into the intestine.


Bilirubin is a yellow compound that occurs in the normal catabolic pathway that breaks down heme in vertebrates. This catabolism is a necessary process in the body's clearance of waste products that arise from the destruction of aged or abnormal red blood cells. First the hemoglobin gets stripped of the heme molecule which thereafter passes through various processes of porphyrin catabolism, depending on the part of the body in which the breakdown occurs. For example, the molecules excreted in the urine differ from those in the feces. The production of biliverdin from heme is the first major step in the catabolic pathway, after which the enzyme biliverdin reductase performs the second step, producing bilirubin from biliverdin.Bilirubin is excreted in bile and urine, and elevated levels may indicate certain diseases. It is responsible for the yellow color of bruises and the yellow discoloration in jaundice. Its subsequent breakdown products, such as stercobilin, cause the brown color of faeces. A different breakdown product, urobilin, is the main component of the straw-yellow color in urine.

It has also been found in plants.


Carotenosis is due to an excess of dietary carotenoids and results in orange discoloration of the outermost skin layer. This is a benign and reversible condition – which is most easily observed in light-skinned people and may be mistaken for jaundice. Carotenoids are lipid-soluble compounds that include alpha- and beta-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin. The primary serum carotenoids are beta-carotene, lycopene, and lutein. Serum levels of carotenoids vary between region, ethnicity, and sex in the healthy population. All are absorbed by passive diffusion from the gastrointestinal tract and are then partially metabolized in the intestinal mucosa and liver to vitamin A. From there they are transported in the plasma into the peripheral tissues. Carotenoids are eliminated via sweat, sebum, urine, and gastrointestinal secretions. Carotenoids contribute to normal-appearing human skin color, and are a significant component of physiologic ultraviolet photoprotection.Carotenemia most commonly occurs in vegetarians and young children. Carotenemia is more easily appreciated in light-complexioned people, and it may present chiefly as an orange discolouration of the palms and the soles in more darkly pigmented persons. Carotenemia does not cause selective orange discoloration of the conjunctival membranes over the sclerae (whites of the eyes), and thus is usually easy to distinguish from the yellowing of the skin and conjunctiva caused by bile pigments in states of jaundice.

Carotenoderma is deliberately caused by beta-carotenoid treatment of certain photo-sensitive dermatitis diseases such as erythropoietic protoporphyria, where beta carotene is prescribed in quantities which discolor the skin. These high doses of beta carotene have been found to be harmless in studies, though cosmetically displeasing to some. In a recent meta analysis of these treatments, however, the effectiveness of the treatment has been called into question.

Common bile duct stone

Common bile duct stone, also known as choledocholithiasis, is the presence of gallstones in the common bile duct (CBD) (thus choledocho- + lithiasis). This condition can cause jaundice and liver cell damage. Treatment is by cholecystectomy and endoscopic retrograde cholangiopancreatography (ERCP).

Courvoisier's law

Courvoisier's law (or Courvoisier syndrome, or Courvoisier's sign or Courvoisier-Terrier's sign) states that in the presence of a palpable enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones. Usually, the term is used to describe the physical examination finding of the right-upper quadrant of the abdomen. This sign implicates possible malignancy of the gallbladder or pancreas and the swelling is unlikely due to gallstones.This observation occurs because gallstones are formed over an extended period of time, resulting in a shrunken, fibrotic gallbladder which does not distend easily and is less likely to be palpable on exam. In contrast, the gallbladder is more often enlarged and thus more easily palpated in pathologies that cause obstruction of the biliary tree over a more acute, shorter period of time such as pancreatic malignancy, leading to passive distention from back pressure.Ludwig Georg Courvoisier's original observations, published in Germany in 1890, were not originally cited as a 'law', and no mention of malignancy or pain (tenderness) was made. These points are commonly misquoted or confused in the medical literature.

Crigler–Najjar syndrome

Crigler–Najjar syndrome is a rare inherited disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of the heme in red blood cells. The disorder results in a form of nonhemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants. The disorder is inherited in an autosomal recessive manner.

This syndrome is divided into types I and II, with the latter sometimes called Arias syndrome. These two types, along with Gilbert's syndrome, Dubin–Johnson syndrome, and Rotor syndrome, make up the five known hereditary defects in bilirubin metabolism. Unlike Gilbert's syndrome, only a few causes of CNS are known.

Gilbert's syndrome

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.

Glucose-6-phosphate dehydrogenase deficiency

Glucose-6-phosphate dehydrogenase deficiency (G6PDD) is an inborn error of metabolism that predisposes to red blood cell breakdown. Most of the time, those who are affected have no symptoms. Following a specific trigger, symptoms such as yellowish skin, dark urine, shortness of breath, and feeling tired may develop. Complications can include anemia and newborn jaundice. Some people never have symptoms.It is an X-linked recessive disorder that results in defective glucose-6-phosphate dehydrogenase enzyme. Red blood cell breakdown may be triggered by infections, certain medication, stress, or foods such as fava beans. Depending on the specific mutation the severity of the condition may vary. Diagnosis is based on symptoms and supported by blood tests and genetic testing.Avoiding triggers is important. Treatment of acute episodes may include medications for infection, stopping the offending medication, or blood transfusions. Jaundice in newborns may be treated with bili lights. It is recommended that people be tested for G6PDD before certain medications, such as primaquine, are taken.About 400 million people have the condition globally. It is particularly common in certain parts of Africa, Asia, the Mediterranean, and the Middle East. Males are affected more often than females. In 2015 it is believed to have resulted in 33,000 deaths. Carriers of the G6PDD allele may be partially protected against malaria.


Hepatitis is inflammation of the liver tissue. Some people have no symptoms whereas others develop yellow discoloration of the skin and whites of the eyes, poor appetite, vomiting, tiredness, abdominal pain, or diarrhea. Hepatitis may be temporary (acute) or long term (chronic) depending on whether it lasts for less than or more than six months. Acute hepatitis can sometimes resolve on its own, progress to chronic hepatitis, or rarely result in acute liver failure. Over time the chronic form may progress to scarring of the liver, liver failure, or liver cancer.The most common causes of hepatitis worldwide are viruses. Other causes include heavy alcohol use, certain medications, toxins, other infections, autoimmune diseases, and non-alcoholic steatohepatitis (NASH). There are five main types of viral hepatitis: type A, B, C, D, and E. Hepatitis A and E are mainly spread by contaminated food and water. Hepatitis B is mainly sexually transmitted, but may also be passed from mother to baby during pregnancy or childbirth. Both hepatitis B and C are commonly spread through infected blood such as may occur during needle sharing by intravenous drug users. Hepatitis D can only infect people already infected with hepatitis B.Hepatitis A, B, and D are preventable with immunization. Medications may be used to treat chronic cases of viral hepatitis. There is no specific treatment for NASH; however, a healthy lifestyle, including physical activity, a healthy diet, and weight loss, is important. Autoimmune hepatitis may be treated with medications to suppress the immune system. A liver transplant may also be an option in certain cases.Worldwide in 2015, hepatitis A occurred in about 114 million people, chronic hepatitis B affected about 343 million people and chronic hepatitis C about 142 million people. In the United States, NASH affects about 11 million people and alcoholic hepatitis affects about 5 million people. Hepatitis results in more than a million deaths a year, most of which occur indirectly from liver scarring or liver cancer. In the United States, hepatitis A is estimated to occur in about 2,500 people a year and results in about 75 deaths. The word is derived from the Greek hêpar (ἧπαρ), meaning "liver", and -itis (-ῖτις), meaning "inflammation".

Intrahepatic cholestasis of pregnancy

Intrahepatic cholestasis of pregnancy (ICP), also known as obstetric cholestasis, cholestasis of pregnancy, jaundice of pregnancy, and prurigo gravidarum, is a medical condition in which cholestasis occurs during pregnancy. It typically presents with itching and can lead to complications for both mother and baby.

Pruritus (itching) is a common symptom of pregnancy, affecting around 20% of women. The majority of times, itching is a minor annoyance caused by changes to the skin, especially that of the abdomen. However, there are instances when itching may be a symptom of ICP. Although typically noticed on the palms of the hands and the soles of the feet, the itching can occur anywhere on the body.

ICP occurs most commonly in the third trimester, but can begin at any time during the pregnancy.


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. Mildly elevated serum bilirubin levels are common in newborns, and neonatal jaundice is not unusual, but bilirubin levels must be carefully monitored in case they start to climb, in which case more aggressive therapy is needed, usually via light therapy but sometimes even via exchange transfusion.


Leptospirosis is an infection caused by corkscrew-shaped bacteria called Leptospira. Signs and symptoms can range from none to mild such as headaches, muscle pains, and fevers to severe with bleeding from the lungs or meningitis. If the infection causes the person to turn yellow, have kidney failure and bleeding, it is then known as Weil's disease. If it also causes bleeding into the lungs then it is known as severe pulmonary haemorrhage syndrome.Up to 10 different genetic types of Leptospira may cause disease in humans. It is transmitted by both wild and domestic animals. The most common animals that spread the disease are rodents. It is often transmitted by animal urine or by water or soil containing animal urine coming into contact with breaks in the skin, eyes, mouth, or nose. In the developing world the disease most commonly occurs in farmers and low-income people who live in cities. In the developed world it most commonly occurs in those involved in outdoor activities in warm and wet areas of the world. Diagnosis is typically by looking for antibodies against the bacterium or finding its DNA in the blood.Efforts to prevent the disease include protective equipment to prevent contact when working with potentially infected animals, washing after this contact, and reducing rodents in areas where people live and work. The antibiotic doxycycline, when used in an effort to prevent infection among travelers, is of unclear benefit. Vaccines for animals exist for certain type of Leptospira which may decrease the risk of spread to humans. Treatment if infected is with antibiotics such as: doxycycline, penicillin, or ceftriaxone. Weil's disease and severe pulmonary haemorrhage syndrome result in death rates greater than 10% and 50%, respectively, even with treatment.It is estimated that seven to ten million people are infected by leptospirosis per year. This results in about 58,900 deaths per year. The disease is most common in tropical areas of the world but may occur anywhere. Outbreaks may occur in slums of the developing world. The disease was first described by physician Adolf Weil in 1886 in Germany. Animals which are infected may have no symptoms, mild symptoms, or severe symptoms. Symptoms may vary by the type of animal. In some animals Leptospira live in the reproductive tract, leading to transmission during mating.

Light therapy

Light therapy—or phototherapy, classically referred to as heliotherapy—consists of exposure to daylight or to specific wavelengths of light using polychromatic polarised light, lasers, light-emitting diodes, fluorescent lamps, dichroic lamps or very bright, full-spectrum light. The light is administered for a prescribed amount of time and, in some cases, at a specific time of day.

One common use of the term is associated with the treatment of skin disorders, chiefly psoriasis, acne vulgaris, eczema and neonatal jaundice.Light therapy which strikes the retina of the eyes is used to treat diabetic retinopathy and also circadian rhythm disorders such as delayed sleep phase disorder and can also be used to treat seasonal affective disorder, with some support for its use also with non-seasonal psychiatric disorders.

Liver function tests

Liver function tests (LFTs or LFs), also referred to as a hepatic panel, are groups of blood tests that provide information about the state of a patient's liver. These tests include prothrombin time (PT/INR), aPTT, albumin, bilirubin (direct and indirect), and others. The liver transaminases aspartate transaminase (AST or SGOT) and alanine transaminase (ALT or SGPT) are useful biomarkers of liver injury in a patient with some degree of intact liver function. Most liver diseases cause only mild symptoms initially, but these diseases must be detected early. Hepatic (liver) involvement in some diseases can be of crucial importance. This testing is performed on a patient's blood sample. Some tests are associated with functionality (e.g., albumin), some with cellular integrity (e.g., transaminase), and some with conditions linked to the biliary tract (gamma-glutamyl transferase and alkaline phosphatase). Several biochemical tests are useful in the evaluation and management of patients with hepatic dysfunction. These tests can be used to detect the presence of liver disease, distinguish among different types of liver disorders, gauge the extent of known liver damage, and monitor the response to treatment. Some or all of these measurements are also carried out (usually about twice a year for routine cases) on those individuals taking certain medications, such as anticonvulsants, to ensure that the medications are not adversely impacting the person's liver.

Mirizzi's syndrome

Mirizzi's syndrome is a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the common bile duct (CBD) or common hepatic duct, resulting in obstruction and jaundice. The obstructive jaundice can be caused by direct extrinsic compression by the stone or from fibrosis caused by chronic cholecystitis (inflammation). A cholecystocholedochal fistula can occur.

Neonatal jaundice

Neonatal jaundice is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels. Other symptoms may include excess sleepiness or poor feeding. Complications may include seizures, cerebral palsy, or kernicterus.In many cases there is no specific underlying disorder (physiologic). In other cases it results from red blood cell breakdown, liver disease, infection, hypothyroidism, or metabolic disorders (pathologic). A bilirubin level more than 34 μmol/l (2 mg/dL) may be visible. Concerns, in otherwise healthy babies, occur when levels are greater than 308 μmol/L (18 mg/dL), jaundice is noticed in the first day of life, there is a rapid rise in levels, jaundice lasts more than two weeks, or the baby appears unwell. In those with concerning findings further investigations to determine the underlying cause are recommended.The need for treatment depends on bilirubin levels, the age of the child, and the underlying cause. Treatments may include more frequent feeding, phototherapy, or exchange transfusions. In those who are born early more aggressive treatment tends to be required. Physiologic jaundice generally lasts less than seven days. The condition affects over half of babies in the first week of life. Of babies that are born early about 80% are affected.


Urobilinogen is a colorless by-product of bilirubin reduction. It is formed in the intestines by bacterial action on bilirubin. About half of the urobilinogen formed is reabsorbed and taken up via the portal vein to the liver, enters circulation and is excreted by the kidney.

Increased amounts of bilirubin are formed in hemolysis, which generates increased urobilinogen in the gut. In liver disease (such as hepatitis), the intrahepatic urobilinogen cycle is inhibited also increasing urobilinogen levels. Urobilinogen is converted to the yellow pigmented urobilin apparent in urine.

The urobilinogen in the intestine is directly reduced to brown stercobilin, which gives the feces their characteristic color. It can also be reduced to stercobilinogen, which can then be further oxidized to stercobilin. This constitutes the normal "enterohepatic urobilinogen cycle."

In biliary obstruction, below-normal amounts of conjugated bilirubin reach the intestine for conversion to urobilinogen. With limited urobilinogen available for reabsorption and excretion, the amount of urobilin found in the urine is low. High amounts of the soluble conjugated bilirubin enter the circulation where they are excreted via the kidneys. These mechanisms are responsible for the dark urine and pale stools observed in biliary obstruction.

Low urine urobilinogen may result from complete obstructive jaundice or treatment with broad-spectrum antibiotics, which destroy the intestinal bacterial flora. (Obstruction of bilirubin passage into the gut or failure of urobilinogen production in the gut.)

Low urine urobilinogen levels may result from congenital enzymatic jaundice (hyperbilirubinemia syndromes) or from treatment with drugs that acidify urine, such as ammonium chloride or ascorbic acid.

Elevated levels may indicate hemolytic anaemia (excessive breakdown of red blood cells RBC), overburdening of the liver, increased urobilinogen production, re-absorption – a large hematoma, restricted liver function, hepatic infection, poisoning or liver cirrhosis.


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