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(jôn`dĭs, jän`–), abnormal condition in which the body fluids and tissues, particularly the skin and eyes, take on a yellowish color as a result of an excess of bilirubin. During the normal breakdown of old erythrocytes (red blood cells), their hemoglobin is converted into bilirubin. Normally the bilirubin is removed from the bloodstream by the liverliver,
largest glandular organ of the body, weighing about 3 lb (1.36 kg). It is reddish brown in color and is divided into four lobes of unequal size and shape. The liver lies on the right side of the abdominal cavity beneath the diaphragm.
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 and eliminated from the body in the bilebile,
bitter alkaline fluid of a yellow, brown, or green color, secreted, in man, by the liver. Bile, or gall, is composed of water, bile acids and their salts, bile pigments, cholesterol, fatty acids, and inorganic salts.
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, which passes from the liver into the intestines. There are several conditions that may interrupt the elimination of bilirubin from the blood and cause jaundice. Hemolytic jaundice is caused by excessive disintegration of erythrocytes; it occurs in hemolytic and other types of anemia and in some infectious diseases like malaria. Another type of jaundice results from obstruction in or about the liver; usually a stone or stricture of the bile duct blocks the passage of bile from the liver into the intestines. A third type of jaundice occurs when the liver cells are damaged by diseases such as hepatitis or cirrhosis of the liver; the damaged liver is unable to remove bilirubin from the blood. Treatment of jaundice is directed to the underlying cause. Many instances of obstructive jaundice may require surgery.



a yellow coloring of the body tissues in man, as a result of excess accumulation in the blood of the bile pigment bilirubin and of its metabolic products. Several types of jaun-dice are discerned, according to the mechanism of its origin—prehepatic and posthepatic.

Prehepatic jaundice is caused by an increased content of free bilirubin circulating in the blood, formed as a result of increased decomposition of the erythrocytes (hemolytic jaundice), or of congenital or acquired deficiency of enzymes that participate in binding bilirubin with glucuronic acid. Hemolytic jaundice appears in hemolytic disease of the new-born and in poisoning with hemolytic toxins; it is characterized by increased excretion of the products of bilirubin metabolism in the urine (urobilin) and feces (stercobilin, which causes the saturated pigmentation of the feces). Other types of jaundice caused by disruption in the capture and bonding of bilirubin and proceeding without substantive affection of liver cells are physiological jaundice of the new-born, nuclear jaundice, and juvenile jaundice. Hepatogenic jaundice (parenchymatous jaundice) is a function of organic (infectious, parasitic, or toxic) affection of the liver itself and is conditioned by the formation of an anastomosis between blood and bile capillaries and also by intrahepatic stasis of bile during inflammations of the liver. There appear, along with other symptoms of liver affection, a saturated pigmentation of the urine and faintly colored feces.

Posthepatic, or mechanical, jaundice develops due to disruption of the patency of the bile ducts, as a result of their stenosis or obstruction or from external pressure, and is manifested by the complete absence of stercobilin in the feces (colorless stools); it sometimes appears as a result of spasm of the sphincter at the point of influx of the bile duct into the duodenum. Pure forms of jaundice are not ordinarily found: in hemolytic jaundice, a mechanical component is added due to concentration of the bile and obstruction of the bile path-ways; affection of the liver cells is added to mechanical jaun-dice and it acquires some features of hepatogenic jaundice. As a result of the increased blood content of the bile components, jaundice is accompanied by itching, which is sometimes extremely distressing. In complete mechanical jaun-dice, there is disruption of the intestinal digestion and of fat and vitamin absorption, and the body is depleted of lime.

In a number of instances, a yellow coloring of the skin and other body tissues may be caused by pigments in food (for example, the carotene contained in carrots) or medications (acrichin).


Bondar’, Z. A.Zheltukhi. Moscow, 1965.
Bondar’, Z. A. Klinicheskaia gepatologiia. Moscow, 1970.



(invertebrate zoology)
Yellow coloration of the skin, mucous membranes, and secretions resulting from hyperbile-rubinemia. Also known as icterus.


yellowing of the skin and whites of the eyes due to the abnormal presence of bile pigments in the blood, as in hepatitis
References in periodicals archive ?
Savoj, "Bile cast nephropathy due to cholestatic jaundice after using stanozolol in 2 amateur bodybuilders," Iran Journal of Kidney Diseases, vol.
To the best of our knowledge, this is one of the first case reports of CAH with cholestatic jaundice, from Pakistan, with only one case of "Lipoid Congenital Adrenal Hyperplasia Presenting with Cholestasis" reported from Iran.
Causes of cholestatic jaundice in a cohort of 74 patients Cause N Biliary atresia 39 (27 evaluable) Non-biliary atresia 34 (31 evaluable) Neonatal hepatitis 10 Choledochal cyst 9 Viral enterocolitis 5 HIV hepatitis 3 Gallstones 1 Auto-immune 1 Miscellaneous 2
Hyperthyroidism is reported to be associated with deterioration of liver function tests as either elevated transaminase levels (1) or findings suggestive of cholestatic jaundice (1,2).
Possible ciprofloxacin-induced acute cholestatic jaundice. Ann Pharmacother.
In present study mortality was seen in 2% of cases, 1% presented with significant hepatocellular jaundice and another 1% presented with significant cholestatic jaundice. These 2% cases were also associated with significant increase in serum creatinine level (>3mg %).
A 21-month-old female infant was referred to the paediatric gastro-enterology clinic with cholestatic jaundice due to biliary atresia.
Cholestatic jaundice is the most common hepatic side effect of methimazole and is reversible when the therapy is stopped.
A 20-year-old HIV infected male with a baseline CD4 count of 17 cells/[mm.sup.3] was referred with cholestatic jaundice.
Although cholestasis (abnormal liver function or cholestatic tests with or without cholestatic jaundice) is a common indication for diagnostic ERCP or MRCP, and MRCP is accepted as the first choice in addition to the diagnostic ERCP is performed only when there is a suspected disease in the absence of abnormal images,2,3,7 intraoperative flexible choledochoscopy may also be used in both the diagnosis and treatment of some hepato-biliary-pancreatic system diseases, particularly in patients in whom laparotomy with or without choledochotomy is performed.1,5,6 It is believed that both ERCP and MRCP are used successfully in the diagnosis of choledocholithiasis.
Definitive exclusion of biliary atresia in the infant with cholestatic jaundice usually requires operative cholangiography (OCG)/ percutaneous cholecysto-cholangiography (PCC) and open liver biopsy/ percutaneous liver biopsy9.
A 35-year-old woman presented with cholestatic jaundice and partial bowel obstruction following 3 months' history of intermittent abdominal pain, nausea and vomiting.