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Related to Hyperbilirubinaemia: hyperbilirubinemia


(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 ?
Results from bilirubinometers cannot be directly compared to serum measurements of bilirubin, and should be followed up with blood tests if they indicate hyperbilirubinaemia.
As soon as the patient stopped taking aspirin, the hyperbilirubinaemia and abnormal liver enzymes began to normalise.
The second reason for hyperbilirubinaemia occurring in the breastfed infant is thought to be related to the constituents of breast milk itself and is termed 'breast milk jaundice' (Paul et al, 2012).
4%), mainly for neonatal hyperbilirubinaemia and sepsis; by 78 of 477 (16.
Term and near-term babies should be assessed for hyperbilirubinaemia soon after birth.
Although in the present study, determination of plasma bilirubin and liver enzymes were not part of the original design, the appearance of bilirubin in urine shows that it is of the conjugated type and by extrapolation, there was conjugated hyperbilirubinaemia in malarial subjects in comparison to the controls, which was significantly higher in P.
Relationship between hyperbilirubinaemia and UDP-glucuronosyltransferase 1A1 polymorphism in adult HIV-infected Thai patients treated with indinavir.
Isolated unconjugated hyperbilirubinaemia (drug-induced Gilbert's syndrome) is generally benign and associated with some PIs (indinavir and atazanavir).
CO-MORBIDITIES AFFECTING CHOICE OF I ANTIRETROVIRALS FOR PEP I Co-morbidity Drug Complication Pregnancy Efavirenz Avoid in the 1st trimester due to teratogenicity Indinavir Hyperbilirubinaemia and nephrolithiasis Tuberculosis Kaletra Additional ritonavir dose of 300 mg bid needed or increase Kaletra dose to 6 tablets bid Epilepsy Pls Increase levels of a number of commonly used anticonvulsants Efavirenz Increased risk of seizures Psychosis Efavirenz Increased risk of psychiatric symptoms Insomnia Pls StJohn's Wort reduces all PI levels Migraine Pls All Pls increase risk of ergotism with ergotamine co-administration Renal failure NRTI Dose adjustments for AZT and D4T.
The main syndromes include acute haemolysis following oxidative stress, neonatal hyperbilirubinaemia and rarely congenital non-spherocytic anaemia.
Capsules can be opened & given with food Give at night to avoid CNS side-effects Anticipate mild transient rash and CNS side-effects Protease inhibitors (PIs) Atazanavir Ideally should always be used (ATV) with RTV boosting (unboosted Reyataz[R] ATV requires a higher dose and gives unpredictable plasma levels) Give with food Unconjugated hyperbilirubinaemia may occur and as long as the patient is comfortable with it, is not a reason to discontinue the drug Fosampre- Room Ideally should always be used navir temparature with RTV boosting (unboosted (fAPV) fAPV requires a higher dose) Telzir[R] Give suspension with food and tablets with or without food Lopinavir/ Capsules Aluvia[R] tabs can be given with ritonavir should be or without food.
A patient taking ritonavir 600 mg twice daily and saquinavir 400 mg twice daily is reported to have developed symptoms of PI toxicity 1 week after itraconozole was increased from 100 mg to 200 mg twice daily, (15) and 2 of 4 patients receiving indinavir developed hyperbilirubinaemia and slightly elevated transaminase levels while on itraconazole.