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jaundice

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jaundice

yellowing of the skin and whites of the eyes due to the abnormal presence of bile pigments in the blood, as in hepatitis
Collins Discovery Encyclopedia, 1st edition © HarperCollins Publishers 2005

jaundice

[′jȯn·dəs]
(invertebrate zoology)
(medicine)
Yellow coloration of the skin, mucous membranes, and secretions resulting from hyperbile-rubinemia. Also known as icterus.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.

Jaundice

 

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).

REFERENCES

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

A. S. MUKHIN

The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.
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References in periodicals archive
Icterometer: a useful screening tool for neonatal jaundice. Indian Pediatr 1991; 28(5): 473-6.
Multivariable logistic regression was used to determine the risk factors of neonatal jaundice. P < 0.05 was considered statistically significant.
Blue light, green light, white light, more light: treatment of neonatal jaundice. Clin Perinatol 1990; 17: 467-81.
Common morbidities were neonatal jaundice, RDS, perinatal asphyxia, infection/sepsis, MAS, and congenital anomalies.
Risk factors of neonatal jaundice includes hemolysis secondary to Rhesus isoimmunisation and ABO incompatibility, sepsis, prematurity and enzyme defects (Uridyl diphosphate glucoronyl transferase enzyme deficiency).11
The high mortality and morbidity from neonatal jaundice is exacerbated by the poor understanding, and mismanagement, of this common neonatal problem by the general populace, leading to dangerous delays and complications.
The frequency of neonatal jaundice among the newborns in Aktobe in different years varies without trends from 4.9 to 7.5% (the rate per 1,000 children in the first year of life is 48.7-75.5).
A total of 258 patients were enrolled for the study after fulfilling the inclusion/ exclusion criteria to compare the decrease in serum bilirubin after applying continuous/intermittent phototherapy for the treatment of neonatal jaundice.
Another 17 percent of hearing loss stems from complications related to birth, such as low birth-weight and neonatal jaundice.
It is estimated that 40% is attributable to genetic causes; 31% to infections such as measles, mumps, rubella and meningitis; and 17% to complications at birth, including prematurity, low birth weight and neonatal jaundice. In addition, an estimated 4% results from expectant mothers and new-borns unknowingly using medicines that are harmful to hearing.To prevent childhood hearing loss, immunizing children against diseases and regulating certain medicines and noise levels are vital.
Ives, "Management of neonatal jaundice," Paediatrics and Child Health, vol.
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