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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 It might be outdated or ideologically biased.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
However, if there is a disruption in this normal metabolism and/or production of bilirubin, jaundice may result.
Calculation from 2x2 table revealed that absence of visual jaundice below the nipple line had sensitivity of 100% and specificity of 73.23% of ruling out significant hyperbilirubinaemia.
The most common symptom of jaundice is yellowing of the skin, eyes, tongue and urine.
This case shows the importance of testing of conjugated bilirubin in neonates with persistent jaundice. Symptoms of pathological and physiological jaundice can be quite similar but the pathophysiology is different.
We have taken cut-off of 15 mg/dL, because less than 15 mg/dL of bilirubin is considered as physiological jaundice. The thyroid hormone levels in the present study were evaluated after 72 hours of postnatal age to avoid physiological changes in the hormonal levels during first 3 days of life.
As per the reports, many people died due to the outbreak of jaundice in the state.
Significant differences were detected between combination therapy and phototherapy alone for serum bilirubin level (MD - 50.25 [micro]mol/L, 95% CI -64.01 to -36.50, 12 =98%; 7 trials, post-hoc decision choosing random effects model), failure of jaundice resolution (RR 0.21, 95% CI 0.14 to 0.32, 12 =0%; 11 trials, fixed effects model), and time to jaundice resolution (MD -2.17 days, 95%CI -2.96 to - 1.38, 12 =98%; 6 trials, random effects model).
Multivariable logistic regression was used to determine the risk factors of neonatal jaundice. P < 0.05 was considered statistically significant.
A 47-year-old African American male presented at Emory University Hospital with jaundice and dark urine.
A 19-year-old Omani female not known to have any significant medical history was referred to our hospital with a history of upper abdominal discomfort more localized to the epigastric region and associated with jaundice and dark urine.
A 1-month-old male neonate with a known antenatal ultrasound (US) diagnosis of fused horseshoe kidneys and bilateral renal hydronephrosis presented in the outpatient clinic with a history of skin jaundice since he was 1 week old.
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