View source for Jaundice

{{Short description|Abnormal pigmentation symptom for liver disease}}
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{{Redirect|Icteric|the physiological event|Ictal|the songbird known as "Icteria"|Yellow-breasted chat}}
{{for|Jaundice in babies|Neonatal jaundice}}
{{Redirect|Yellowing|the yellowing of ABS plastic|Retrobright|the documentary|Yellowing (film)}}
{{Use dmy dates|date=July 2022}}
{{Infobox medical condition (new)
| name = Jaundice
| synonyms = Icterus<ref>{{cite book | vauthors = Ziebert M | chapter = Jaundice | veditors = Torre DM, Lamb GC, van Ruiswyk J, Schapira RM |title=Kochar's Clinical Medicine for Students |date=2009 |publisher=Lippincott Williams & Wilkins |isbn=978-0-7817-6699-9 |page=101 | chapter-url = https://books.google.com/books?id=S0Jz_3WEPYMC&pg=PA101 |language=en}}</ref>
| image = Jaundice08.jpg
| caption = Jaundice of the skin caused by [[pancreatic cancer]]
| field = [[Gastroenterology]], [[hepatology]], [[general surgery]]
| pronounce = {{IPAc-en|ˈ|dʒ|ɔː|n|d|ɪ|s}} {{respell|JAWN|diss}}
| symptoms = [[Yellow]]ish coloration of skin and [[sclera]], itchiness<ref name=Bas2015/><ref name=NIH2016/>
| complications =
| onset =
| duration =
| causes = [[hyperbilirubinemia|High bilirubin levels]]<ref name=NIH2016/>
| risks = [[Pancreatic cancer]], [[pancreatitis]], [[liver disease]], certain infections
| diagnosis = Blood bilirubin, [[liver panel]]<ref name=NIH2016/>
| differential = [[Carotenemia]], taking [[rifampin]]<ref name=Rog2004/>
| prevention =
| treatment = Based on the underlying cause<ref name=Fer2014/>
| medication =
| prognosis =
| frequency =
| deaths =
}}
<!-- Definition and symptoms -->

'''Jaundice''', also known as '''icterus''', is a yellowish or, less frequently, greenish pigmentation of the [[Human skin|skin]] and [[sclera]] due to [[hyperbilirubinemia|high bilirubin levels]].<ref name="NIH2016">{{cite web |title=Jaundice |date=25 June 2025 |url=https://medlineplus.gov/jaundice.html|publisher=MedlinePlus, US National Library of Medicine|access-date=24 October 2025}}</ref><ref name="But2012">{{cite book| vauthors = Buttaro TM, Trybulski JA, Polgar-Bailey P, Sandberg-Cook J |title=Primary Care: A Collaborative Practice|date=2012|publisher=Elsevier Health Sciences|isbn=978-0-323-07585-5|page=690|edition=4th|url=https://books.google.com/books?id=YBcHR-wQOWQC&pg=PA690|language=en|url-status=live|archive-url=https://web.archive.org/web/20170908204555/https://books.google.com/books?id=YBcHR-wQOWQC&pg=PA690|archive-date=2017-09-08}}</ref> Jaundice in adults typically indicates the presence of underlying diseases involving abnormal [[heme]] [[Heme oxygenase|metabolism]], [[liver dysfunction]], or [[biliary tract|biliary-tract]] obstruction.<ref>{{cite book| vauthors = Al-Tubaikh JA |date=2017 |title= Internal Medicine|doi=10.1007/978-3-319-39747-4|isbn=978-3-319-39746-7}}</ref> The prevalence of jaundice in adults is rare, while [[Neonatal jaundice|jaundice in babies]] is common, with an estimated 80% affected during their first week of life.<ref name="Kap2017">{{cite book |doi=10.1016/b978-0-323-35214-7.00097-4 |chapter=Hereditary Contribution to Neonatal Hyperbilirubinemia |title=Fetal and Neonatal Physiology |date=2017 |last1=Kaplan |first1=Michael |last2=Hammerman |first2=Cathy |pages=933–942.e3 |isbn=978-0-323-35214-7 }}</ref> The most commonly associated symptoms of jaundice are [[Biliary pruritus|itchiness]],<ref name="Bas2015">{{cite journal|vauthors=Bassari R, Koea JB|date=February 2015|title=Jaundice associated {{sic|hide=y|pruritis}}: a review of pathophysiology and treatment|journal=World Journal of Gastroenterology|volume=21|issue=5|pages=1404–1413|doi=10.3748/wjg.v21.i5.1404|pmc=4316083|pmid=25663760 |doi-access=free }}</ref> pale [[Human feces|feces]], and [[dark urine]].<ref name="Rog2004" />

<!-- Pathophysiology -->
Normal levels of bilirubin in [[blood plasma|blood]] are below 1.0&nbsp;[[milligram|mg]]/[[decilitre|dl]] (17&nbsp;[[Mole (unit)|μmol]]/[[litre|L]]), while levels over 2–3&nbsp;mg/dl (34–51&nbsp;μmol/L) typically result in jaundice.<ref name=Rog2004>{{cite book | vauthors = Roger J |title=Oxford Textbook of Primary Medical Care|date=2004|publisher=Oxford University Press|isbn=978-0-19-856782-0|page=758|url=https://books.google.com/books?id=2LB0PC17uFsC&pg=PA758|language=en|url-status=live|archive-url= https://web.archive.org/web/20170908204555/https://books.google.com/books?id=2LB0PC17uFsC&pg=PA758|archive-date=2017-09-08}}</ref><ref name=CMAJ2015/> [[Hyperbilirubinemia|High blood bilirubin]] is divided into two types: [[unconjugated bilirubin|unconjugated]] and [[conjugated bilirubin]].<ref name=Win2011>{{cite journal | vauthors = Winger J, Michelfelder A | title = Diagnostic approach to the patient with jaundice | journal = Primary Care | volume = 38 | issue = 3 | pages = viii, 469–482 | date = September 2011 | pmid = 21872092 | doi = 10.1016/j.pop.2011.05.004 }}</ref>

<!-- Cause and differential-->
Causes of jaundice vary from relatively benign to potentially fatal.<ref name=Win2011/> High unconjugated bilirubin may be due to [[haemolytic anemia|excess red blood cell breakdown]], [[large bruise]]s, genetic conditions such as [[Gilbert's syndrome]], not eating for a prolonged period of time, newborn jaundice, or [[thyroid disease|thyroid problems]].<ref name=Rog2004/><ref name=Win2011/> High conjugated bilirubin may be due to liver diseases such as [[cirrhosis]] or [[hepatitis]], infections, [[medication]]s, or [[blockage of the bile duct]],<ref name=Rog2004/> due to factors including [[gallstones]], [[cancer]], or [[pancreatitis]].<ref name=Rog2004/> Other conditions can also cause yellowish skin, but are not jaundice, including [[carotenemia]], which can develop from eating large amounts of foods containing [[carotene]]—or medications such as [[rifampin]].<ref name="Rog2004" />

<!-- Treatment and etymology -->
Treatment of jaundice is typically determined by the underlying cause.<ref name=Fer2014/> If a bile duct blockage is present, [[surgery]] is typically required; otherwise, management is medical.<ref name=Fer2014/> Medical management may involve treating infectious causes and stopping medication that could be contributing to the jaundice.<ref name=Fer2014>{{cite book | vauthors = Ferri FF |title= Ferri's Clinical Advisor 2015: 5 Books in 1 |date= 2014 |publisher= Elsevier Health Sciences |isbn= 978-0-323-08430-7 |page= 672 |url= https://books.google.com/books?id=icTsAwAAQBAJ&pg=PA672 |language= en |url-status= live |archive-url= https://web.archive.org/web/20170908204555/https://books.google.com/books?id=icTsAwAAQBAJ&pg=PA672 |archive-date= 2017-09-08 }}</ref> Jaundice in newborns may be treated with [[phototherapy]] or [[exchanged transfusion]] depending on age and [[premature birth|prematurity]] when the bilirubin is greater than 4–21&nbsp;mg/dl (68–365&nbsp;μmol/L).<ref name=CMAJ2015>{{cite journal | vauthors = Maisels MJ | title = Managing the jaundiced newborn: a persistent challenge | journal = CMAJ | volume = 187 | issue = 5 | pages = 335–343 | date = March 2015 | pmid = 25384650 | pmc = 4361106 | doi = 10.1503/cmaj.122117 }}</ref> The itchiness may be helped by [[Cholecystostomy|draining the gallbladder]], [[ursodeoxycholic acid]], or [[opioid]] antagonists such as [[naltrexone]].<ref name=Bas2015/> The word ''jaundice'' is from the [[French language|French]] ''[[wikt:jaune#French|jaunisse]]'', meaning 'yellow disease'.<ref>{{cite book |title= Dr. Chase's Family Physician, Farrier, Bee-keeper, and Second Receipt Book: Being an Entirely New and Complete Treatise ... |date= 1873 |publisher= Chase Publishing Company |page= 542 |url= https://books.google.com/books?id=bC7iAAAAMAAJ&pg=PA542 |language= en |url-status= live |archive-url= https://web.archive.org/web/20170908204555/https://books.google.com/books?id=bC7iAAAAMAAJ&pg=PA542 |archive-date= 2017-09-08 }}</ref><ref>{{cite book |doi=10.1016/b978-1-4377-0774-8.10017-x |chapter=Jaundice |title=Pediatric Gastrointestinal and Liver Disease |date=2011 |last1=Sullivan |first1=Kara M. |last2=Gourley |first2=Glenn R. |pages=176–186.e3 |isbn=978-1-4377-0774-8 }}</ref>

== Signs and symptoms ==
[[File:Jaundice.jpg|thumb|A 4-year-old boy with icteric sclera due to [[G6PD deficiency]]]]
The most common signs of jaundice in adults are a yellowish discoloration of the white area of the eye ([[sclera]]) and skin,<ref>{{cite journal | vauthors = Gondal B, Aronsohn A | title = A Systematic Approach to Patients with Jaundice | journal = Seminars in Interventional Radiology | volume = 33 | issue = 4 | pages = 253–258 | date = December 2016 | pmid = 27904243 | pmc = 5088098 | doi = 10.1055/s-0036-1592331 }}</ref> with scleral icterus presence indicating a serum bilirubin of at least 3&nbsp;mg/dl.<ref name="Reuben_2012" /> Other common signs include dark urine ([[bilirubinuria]]) and pale ([[acholia]]) fatty stool ([[steatorrhea]]).<ref>{{cite book | vauthors = Goroll AH |title= Primary care medicine: office evaluation and management of the adult patient |date= 2009 |publisher= Wolters Kluwer Health/Lippincott Williams & Wilkins |location= Philadelphia |isbn= 978-0-7817-7513-7 |page= 496 |edition= 6th |url= https://books.google.com/books?id=bIZvJPcSEXMC&pg=PA496 |url-status= live |archive-url= https://web.archive.org/web/20170908204555/https://books.google.com/books?id=bIZvJPcSEXMC&pg=PA496 |archive-date= 2017-09-08 }}</ref> Because bilirubin is a skin irritant, jaundice is commonly associated with severe itchiness.<ref>{{cite book| vauthors = James WD |title=Andrews' diseases of the skin: clinical dermatology|date=2006|publisher=Saunders Elsevier|others=Berger, Timothy G.; Elston, Dirk M.; Odom, Richard B.|isbn=0-7216-2921-0|edition=10th|location=Philadelphia|oclc=62736861}}</ref><ref>{{cite journal | vauthors = Bassari R, Koea JB | title = Jaundice associated pruritis: a review of pathophysiology and treatment | journal = World Journal of Gastroenterology | volume = 21 | issue = 5 | pages = 1404–1413 | date = February 2015 | pmid = 25663760 | pmc = 4316083 | doi = 10.3748/wjg.v21.i5.1404 | doi-access = free }}</ref>

Eye [[conjunctiva]] has a particularly high affinity for bilirubin deposition due to high elastin content. Slight increases in serum bilirubin can, therefore, be detected early on by observing the yellowing of sclerae. Traditionally referred to as scleral icterus, this term is actually a misnomer, because bilirubin deposition technically occurs in the [[Conjunctiva|conjunctival membranes]] overlying the avascular sclera. Thus, the proper term for the yellowing of "white of the eyes" is conjunctival icterus.<ref>{{cite book | vauthors = McGee SR |title=Evidence-Based Physical Diagnosis |date=2018 |publisher=Elsevier |location=Philadelphia |isbn=978-0-323-39276-1 |pages=59–68 |edition=4th |chapter=Jaundice}}</ref>

In individuals with darker skin tones, jaundice may be less readily apparent on the skin and is more reliably observed in areas such as the sclera, palms, soles, and oral mucosa. Educational resources have increasingly highlighted this variation to support accurate clinical assessment across diverse populations.<ref>{{cite web |author1=Malone Mukwende |title=Mind the Gap: A handbook of clinical signs in Black and Brown skin |url=https://sgul.figshare.com/articles/online_resource/Mind_the_Gap_A_handbook_of_clinical_signs_in_Black_and_Brown_skin/12769988 |website=St George's University of London |date=2020 |doi=10.24376/rd.sgul.12769988.v1 |access-date=2025-05-19}}</ref><ref>{{cite journal |last=Ferdinand |first=Joshua |title=Recognising Clinical Signs and Symptoms on Black, Asian and Minority Ethnic (BAME) Skin Types |journal=Atomic Academia |date=2024 |doi=10.62594/LTHW5053}}</ref>

A rare sign of jaundice in childhood is the appearance of yellowish or greenish teeth. In developing children, hyperbilirubinemia can lead to yellow or green tooth discoloration as bilirubin deposits during tooth calcification.<ref>{{cite book| vauthors = Neville BW |title=Oral and Maxillofacial Pathology |publisher=Elsevier |year=2012 |isbn=978-981-4371-07-0 |edition=3rd |location=Singapore |page=798 }}</ref> While this may occur in children with hyperbilirubinemia, tooth discoloration due to hyperbilirubinemia is not observed in individuals with adult-onset liver disease. Disorders associated with a rise in serum levels of conjugated bilirubin during early development can also cause [[Enamel hypoplasia|dental hypoplasia]].<ref>{{cite journal | vauthors = Amin SB, Karp JM, Benzley LP | title = Unconjugated hyperbilirubinemia and early childhood caries in a diverse group of neonates | journal = American Journal of Perinatology | volume = 27 | issue = 5 | pages = 393–397 | date = May 2010 | pmid = 20013583 | pmc = 3264945 | doi = 10.1055/s-0029-1243314 }}</ref>

== Causes ==
[[File:Jaundice-types.png|thumb|upright=1.6|Types of jaundice]]
Jaundice is a sign indicating the presence of an underlying diseases involving abnormal bilirubin metabolism, liver dysfunction, or biliary-tract obstruction. In general, jaundice is present when blood levels of bilirubin exceed 3&nbsp;mg/dl.<ref name="Reuben_2012">{{cite book | vauthors = Reuben A |chapter=Jaundice |date=2012|title=Textbook of Clinical Gastroenterology and Hepatology|pages=84–92|publisher=John Wiley & Sons, Ltd|language=en|doi=10.1002/9781118321386.ch15|isbn=978-1-118-32138-6}}</ref> Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

{| class="wikitable mw-collapsible"
|-
!Category
!Definition
|-
|Prehepatic/hemolytic
|The pathology occurs prior to the liver metabolism, due to either intrinsic causes to red blood cell rupture or extrinsic causes to red blood cell rupture.
|-
|Hepatic/hepatocellular
|The pathology is due to damage of parenchymal liver cells.
|-
|Posthepatic/cholestatic
|The pathology occurs after bilirubin conjugation in the liver, due to obstruction of the biliary tract and/or decreased bilirubin excretion.{{cn|date=April 2024}}
|}

=== Prehepatic causes ===
Prehepatic jaundice is most commonly caused by a pathological increased rate of red blood cell (erythrocyte) [[hemolysis]]. The increased breakdown of erythrocytes → increased unconjugated serum bilirubin → increased deposition of unconjugated bilirubin into mucosal tissue.<ref>{{cite book | vauthors = Joseph A, Samant H | chapter = Jaundice |date=2022 | chapter-url = https://www.ncbi.nlm.nih.gov/books/NBK544252/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=31334972 |access-date=2022-04-23 }}</ref> These diseases may cause jaundice due to increased erythrocyte hemolysis:<ref>{{cite web |title=What causes jaundice in hemolytic anemia? |url=https://www.medscape.com/answers/201066-27045/what-causes-jaundice-in-hemolytic-anemia |access-date=2022-04-26 |website=www.medscape.com |language=en}}</ref>
* [[Sickle-cell anemia]]<ref>{{cite web|title=What Is Sickle Cell Disease?|url=https://www.nhlbi.nih.gov/health/sickle-cell-disease|website=National Heart, Lung, and Blood Institute|access-date=8 March 2016|date=12 June 2015|url-status=live|archive-url=https://web.archive.org/web/20160306021706/http://www.nhlbi.nih.gov/health/health-topics/topics/sca/|archive-date=6 March 2016}}</ref>
* [[Spherocytosis]]<ref>{{cite book| vauthors = Hillman RS, Ault KA, Rinder HM |title=Hematology in clinical practice: a guide to diagnosis and management|url=https://books.google.com/books?id=NJs1VpA8SEoC&pg=PA146|access-date=15 November 2010|year=2005|publisher=McGraw-Hill Professional|isbn=978-0-07-144035-6|pages=146–}}</ref>
* [[Thalassemia]]<ref>{{cite web |url=https://www.lecturio.com/concepts/thalassemia/ | title= Thalassemia
|website=The Lecturio Medical Concept Library |access-date= 27 July 2021}}</ref>
* [[Pyruvate kinase deficiency]]
* [[Glucose-6-phosphate dehydrogenase deficiency]]
* [[Microangiopathic hemolytic anemia]]
* [[Hemolytic–uremic syndrome]]
* Some infections can also cause increased red blood cell turnover, including [[malaria]] and [[bartonellosis]]<ref>{{Cite book |last1=McKean |first1=Sylvia |title=Principles and Practice of Hospital Medicine |last2=Ross |first2=John |last3=Dressler |first3=Daniel |last4=Scheurer |first4=Danielle |publisher=McGraw-Hill Education LLC |year=2016 |isbn=978-0-07-184313-3 |edition=2nd}}</ref>

=== Hepatic causes ===
[[File:Bilirubin pigment in cholestatic liver 40X.jpg|thumbnail|Microscopy of a biopsy of a cholestatic liver showing bilirubin pigment (brown pigment), [[H&E]] stain]]
Hepatic jaundice is caused by abnormal liver metabolism of bilirubin.<ref>{{cite book | vauthors = Kalakonda A, Jenkins BA, John S | chapter = Physiology, Bilirubin |date=2022 |url= https://www.ncbi.nlm.nih.gov/books/NBK470290/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29261920 |access-date=2022-04-23 }}</ref> The major causes of hepatic jaundice are significant damage to hepatocytes due to infectious, drug/medication-induced, autoimmune etiology, or less commonly, due to inheritable genetic diseases.<ref>{{cite book | vauthors = Tripathi N, Jialal I | chapter = Conjugated Hyperbilirubinemia |date=2022 | chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK562172/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32965843 |access-date=2022-04-23 }}</ref> The following is a partial list of hepatic causes to jaundice:<ref>{{cite book | vauthors = Tholey D | chapter = Jaundice |date=January 2023 |url= https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/approach-to-the-patient-with-liver-disease/jaundice | title = Merck Manual. Professional Version |publisher=Merck|access-date=2022-04-12}}</ref>
* [[Acute hepatitis]]
* [[Chronic hepatitis]]
* [[Hepatotoxicity]]
* [[Cirrhosis]]
* [[Drug-induced hepatitis]]
* [[Alcoholic liver disease]]
* [[Gilbert's syndrome]] (found in about 5% of the population, results in induced mild jaundice)
* [[Crigler–Najjar syndrome, type I]]
* [[Crigler–Najjar syndrome, type II]]
* [[Leptospirosis]]

===Posthepatic causes (Obstructive jaundice)===
Posthepatic jaundice (obstructive jaundice) is caused by a blockage of bile ducts that transport bile containing conjugated bilirubin out of the liver for excretion.{{fact|date=March 2025}} This is a list of conditions that can cause posthepatic jaundice:
* [[Common bile duct stone|Choledocholithiasis]] (common bile duct gallstones). It is the most common cause of obstructive jaundice.
* [[Pancreatic cancer]] of the pancreatic head
* Biliary tract strictures
* [[Biliary atresia]]
* [[Primary biliary cholangitis]]
* [[Cholestasis of pregnancy]]
* [[Acute pancreatitis|Acute Pancreatitis]]
* [[Chronic pancreatitis|Chronic Pancreatitis]]
* [[Pancreatic pseudocyst]]s
* [[Mirizzi's syndrome]]
* Parasites ("[[liver fluke]]s" of the [[Opisthorchiidae]] and [[Fasciolidae]])<ref>{{cite web|date=2019-04-18|title=CDC – Liver Flukes|url=https://www.cdc.gov/parasites/liver_flukes/index.html|access-date=2020-06-05|website=www.cdc.gov|language=en-us}}</ref>

== Pathophysiology ==
[[File:Heme Breakdown.png|thumb]]Jaundice is typically caused by an underlying pathological process that occurs at some point along the normal physiological pathway of heme metabolism. A deeper understanding of the anatomical flow of normal heme metabolism is essential to appreciate the importance of prehepatic, hepatic, and posthepatic categories. Thus, an anatomical approach to heme metabolism precedes a discussion of the pathophysiology of jaundice.{{citation needed|date=August 2020}}

=== Normal heme metabolism ===

==== Prehepatic metabolism ====
When [[red blood cell]]s complete their lifespan of about 120 days, or if they are damaged, they rupture as they pass through the [[reticuloendothelial system]], and cell contents including [[hemoglobin]] are released into circulation. Macrophages phagocytose free hemoglobin and split it into [[heme]] and [[globin]]. 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 [[tetrapyrrole]] pigment called bilirubin by cytosolic enzyme [[biliverdin reductase]]. This bilirubin is "unconjugated", "free", or "indirect" bilirubin. Around 4&nbsp;mg of bilirubin per kg of blood are produced each day.<ref name="PedRev">{{cite journal|vauthors=Pashankar D, Schreiber RA |date=July 2001|title=Jaundice in older children and adolescents|journal=Pediatrics in Review|volume=22|issue=7|pages=219–226|doi=10.1542/pir.22-7-219|pmid=11435623}}</ref> The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. Roughly 20% comes from other heme sources, however, including ineffective [[erythropoiesis]], and the breakdown of other heme-containing proteins, such as muscle [[myoglobin]] and [[cytochrome]]s.<ref name="PedRev" /> The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, it is transported through the blood bound to [[serum albumin]].<ref name=":1" />

==== Hepatic metabolism ====
Once unconjugated bilirubin arrives in the liver, liver enzyme [[UDP-glucuronyl-transferase|UDP-glucuronyl transferase]] conjugates bilirubin + [[glucuronic acid]] → [[bilirubin diglucuronide]] (conjugated bilirubin). Bilirubin that has been conjugated by the liver is water-soluble and excreted into the gallbladder.{{citation needed|date=August 2020}}

==== Posthepatic metabolism ====
Bilirubin enters the intestinal tract via bile. In the intestinal tract, bilirubin is converted into [[urobilinogen]] by symbiotic intestinal bacteria. Most urobilinogen is converted into [[stercobilinogen]] and further oxidized into [[stercobilin]]. Stercobilin is excreted via [[feces]], giving stool its characteristic brown coloration.<ref name="Berthelot_2018">{{cite book | vauthors = Berthelot P, Duvaldestin P, Fevery J | chapter = Physiology and Disorders of Human Bilirubin Metabolism|date=2018| title = Bilirubin|pages=173–214|publisher=CRC Press|isbn=978-1-351-07011-9 |doi=10.1201/9781351070119-6}}</ref> A small portion of urobilinogen is reabsorbed back into the gastrointestinal cells. Most reabsorbed urobilinogen undergoes hepatobiliary recirculation. A smaller portion of reabsorbed urobilinogen is filtered into the kidneys. In the urine, urobilinogen is converted to [[urobilin]], which gives urine its characteristic yellow color.<ref name="Berthelot_2018" />

=== Abnormalities in heme metabolism and excretion ===
One way to understand jaundice pathophysiology is to organize it into disorders that cause increased bilirubin production (abnormal heme metabolism) or decreased bilirubin excretion (abnormal heme excretion).{{citation needed|date=August 2020}}

==== Prehepatic pathophysiology ====
Prehepatic jaundice results from a pathological increase in bilirubin production, most often as a result of an increased rate of red blood cell hemolysis, leading to an increased deposition of bilirubin in mucosal tissues and the appearance of a yellow hue.<ref>{{Cite book |last1=McKean |first1=Sylvia |title=Principles and Practice of Hospital Medicine |last2=Ross |first2=John |last3=Dressler |first3=Daniel |last4=Scheurer |first4=Danielle |publisher=McGraw-Hill Education LLC |year=2016 |isbn=978-0-07-184313-3 |edition=2nd}}</ref>

==== Hepatic pathophysiology ====
Hepatic jaundice (hepatocellular jaundice) is due to significant disruption of liver function, leading to hepatic cell death and necrosis and impaired bilirubin transport across [[hepatocyte]]s. Bilirubin transport across hepatocytes may be impaired at any point between hepatocellular uptake of unconjugated bilirubin and hepatocellular transport of conjugated bilirubin into the gallbladder. In addition, subsequent cellular [[oedema|edema]] due to inflammation causes mechanical obstruction of the intrahepatic biliary tract. Most commonly, interferences in all three major steps of bilirubin metabolism—uptake, conjugation, and excretion—usually occur in hepatocellular jaundice. Thus, an abnormal rise in both unconjugated and conjugated bilirubin (formerly called '''cholemia''') will be present. Because excretion (the rate-limiting step) is usually impaired to the greatest extent, conjugated hyperbilirubinemia predominates.<ref>{{cite book|title=Medicine: Prep Manual for Undergraduates|vauthors=Mathew KG|date=2008|publisher=Elsevier India|isbn=978-81-312-1154-0|edition=3rd|pages=296–297}}</ref>

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]] exiting 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 the intestine to become [[urobilinogen]], gives the urine a dark color.<ref>{{cite book|title=Textbook of Medical Physiology|vauthors=Hall JE, Guyton AC|date=2011|publisher=Saunders/Elsevier|isbn=978-1-4160-4574-8|page=841}}</ref>{{what|date=May 2022}}

There are other causes of hepatic jaundice that are not due to significant liver dysfunction and are associated solely with the conjugation of bilirubin.<ref name=":2">{{Cite book |last1=Wing |first1=Edward J. |title=Cecil Essentials of Medicine |last2=Schiffman |first2=Fred J. |publisher=Elsevier |year=2021 |isbn=978-0-323-72271-1 |edition=10th}}</ref> One example is [[Gilbert's syndrome|Gilbert syndrome]] where affected individuals have normal liver function but have genetic variants in their UDP-glucuronyl transferase enzyme, causing the enzyme to be less efficient in conjugating unconjugated bilirubin.<ref name=":2" /> Individuals typically experience mild episodes of jaundice during periods of stress.<ref name=":2" /> Another example is [[Crigler–Najjar syndrome|Crigler-Najjar syndrome]] where genetic variants in the UDP-glucuronyl transferase enzyme result in partial or complete loss of enzyme activity, and affected individuals experience significant hyperbilirubinemia as a result.<ref name=":2" />
<!-- Bilirubinuria is due to excess conjugated bilirubin excreted in the urine.{{citation needed|date=August 2020}}
 -->

==== Posthepatic pathophysiology ====
Posthepatic jaundice, also called obstructive jaundice, is due to the blockage of bile excretion from the biliary tract, which leads to increased conjugated bilirubin and bile salts there. In complete obstruction of the bile duct, conjugated bilirubin cannot access the intestinal tract, disrupting further bilirubin conversion to urobilinogen and, therefore, no [[stercobilin]] or [[urobilin]] is produced. In obstructive jaundice, excess conjugated bilirubin is filtered into the urine without urobilinogen. Conjugated bilirubin in urine (bilirubinuria) gives urine an abnormally dark brown color. Thus, the presence of pale stool (stercobilin absent from feces) and dark urine (conjugated bilirubin present in urine) suggests an obstructive cause of jaundice. Because these associated signs are also positive in many hepatic jaundice conditions, they cannot be a reliable clinical feature to distinguish obstructive versus hepatocellular jaundice causes.<ref>{{cite journal|vauthors=Beckingham IJ, Ryder SD|date=January 2001|title=ABC of diseases of liver, pancreas, and biliary system. Investigation of liver and biliary disease|journal=BMJ|volume=322|issue=7277|pages=33–36|doi=10.1136/bmj.322.7277.33|pmc=1119305|pmid=11141153}}</ref>

== Diagnosis ==
[[File:Obstructivebiliarydilation.png|thumb|Biliary-tract dilation due to obstruction as seen on CT scan (frontal plane)]]
[[File:Obstructivebiliarydilation2.png|thumb|Biliary-tract dilation due to obstruction as seen on CT scan (axial plane)]]
Most people presenting with jaundice have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel includes 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, [[Blood proteins|total protein]] and [[albumin]]. Other primary lab tests for liver function include [[gamma glutamyl transpeptidase]] (GGT) and [[prothrombin time]] (PT).<ref>{{cite web |title=Liver Function Tests |url=https://medlineplus.gov/lab-tests/liver-function-tests/ |website=MedlinePlus |publisher=US National Library of Medicine |access-date=16 January 2021}}</ref> No single test can differentiate between various classifications of jaundice. A combination of [[liver function tests]] and other physical examination findings is essential to arrive at a diagnosis.<ref>{{cite journal | vauthors = Roche SP, Kobos R | title = Jaundice in the Adult Patient | journal = American Family Physician | year=2004 | url = https://www.aafp.org/afp/2004/0115/p299.html | volume = 69 | issue = 2 | pages = 299–304 | pmid = 14765767 | access-date = 22 September 2020 }}</ref>

=== Laboratory tests ===
{| class="wikitable"
!
!Prehepatic jaundice
!Hepatic jaundice
!Posthepatic jaundice
|-
!Total serum bilirubin
|Normal / increased
|Increased
|Increased
|-
!Conjugated bilirubin
|Normal
|Increased
|Increased
|-
!Unconjugated bilirubin
|Normal / increased
|Increased
|Normal
|-
!Urobilinogen
|Normal / increased
|Decreased
|Decreased / negative
|-
!Urine color
|Normal<ref>{{cite book| vauthors =Llewelyn H, Ang HA, Lewis K, Al-Abdullah A |url=https://books.google.com/books?id=rNFLBAAAQBAJ&pg=PA18|title=Oxford Handbook of Clinical Diagnosis |date=2014|publisher=Oxford University Press|isbn=978-0-19-967986-7|page=18|language=en |archive-url=https://web.archive.org/web/20170908204555/https://books.google.com/books?id=rNFLBAAAQBAJ&pg=PA18|archive-date=2017-09-08|url-status=live}}</ref>
|Dark (urobilinogen, conjugated bilirubin)
|Dark (conjugated bilirubin)
|-
!Stool color
|Brown
|Slightly pale
|Pale, white
|-
!Alkaline phosphatase levels
| rowspan="2" |Normal
|Increased
|Highly increased
|-
!Alanine transferase and aspartate transferase levels
|Highly increased
|Increased
|-
!Conjugated bilirubin in urine
|Not present
|Present
|Present
|}

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 are only elevated in liver-specific conditions. The second step is distinguishing from biliary (cholestatic) or liver causes of jaundice and altered laboratory results. ALP and GGT levels 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 IU/L) levels rise proportionately as high as the AST (12–38 IU/L) and ALT (10–45 IU/L) levels, this indicates a cholestatic problem. If the AST and ALT rise is significantly higher than the ALP and GGT rise, though, this indicates a liver problem. Finally, distinguishing between liver causes of jaundice, comparing levels of AST and ALT can prove useful. AST levels typically are higher than ALT. This remains the case in most liver disorders except for hepatitis (viral or hepatotoxic). Alcoholic liver damage may have fairly normal ALT levels, with AST 10 times higher than ALT. If ALT is higher than AST, however, 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 the level is normal in hepatitis and cholestasis.{{citation needed|date=July 2015}}

Laboratory 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 10 times normal could indicate neoplastic or intrahepatic cholestasis. Levels lower than this tend to indicate hepatocellular causes. AST levels greater than 15 times normal tend to indicate acute hepatocellular damage. Less than this tend to indicate obstructive causes. ALP levels greater than 5 times normal tend to indicate obstruction, while levels greater than 10 times normal can indicate drug (toxin) induced cholestatic hepatitis or [[cytomegalovirus]] infection. Both of these conditions can also have ALT and AST greater than 20 times normal. GGT levels greater than 10 times normal typically indicate cholestasis. Levels 5–10 times tend to indicate viral hepatitis. Levels less than 5 times normal tend to indicate drug toxicity. Acute hepatitis typically has ALT and AST levels rising 20–30 times normal (above 1000) and may remain significantly elevated for several weeks. [[Acetaminophen]] toxicity can result in ALT and AST levels greater than 50 times than normal.{{citation needed|date=July 2015}}

Laboratory findings depend on the cause of jaundice:
* Urine: conjugated bilirubin present, urobilinogen > 2 units but variable (except in children)
* [[Plasma protein]]s show characteristic changes.
* Plasma albumin level is low, but plasma [[globulin]]s are raised due to an increased formation of [[Antibody|antibodies]].

Unconjugated bilirubin is hydrophobic, so cannot be excreted in urine. Thus, the finding of increased urobilinogen in the urine without the presence of bilirubin in the urine (due to its unconjugated state) suggests [[hemolytic jaundice]] as the underlying disease process.<ref>{{cite web| vauthors = Cadogen M |date=2019-04-21|title=Bilirubin and Jaundice|url=https://litfl.com/bilirubin-and-jaundice/|access-date=2019-11-19|website=Life in the Fast Lane|language=en-US}}</ref> Urobilinogen will be greater than 2 units, as hemolytic anemia causes increased heme metabolism; one exception being the case of infants, where the [[gut flora]] has not developed). Conversely, conjugated bilirubin is hydrophilic and thus can be detected as present in the urine—[[bilirubinuria]]—in contrast to unconjugated bilirubin, which is absent in the urine.<ref name="AFP2004">{{cite journal|vauthors=Roche SP, Kobos R|date=January 2004|title=Jaundice in the adult patient|journal=American Family Physician|volume=69|issue=2|pages=299–304|pmid=14765767}}</ref>

=== Imaging ===
[[Medical imaging]] such as [[ultrasound]], [[CT scan]] with contrast, and [[Cholescintigraphy|HIDA scan]] are useful for detecting bile-duct blockage.<ref name="AFP2004" /><ref name="nelson">{{Cite journal |last1=Nelson |first1=Michelle |last2=Mulani |first2=Shaunak R. |last3=Saguil |first3=Aaron |year=2025 |title=Evaluation of Jaundice in Adults |journal=American Family Physician |volume=111 |issue=1 |pages=25–30 |issn=1532-0650 |pmid=39823630}}</ref> Ultrasound and CT scans are routinely first line as they provide rapid results while remaining noninvasive and cost-effective.<ref name=nelson/> Other imaging modalities may also be effective and utilized when a particular etiology is suspected, such as endoscopic retrograde cholangiopancreatography ([[Endoscopic retrograde cholangiopancreatography|ERCP]]) or magnetic resonance cholangiopancreatography ([[Magnetic resonance cholangiopancreatography|MRCP]]) in the setting of suspected bile duct obstruction.<ref name=nelson/>

=== Liver biopsy ===
Liver biopsy may be indicated if labs, imaging, or other diagnostic tests do not determine the cause of jaundice.<ref name=nelson/> There is a substantial risk of bleeding of up to 10% associated with liver biopsy, although significant life-threatening bleeding is much less likely.<ref name=nelson/> Given this, liver biopsy should be reserved for cases in which it will significantly impact diagnosis or management.<ref name=nelson/>

===Differential diagnosis===
Other etiologies of yellow discoloration of the skin not related to deposition of bilirubin include:
* Yellow discoloration of the skin, especially on the palms and the soles, but not of the sclera or inside the mouth, is often due to [[carotenemia]]—a harmless condition.<ref>{{EMedicine|article|1104368|Carotenemia}}</ref> Overconsumption of foods containing carotene such as carrots, leafy vegetables, squash, peaches, and oranges are the most common cause.<ref name=":1">{{Cite book |last1=Longo |first1=Dan |title=Harrison's Principles of Internal Medicine |last2=Fauci |first2=Anthony |last3=Kasper |first3=Dennis |last4=Hauser |first4=Stephen |last5=Jameson |first5=J. Larry |last6=Loscalzo |first6=Joseph |last7=Holland |first7=Steven |last8=Langford |first8=Carol |publisher=McGraw Hill |year=2025 |isbn=978-1-265-97931-7 |edition=22nd |location=New York}}</ref> However, it can also be associated with medical conditions such as diabetes, hypothyroidism, and anorexia nervosa.<ref name=":1" /> On physical exam, the two are differentiable where jaundice typically has diffuse yellowing of the skin throughout the body and carotenemia displays concentration of yellowing in specific areas of the body.<ref name=":1" />
* Certain medications are associated with yellowing of the skin as a side effect: [[quinacrine]], [[sunitinib]], and [[sorafenib]].<ref name=":1" />
* Yellow discoloration of the skin can also rarely occur with [[copper toxicity|hypercupremia]], whether from [[Wilson's disease]] or from another metabolic derangement. Similarly, a golden-ish ring at the edges of the [[iris (anatomy)|irises]] can occur ([[:File:Kayser-Fleischer ring.jpg|Kayser-Fleischer ring]]).<!--Sanders 2009 is an example of a [[WP:RS]] ref for this sign in DDx.-->{{cn|date=March 2025}}

== Treatment ==
Treatment of jaundice varies depending on the underlying cause.<ref name="Fer2014" /> If a bile duct blockage is present, surgery is typically required; otherwise, management is pharmacological.<ref name="Fer2014" /><ref>{{cite journal | vauthors = Wang L, Yu WF | title = Obstructive jaundice and perioperative management | journal = Acta Anaesthesiologica Taiwanica | volume = 52 | issue = 1 | pages = 22–29 | date = March 2014 | pmid = 24999215 | doi = 10.1016/j.aat.2014.03.002 | doi-access =  }}</ref><ref>{{cite book|date=2015| veditors = Dixon E, Vollmer CM, May GR |title=Management of Benign Biliary Stenosis and Injury|doi=10.1007/978-3-319-22273-8|isbn=978-3-319-22272-1|doi-access=free}}</ref><ref>{{cite journal | vauthors = Lorenz JM | title = Management of Malignant Biliary Obstruction | journal = Seminars in Interventional Radiology | volume = 33 | issue = 4 | pages = 259–267 | date = December 2016 | pmid = 27904244 | pmc = 5088103 | doi = 10.1055/s-0036-1592330 }}</ref>

==Epidemiology==
Jaundice in adults is rare.<ref>{{cite book| vauthors = Ahmad J, Friedman SL, Dancygier H |url=https://books.google.com/books?id=4uLAAgAAQBAJ&pg=PT60|title=Mount Sinai Expert Guides: Hepatology|date=2014|publisher=John Wiley & Sons|isbn=978-1-118-74252-5|language=en |archive-url=https://web.archive.org/web/20170908204555/https://books.google.com/books?id=4uLAAgAAQBAJ&pg=PT60|archive-date=2017-09-08|url-status=live}}</ref><ref>{{cite journal | vauthors = Björnsson E, Gustafsson J, Borkman J, Kilander A | title = Fate of patients with obstructive jaundice | journal = Journal of Hospital Medicine | volume = 3 | issue = 2 | pages = 117–123 | date = March 2008 | pmid = 18438808 | doi = 10.1002/jhm.272 }}</ref><ref name="Bansal_2006">{{cite journal | vauthors = Bansal V, Schuchert VD | title = Jaundice in the intensive care unit | journal = The Surgical Clinics of North America | volume = 86 | issue = 6 | pages = 1495–1502 | date = December 2006 | pmid = 17116459 | doi = 10.1016/j.suc.2006.09.007 }}</ref> Under the five year DISCOVERY programme in the UK, annual incidence of jaundice was 0.74 per 1000 individuals over age 45, although this rate may be slightly inflated due to the main goal of the programme collecting and analyzing cancer data in the population.<ref>{{cite journal | vauthors = Taylor A, Stapley S, Hamilton W | title = Jaundice in primary care: a cohort study of adults aged >45 years using electronic medical records | journal = Family Practice | volume = 29 | issue = 4 | pages = 416–420 | date = August 2012 | pmid = 22247287 | doi = 10.1093/fampra/cmr118 | doi-access = free }}</ref> Jaundice is commonly associated with severity of disease with an incidence of up to 40% of patients requiring intensive care in ICU experiencing jaundice.<ref name="Bansal_2006" /> The causes of jaundice in the intensive care setting are both due to jaundice as the primary reason for ICU stay or as a morbidity to an underlying disease (i.e. sepsis).<ref name="Bansal_2006" />

In the developed world, the most common causes of jaundice are blockage of the bile duct or medication-induced. In the developing world, the most common cause of jaundice is infectious, such as [[viral hepatitis]], [[leptospirosis]], [[schistosomiasis]], or [[malaria]].<ref name="Rog2004" />

=== Risk factors ===
Risk factors associated with high serum bilirubin levels include male gender, white ethnicities, and active smoking.<ref name="Zucker 827–835">{{cite journal | vauthors = Zucker SD, Horn PS, Sherman KE | title = Serum bilirubin levels in the U.S. population: gender effect and inverse correlation with colorectal cancer | journal = Hepatology | volume = 40 | issue = 4 | pages = 827–835 | date = October 2004 | pmid = 15382174 | doi = 10.1002/hep.1840400412 | doi-access =  }}</ref> Mean serum total bilirubin levels in adults were found to be higher in men (0.72 ± 0.004&nbsp;mg/dl) than women (0.52 ± 0.003&nbsp;mg/dl).<ref name="Zucker 827–835" /> Higher bilirubin levels in adults are found also in non-Hispanic white population (0.63 ± 0.004&nbsp;mg/dl) and Mexican American population (0.61 ± 0.005&nbsp;mg/dl) while lower in non-Hispanic black population (0.55 ± 0.005&nbsp;mg/dl).<ref name="Zucker 827–835" /> Bilirubin levels are higher in active smokers.<ref name="Zucker 827–835" />

== Special populations ==

=== Neonatal jaundice ===
{{main|Neonatal jaundice}}
==== Symptoms ====
Jaundice in infants presents with yellowed skin and icteral sclerae. Neonatal jaundice spreads in a cephalocaudal pattern, affecting the face and neck before spreading down to the trunk and lower extremities in more severe cases.<ref>{{cite book | vauthors = Telega GW |chapter=Jaundice|date=2018|title=Nelson Pediatric Symptom-Based Diagnosis|pages=255–274.e1|publisher=Elsevier|doi=10.1016/b978-0-323-39956-2.00015-7|isbn=978-0-323-39956-2}}</ref> Other symptoms may include drowsiness, poor feeding, and in severe cases, unconjugated bilirubin can cross the blood-brain barrier and cause permanent neurological damage ([[kernicterus]]).

==== Causes ====
The most common cause of jaundice in infants is [[Physiologic jaundice|normal physiologic jaundice]]. Pathologic causes of neonatal jaundice include:
* Formula jaundice<ref>{{cite journal|vauthors=Bertini G, Dani C, Tronchin M, Rubaltelli FF|date=March 2001|title=Is breastfeeding really favoring early neonatal jaundice?|journal=Pediatrics|volume=107|issue=3|article-number=E41|doi=10.1542/peds.107.3.e41|pmid=11230622|doi-access=free}}</ref>
* [[Hereditary spherocytosis]]
* [[Glucose-6-phosphate dehydrogenase deficiency]]
* [[Pyruvate kinase deficiency]]
* [[ABO blood group system|ABO]]/[[Rh blood group system|Rh]] blood type autoantibodies
* [[Alpha 1-antitrypsin deficiency]]
* [[Alagille syndrome]] (genetic defect resulting in hypoplastic intrahepatic bile ducts)
* [[Progressive familial intrahepatic cholestasis]]
* [[Pyknocytosis]] (due to vitamin deficiency)
* [[Cretinism]] (congenital hypothyroidism)
* Sepsis or other infectious causes

==== Pathophysiology ====
Transient [[neonatal jaundice]] is one of the most common conditions occurring in newborns (children under 28 days of age) with more than 80 per cent experienceing jaundice during their first week of life.<ref>{{cite journal | vauthors = Maisels MJ | title = Managing the jaundiced newborn: a persistent challenge | journal = CMAJ | volume = 187 | issue = 5 | pages = 335–343 | date = March 2015 | pmid = 25384650 | pmc = 4361106 | doi = 10.1503/cmaj.122117 }}</ref> Jaundice in infants, as in adults, is characterized by increased bilirubin levels (infants: total serum bilirubin greater than 5&nbsp;mg/dL).{{cn|date=March 2025}}

Normal physiological neonatal jaundice is due to immaturity of liver enzymes involved in bilirubin metabolism, immature gut microbiota, and increased breakdown of fetal hemoglobin (HbF).<ref>{{cite book|title=Oxford Handbook of Clinical Specialties|vauthors=Collier J, Longore M, Turmezei T, Mafi AR|publisher=Oxford University Press|year=2010|isbn=978-0-19-922888-1|chapter=Neonatal jaundice}}{{page needed|date=July 2015}}</ref> Breast milk jaundice is caused by an increased concentration of [[β-glucuronidase]] in breast milk, which increases bilirubin deconjugation and reabsorption of bilirubin, leading to persistence of physiologic jaundice with unconjugated hyperbilirubinemia. Onset of breast milk jaundice is within 2 weeks after birth and lasts for 4–13 weeks.{{cn|date=May 2022}}

While most cases of newborn jaundice are not harmful, when bilirubin levels are very high, brain damage—[[kernicterus]]—may occur<ref>{{cite web|date=February 23, 2015|title=Facts about Jaundice and Kernicterus|url=https://www.cdc.gov/ncbddd/jaundice/facts.html|url-status=live|archive-url=https://web.archive.org/web/20160808204002/http://www.cdc.gov/ncbddd/jaundice/facts.html|archive-date=8 August 2016|access-date=13 August 2016|website=CDC}}</ref><ref name="Kap2017" /> leading to significant disability.<ref name="family">{{cite journal|vauthors=Click R, Dahl-Smith J, Fowler L, DuBose J, Deneau-Saxton M, Herbert J|year=2013|title=An osteopathic approach to reduction of readmissions for neonatal jaundice|journal=Osteopathic Family Physician|volume=5|issue=1|pages=17–23|doi=10.1016/j.osfp.2012.09.005}}</ref> Kernicterus is associated with increased unconjugated bilirubin (bilirubin which is not carried by [[albumin]]). Newborns are especially vulnerable to this damage, due to increased permeability of the [[blood–brain barrier]] occurring with increased unconjugated bilirubin, simultaneous to the breakdown of fetal hemoglobin and the immaturity of gut flora. This condition has been rising in recent years, as babies spend less time in sunlight.{{Citation needed|date=June 2020}}

==== Treatment ====
Jaundice in newborns is usually transient and dissipates without medical intervention. In cases when serum bilirubin levels are greater than 4–21&nbsp;mg/dl (68–360&nbsp;μmol/L), infant may be treated with [[phototherapy]] or [[exchanged transfusion]] depending on the infant's age and prematurity status.<ref name="CMAJ2015" /> A [[bili light]] is often the tool used for early treatment, which consists of exposing the baby to intensive [[phototherapy]], which may be intermittent or continuous.<ref>{{cite journal | vauthors = Gottimukkala SB, Lobo L, Gautham KS, Bolisetty S, Fiander M, Schindler T | title = Intermittent phototherapy versus continuous phototherapy for neonatal jaundice | journal = The Cochrane Database of Systematic Reviews | volume = 2023 | issue = 3 | article-number = CD008168 | date = March 2023 | pmid = 36867730 | pmc = 9979775 | doi = 10.1002/14651858.CD008168.pub2 | collaboration = Cochrane Neonatal Group }}</ref><ref>{{cite web |title=Bili Lights for Jaundice: Effectiveness for Neonatal and Adults {{!}} Heliotherapy Research Institute |url=https://heliotherapy.institute/bili-lights/ |access-date=2022-07-24 |language=en-US}}</ref> A 2014 systematic review found no evidence indicating whether outcomes were different for hospital-based versus home-based treatment.<ref>{{cite journal | vauthors = Malwade US, Jardine LA | title = Home- versus hospital-based phototherapy for the treatment of non-haemolytic jaundice in infants at more than 37 weeks' gestation | journal = The Cochrane Database of Systematic Reviews | issue = 6 | article-number = CD010212 | date = June 2014 | volume = 2014 | pmid = 24913724 | doi = 10.1002/14651858.cd010212.pub2 | pmc = 10750451 }}</ref> A 2021 Cochrane systematic review found that sunlight can be used to supplement phototherapy, as long as care is taken to prevent overheating and skin damage.<ref name="Horn_2021">{{cite journal | vauthors = Horn D, Ehret D, Gautham KS, Soll R | title = Sunlight for the prevention and treatment of hyperbilirubinemia in term and late preterm neonates | journal = The Cochrane Database of Systematic Reviews | volume = 2021 | issue = 7 | article-number = CD013277 | date = July 2021 | pmid = 34228352 | pmc = 8259558 | doi = 10.1002/14651858.CD013277.pub2 | collaboration = Cochrane Neonatal Group }}</ref> There was not sufficient evidence to conclude that sunlight by itself is an effective treatment.<ref name="Horn_2021" />  Bilirubin count is also lowered through excretion—bowel movements and urination—so frequent and effective feedings are vital measures to decrease jaundice in infants.<ref>{{cite journal| vauthors = O'Keefe L |date=May 2001|title=Increased vigilance needed to prevent kernicterus in newborns|url=http://aapnews.aappublications.org/cgi/content/full/18/5/231|url-status=live|journal=American Academy of Pediatrics|volume=18|issue=5|page=231|archive-url=https://web.archive.org/web/20070927203356/http://aapnews.aappublications.org/cgi/content/full/18/5/231|archive-date=2007-09-27}}</ref>

==Etymology==
Jaundice comes from the French {{Lang|fr|jaune}}, meaning 'yellow'; {{Lang|fr|jaunisse}} meaning 'yellow disease'. The medical term is ''icterus,'' from the Greek word {{Lang|grc-latn|ikteros}}.<ref name="medicinenet">{{cite web|title=Definition of Icterus| work=Medterms |url=http://www.medterms.com/script/main/art.asp?articlekey=3890|year=2011|publisher=MedicineNet.com|url-status=live|archive-url=https://web.archive.org/web/20120807091718/http://www.medterms.com/script/main/art.asp?articlekey=3890|archive-date=7 August 2012|access-date=3 February 2013}}</ref> The term ''icterus'' is sometimes incorrectly used to refer to jaundice specifically of sclera.<ref name="medicinenet" /><ref>[http://dictionary.reference.com/browse/icterus Icterus | Define Icterus at Dictionary.com] {{webarchive|url=https://web.archive.org/web/20101231025038/http://dictionary.reference.com/browse/icterus|date=2010-12-31}}. Dictionary.reference.com. Retrieved on 2013-12-23.</ref> It is also referenced in the [[scientific name]] of the [[yellow-breasted chat]] (''Icteria virens''), whose sight was believed to cure jaundice.<ref>{{cite journal |last1=Hoenig |first1=Leonard J. |title=True Colors |journal=JAMA Dermatology |date=June 2015 |volume=151 |issue=6 |page=641 |doi=10.1001/jamadermatol.2015.107 |pmid=26061953 }}</ref>

== References ==
{{Reflist}}

== External links ==
* {{Wiktionary-inline|jaundice}}
* {{Commons category-inline}}
{{Medical condition classification and resources

| ICD10          = {{ICD10|R|17||r|10}}
 | ICD9           = {{ICD9|782.4}}
 | OMIM           =
 | MedlinePlus    = 003243
 | eMedicineSubj  =
 | eMedicineTopic =
 | DiseasesDB     = 7038
 | MeshID         = D007565
}}
{{Digestive system and abdomen symptoms and signs}}

{{Authority control}}

[[Category:Symptoms and signs: Digestive system and abdomen]]
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