Jaundice

Author(s):  
Satish Keshav ◽  
Alexandra Kent

Jaundice, also known as icterus, is the yellowish discolouration seen in skin, mucous membranes, and sclerae when the plasma bilirubin concentration is >40 μ‎mol/l. Jaundice may arise from increased production of bilirubin, for instance, in haemolysis; from reduced conjugation in the liver, as in Gilbert’s syndrome; or from reduced excretion via bile, as in intra-hepatic cholestasis. Jaundice also occurs when the flow of bile is obstructed, for instance, by gallstones or pancreatic cancer (extra-hepatic cholestasis). The clinical approach to the jaundiced patient is described in this topic.

1984 ◽  
Vol 66 (4) ◽  
pp. 493-496 ◽  
Author(s):  
Giovanni L. Ricci ◽  
Riccardo R. Ricci

1. To test the hypothesis that the presence of food in the intestine plays a role in the control of serum bilirubin levels, the effect of a 1674 kJ (400 kcal) diet, including non-absorbable material able to produce an intestinal bulk, was compared with the effect of caloric restriction alone. 2. In normal individuals (n = 10) the rise of plasma bilirubin was comparable after the two trials. In patients with Gilbert's syndrome (n = 18), bilirubin concentration rose to a much greater extent during the caloric restriction as compared with controls, and to a lesser extent (P<0.001) after the bulky diet, as compared with caloric restriction alone in the same patient. 3. It is proposed that a factor originating from the intestine, perhaps a hormone, the release of which is dependent on the presence of food-bulk, plays a role in the control of hyperbilirubinaemia associated with caloric restriction.


1974 ◽  
Vol 46 (1) ◽  
pp. 1-17 ◽  
Author(s):  
M. Black ◽  
J. Fevery ◽  
D. Parker ◽  
J. Jacobson ◽  
Barbara H. Billing ◽  
...  

1. The clearance of a tracer dose of [14C]bilirubin from the plasma was studied in patients with Gilbert's syndrome, congenital non-haemolytic jaundice, haemolytic jaundice and in normal subjects. Clearance was significantly impaired in the patients with Gilbert's syndrome and in those with congenital non-haemolytic jaundice when compared with the normal subjects, and was normal in the patient with haemolytic jaundice. 2. Treatment for 2 weeks with phenobarbitone (180 mg/day) lowered the plasma bilirubin concentration and improved all indices of plasma clearance of the isotope in patients with Gilbert's syndrome, so that they became indistinguishable from those of normal subjects. The improvement in plasma [14C]bilirubin clearance in these patients was associated with modest increases in hepatic bilirubin glucuronyl transferase in some subjects. 3. Phenobarbitone treatment improved plasma bilirubin concentrations and plasma [14C]bilirubin clearance in patients with congenital non-haemolytic jaundice, so that they resembled those seen in patients with untreated Gilbert's syndrome. Despite this improvement hepatic bilirubin glucuronyl transferase activity remained undetectable. 4. These results are compatible with the hypothesis that Gilbert's syndrome is a manifestation of a relative deficiency of hepatic bilirubin glucuronyl transferase, and differs from congenital non-haemolytic jaundice only in severity.


1978 ◽  
Vol 55 (1) ◽  
pp. 63-71 ◽  
Author(s):  
C. A. Goresky ◽  
Ellen R. Gordon ◽  
E. A. Shaffer ◽  
P. Paré ◽  
D. Carassavas ◽  
...  

1. Intravenous doses of bilirubin (3.4 μmol/kg) were given to normal subjects and patients with Gilbert's syndrome. Both groups displayed an identical initial disappearance of a substantial proportion of the bilirubin but, late in time, the Gilbert's patients exhibited reduced clearance with a sustained elevation of the plasma bilirubin and no reflux into the plasma space of conjugated bilirubin. Increasing the dose in normal subjects (by factors of 3 and 6) failed to reproduce the response found in the Gilbert's patients. 2. In the bile-containing duodenal aspirates of Gilbert's patients the average proportion of bilirubin found as bilirubin diglucuronide was 68% (normal 88%) and of bilirubin monoglucuronide, 23% (normal 7%). Both differences were significant at the P < 0.001 level. In the Gilbert's patients restriction of caloric intake to 1569 kJ/day for 2 days characteristically raised the serum bilirubin with no modification of the biliary pigment pattern; phenobarbital (180 mg/day for 2 weeks) decreased the plasma bilirubin to the normal range with, concomitantly, a reversion of the biliary pigment pattern towards normal. 3. We conclude that there is no hepatic uptake defect in Gilbert's syndrome but that there is decreased activity in the conjugation process underlying the addition of the second glucuronic acid moiety to bilirubin, to form bilirubin diglucuronide.


2019 ◽  
Vol 6 (2) ◽  
Author(s):  
Suneed Kumar ◽  
Sneha Jha ◽  
Anshuman Pandey ◽  
Shibumon M Madhavan ◽  
Dinesh Kumar ◽  
...  

Gallstones are the commonest ailment affecting the hepato-biliary system. Associated jaundice is usually direct, commonly due to biliary obstructive lesions. Unconjugated hyperbilirubinemia with cholelithiasis is commonly seen with hemolytic disease. In the absence of hemolysis or systemic causes, congenital causes prevail, commonest of which is Gilbert’ Syndrome. This study aims to ascertain a clinical approach to the patient of gallstones with Gilbert’s syndrome. This is retrospective study of 58 patients with gallstone associated unconjugated hyperbilirubinemia, who underwent surgery over a two-year period. Patients underwent repeat blood investigations and ultrasound to confirm the diagnosis. Obstructive biliary pathology was ruled out by MRCP images; EUS added if indicated. The remaining patients underwent genetic test for Gilbert’s syndrome – namely UGT1A1 gene assessment by PCR. All patients underwent laparoscopic cholecystectomy as routine; with addition of intra-operative liver biopsy. Sixteen of the 58 patients were short-listed to be high risk factors for harboring Gilbert’s syndrome after ruling out other systemic causes. On gene study, 14 patients tested positive for UGT1A1 gene, hence Gilbert’s syndrome. The other two were kept on follow up for jaundice recurrence in future. The management algorithm is depicted as flowchart. Gilbert’s syndrome can be identified in select “high-risk” individuals presenting with gallstone disease. Genetic testing is gold standard, and helps in effective management and better patient counselling.


2021 ◽  
Author(s):  
Yuki Fujimaki ◽  
Takehiko Soutome ◽  
Takayuki Tanaka ◽  
Takeshi Shiba ◽  
Misa Watanabe

2016 ◽  
Vol 56 (12) ◽  
pp. 1164-1166
Author(s):  
Jonathan Leong ◽  
Maria-Stella Serrano

The Lancet ◽  
1995 ◽  
Vol 346 (8988) ◽  
pp. 1494 ◽  
Author(s):  
Yoko Soeda ◽  
Kazuo Yamamoto ◽  
Yukihiko Adachi ◽  
Takeshi Hori ◽  
Sachiko Aono ◽  
...  

The Lancet ◽  
1970 ◽  
Vol 295 (7661) ◽  
pp. 1359-1362 ◽  
Author(s):  
Martin Black ◽  
Sheila Sherlock

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