eMedicine Specialties > Gastroenterology > Liver

Gilbert Syndrome: Differential Diagnoses & Workup

Author: Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Contributor Information and Disclosures

Updated: Nov 19, 2009

Differential Diagnoses

Biliary Disease

Other Problems to Be Considered

Hemolysis
Hematoma
Acute and chronic liver disease
Primary hyperbilirubinemia from ineffective erythropoiesis
Glucuronyl transferase deficiency
Infections
Cardiac disease (eg, congestive heart failure, prosthetic heart valves)
Rhabdomyolysis
High-altitude living
Medications (eg, probenecid, rifamycin, other antibiotics)
Thyrotoxicosis

As can be inferred from the above list, Gilbert syndrome has a broad differential diagnosis because causes of unconjugated hyperbilirubinemia must be considered.

Workup

Laboratory Studies

  • CBC count (including reticulocyte count and blood smear): This is a useful screening test to exclude hemolysis. Rarely, red blood cell abnormalities resembling variegate porphyria have been described in persons with Gilbert syndrome, possibly due to the increased hepatocellular bilirubin concentration.
  • Lactate dehydrogenase: Levels are elevated in persons with hemolysis but are normal in those with Gilbert syndrome.
  • Liver function tests: With the exception of unconjugated hyperbilirubinemia, standard liver function test results are normal. However, a familial increase in serum alkaline phosphatase levels has been reported in persons with Gilbert syndrome.

Imaging Studies

  • Imaging studies are not required to confirm a diagnosis of Gilbert syndrome.

Other Tests

  • Additional tests are rarely required because a diagnosis of Gilbert syndrome can be made in the presence of (1) unconjugated hyperbilirubinemia noted on several occasions; (2) normal results from CBC count, reticulocyte count, and blood smear; (3) normal liver function test results; and (4) an absence of other disease processes.
  • The following investigations are occasionally performed to confirm a diagnosis of Gilbert syndrome. Those of historical interest, as well as the newer molecular genetic techniques, are included. They are described to introduce the clinician to the broad diagnostic armamentarium available for diagnosing Gilbert syndrome. Recourse to these specialized tests should be rare and is usually difficult to justify in clinical practice because the diagnosis of Gilbert syndrome is usually straightforward.
    • Fasting: This usually results in a 2- to 3-fold rise in the plasma unconjugated bilirubin level within 48 hours of a fast that returns to normal levels within 24 hours of resuming a normal diet. Although unconjugated bilirubin levels also rise with fasting in patients with hemolysis or liver disease, the magnitude of the rise is less than that observed with Gilbert syndrome. A similar rise in plasma bilirubin is also observed with normocaloric diets deficient in lipids and reverses promptly with lipid replacement. The precise mechanism of fasting and dietary-induced hyperbilirubinemia remains unclear. The fasting test remains of historic interest and has limited usefulness in the diagnosis of Gilbert syndrome.
    • Nicotinic acid: Intravenous administration of 50 mg of nicotinic acid results in a 2- to 3-fold rise in plasma unconjugated hyperbilirubinemia within 3 hours. The mechanisms are multifactorial and probably related to (1) elevated osmotic fragility of red blood cells, (2) increase in splenic production of bilirubin, (3) transient inhibition of hepatic bilirubin-UGT activity, and (4) increased splenic heme oxygenase activity. Although a similar but less impressive increase is observed in healthy individuals and those with hemolysis or liver disease, the nicotinic test, similar to fasting, does not clearly distinguish patients with Gilbert syndrome from those who are healthy or who have other disease processes.
    • Phenobarbital: Phenobarbital and other enzyme inducers of the bilirubin-UGT system will normalize plasma bilirubin in patients with Gilbert syndrome. This is predominantly due to accelerated bilirubin clearance from enzyme induction but is also due to reduced bilirubin turnover. Steroids can also reduce plasma bilirubin levels in Gilbert syndrome by increasing hepatic uptake and storage of bilirubin.
    • Radioactive-labeled chromium: This is used to measure red blood cell survival. As many as 60% of patients with Gilbert syndrome have a mild and fully compensated state of hemolysis together with increased hepatic heme production. As a result, hyperbilirubinemia may be due to reduced bilirubin clearance and increased production, the latter from increased erythroid or hepatic heme turnover.
    • Thin-layer chromatography: This test is diagnostic for Gilbert syndrome when it shows a significantly higher proportion of unconjugated bilirubin compared with individuals with chronic hemolysis or liver disease or those who are healthy. If confirmation of the diagnosis is truly essential, chromatographic determination is of potential use. This shows an increased ratio of bilirubin monoglucuronide to diglucuronide, reflecting reduced bilirubin-UGT activity.
    • Drug clearance: Approximately 30% of patients have impaired clearance of bromosulfophthalein, indocyanine green, and free fatty acid, suggesting an abnormality in hepatic uptake, transport, or both. The metabolic clearance of tolbutamide is also reduced in persons with Gilbert syndrome, but, because it does not undergo glucuronidation, hepatic uptake appears to be defective. Plasma clearance of most drugs that undergo glucuronidation (eg, benzodiazepines) is unaffected. However, with regard to acetaminophen, patients with Gilbert syndrome are a heterogeneous group, with some demonstrating normal metabolism and others exhibiting marked reduction in glucuronidation and an increase in oxidation. These changes could mean that people in this subgroup could be more susceptible to liver injury after an acetaminophen overdose, although no such adverse events have been reported.
    • Polymerase chain reaction: Polymerase chain reaction is a novel and rapid method of identifying genetic polymorphisms in the TATA box of the UGT1*1 gene using fluorescence resonance energy transfer.

Procedures

  • Liver biopsies are not performed routinely and are rarely necessary.

Histologic Findings

The liver is normal histologically, except for occasional accumulation of a lipofuscinlike pigment around the terminal hepatic venules.

More on Gilbert Syndrome

Overview: Gilbert Syndrome
Differential Diagnoses & Workup: Gilbert Syndrome
Treatment & Medication: Gilbert Syndrome
Follow-up: Gilbert Syndrome
References
Further Reading
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References

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Further Reading

Clinical guideline

ACR Appropriateness Criteria® jaundice.
American College of Radiology - Medical Specialty Society. 1996 (revised 2008). 7 pages. NGC:006987

Clinical trial
The Effects of Atazanavir-Induced Hyperbilirubinemia During Human Endotoxemia

Related eMedicine topics
Crigler-Najjar Syndrome

Hyperbilirubinemia, Unconjugated

Breast Milk Jaundice

Jaundice, Neonatal

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Keywords

Gilbert syndrome, jaundice, bilirubin levels, high bilirubin, bilirubin level, elevated bilirubin, serum bilirubin, Gilbert's syndrome, unconjugated hyperbilirubinemia, unconjugated bilirubin, constitutional hyperbilirubinemia, familial nonhemolytic jaundice, hereditary nonhemolytic bilirubinemia, low-grade chronic hyperbilirubinemia

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Contributor Information and Disclosures

Author

Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Medical Editor

Manoop S Bhutani, MD, FACG, FACP, Professor, Department of Medicine, Division of Gastroenterology, Director, Center for Endoscopic Ultrasound, Co-Director, Center for Endoscopic Research, Training and Innovation, University of Texas Medical Branch at Galveston
Manoop S Bhutani, MD, FACG, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Institute of Ultrasound in Medicine, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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