Bilirubin, Total
| Bilirubin, Total | | | |
| Number | | 001099 |
| CPT | | 82247 |
| Synonyms | | TBili |
| Specimen | | Serum |
| Volume | | 1 mL |
| Minimum Volume | | 0.5 mL |
| Container | | Red-top tube or gel-barrier tube |
| Collection | | Separate serum from cells within 45 minutes of collection. |
| Storage Instructions | | Refrigerate |
| Causes for Rejection | | Gross hemolysis; improper labeling; gross lipemia |
| Reference Interval | | 0.1-1.2 mg/dL |
| Use | | Causes of high bilirubin: Liver disease: hepatitis, cholangitis, cirrhosis, other types of liver disease (including primary or secondary neoplasia); alcoholism (usually with high AST (SGOT), GGT, MCV, or some combination of these findings); biliary obstruction (intrahepatic or extrahepatic); infectious mononucleosis (look also for increased LD (LDH), lymphocytosis); Dubin-Johnson syndrome; Gilbert disease1 (familial hyperbilirubinemia) is encountered as a moderate elevation with otherwise unremarkable chemistries. Anorexia or prolonged fasting: 36 hours or more may cause moderate rise. Pernicious anemia, hemolytic anemias, erythroblastosis fetalis, other neonatal jaundice, hematoma, and following a blood transfusion, especially if several units are given in a short time. Pulmonary embolism and/or infarct, congestive heart failure. Drugs: A large number of drugs can cause jaundice by in vivo action or by chemistry methodology. Drugs causing cholestasis and/or hepatocellular damage include diphenylhydantoin, azathioprine, phenothiazines, erythromycin, penicillin, sulfonamides, oral contraceptives, anabolic-androgenic steroids, halothane, aminosalicylic acid, isoniazid, methyldopa, indomethacin, pyrazinamide, and others. |
| Methodology | | Colorimetric |
| Additional Information | | Interpretation of increased bilirubin is greatly enhanced by other chemistry results. In acute viral hepatitis with jaundice, for instance, the transaminases ALT (SGPT) and AST (SGOT) are consistently increased, while an isolated elevation of bilirubin is seen in Gilbert disease.1 Obstruction causes increases in bilirubin and alkaline phosphatase greater than and out of proportion to the transaminases.2 Amylase and lipase are useful in differential diagnosis of obstructive jaundice. In intrahepatic cholestasis, the transaminases are not as increased, relative to bilirubin, as they are in hepatitis.3 Work-up of jaundice has been outlined.4,5 Nicotinic acid increases the formation of bilirubin in the spleen, leading to a rise in unconjugated bilirubin. This can be used as a test for Gilbert disease1 in which there is a decreased hepatic clearance of unconjugated bilirubin. Although the indirect bilirubin level is increased in normal controls when nicotinic acid is given, the increase is much greater in patients with Gilbert disease. In the Crigler-Najjar syndrome type I, the unconjugated bilirubin is >20 μg/dL. In type II, the level is <20 μg/dL. |
| Footnotes | | - Ohkubo H and Okuda K, “The Nicotinic Acid Test in Constitutional Conjugated Hyperbilirubinemia and Effects of Steroids,” Hepatology, 1984, 4(6):1206-8.
- Scharschmidt BF, Goldberg HI, and Schmid R, “Current Concepts in Diagnosis. Approach to the Patient With Cholestatic Jaundice,” N Engl J Med, 1983, 308(25):1515-9.
- Goldberg DM, Spooner RJ, Ellis G, et al, “Biochemical Features of Intrahepatic Cholestasis,” Am J Clin Pathol, 1979, 71(5):557-63.
- Ostrow JD, “Jaundice in Older Children and Adults,” Using the Clinical Laboratory in Medical Decision Making, Lundberg GD, ed, Chicago, IL: American Society of Clinical Pathologists, 1983, 41-8.
- Fischer MG, Gelb AM, and Weingarten LA, “Cholestatic Jaundice in Adults,” Using the Clinical Laboratory in Medical Decision Making, Lundberg GD, ed, Chicago, IL: American Society of Clinical Pathologists, 1983, 49-54
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