Skip to main content

Assessment of Liver Function

  • Chapter
  • First Online:
Liver Diseases

Abstract

This chapter explores various liver pathologies and their respective laboratory test abnormalities. Particular emphasis is placed on viral hepatitis, in addition to alcohol-induced, metabolic, and cholestatic liver disease. The chapter concludes with a discussion on the numerous complications of chronic liver disease with a focus on diagnosis and management, followed by a brief look into the future of hepatobiliary diagnostic workup.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 99.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 129.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 179.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Sticova E, Jirsa M. New insights in bilirubin metabolism and their clinical implications. World J Gastroenterol. 2013;19:6398.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  2. Raymond GD, Galambos JT. Hepatic storage and excretion of bilirubin in man. Am J Gastroenterol. 1971;55:135.

    CAS  PubMed  Google Scholar 

  3. Schmid R, Diamond I, Hammaker L, Gundersen CB. Interaction of bilirubin with albumin. Nature. 1965;206:1041.

    Article  CAS  PubMed  Google Scholar 

  4. VanWagner LB, Green RM. Evaluating elevated bilirubin levels in asymptomatic adults. JAMA. 2015;313:516–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Karmen A, Wroblewski F, Ladue JS. Transaminase activity in human blood. J Clin Invest. 1955;34(1):126–31.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Kwo PY, Cohen SM, Lim JK. ACG clinical guideline: evaluation of abnormal liver chemistries. Am J Gastroenterol. 2017;112:18.

    Article  CAS  PubMed  Google Scholar 

  7. Moussavian SN, Becker RC, Piepmeyer JL, et al. Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease. Dig Dis Sci. 1985;30:211.

    Article  CAS  PubMed  Google Scholar 

  8. Cohen JA, Kaplan MM. The SGOT/SGPT ratio-an indicator of alcoholic liver disease. Dig Dis Sci. 1979;24:835.

    Article  CAS  PubMed  Google Scholar 

  9. Sharma U, Pal D, Prasad R. Alkaline phosphatase: an overview. Indian J Clin Biochem. 2014;29(3):269–78.

    Article  CAS  PubMed  Google Scholar 

  10. Goldberg DM. Structural, functional, and clinical aspects of gamma-glutamyltransferase. CRC Crit Rev Clin Lab Sci. 1980;12:1.

    Article  CAS  PubMed  Google Scholar 

  11. Lum G, Gambino SR. Serum gamma-glutamyl transpeptidase activity as an indicator of disease of liver, pancreas, or bone. Clin Chem. 1972;18:358.

    CAS  PubMed  Google Scholar 

  12. Rothschild MA, Oratz M, Schreiber SS. Serum albumin. Hepatology. 1988;8:385.

    Article  CAS  PubMed  Google Scholar 

  13. Farrugia A. Albumin usage in clinical medicine: tradition or therapeutic? Transfus Med Rev. 2010;24(1):53–63.

    Article  PubMed  Google Scholar 

  14. Eschar J, Rudzki C, Zimmerman HJ. Serum levels of 5′-nucleotidase in disease. Am J Clin Pathol. 1967;47:598.

    Article  CAS  PubMed  Google Scholar 

  15. Hill PG, Sammons HG. An assessment of 5′-nucleotidase as a liver-function test. Q J Med. 1967;36:457.

    CAS  PubMed  Google Scholar 

  16. Brewer GJ, Yuzbasiyan-Gurkan V. Wilson disease. Medicine (Baltimore). 1992;71:139.

    Article  CAS  Google Scholar 

  17. Gibbs K, Walshe JM. A study of the caeruloplasmin concentrations found in 75 patients with Wilson’s disease, their kinships and various control groups. Q J Med. 1979;48:447.

    CAS  PubMed  Google Scholar 

  18. Marrero JA, Feng Z, Wang Y, et al. Alpha-fetoprotein, des-gamma carboxyprothrombin, and lectin-bound alpha-fetoprotein in early hepatocellular carcinoma. Gastroenterology. 2009;137:110.

    Article  CAS  PubMed  Google Scholar 

  19. Lok AS, Sterling RK, Everhart JE, et al. Des-gamma-carboxy prothrombin and alpha-fetoprotein as biomarkers for the early detection of hepatocellular carcinoma. Gastroenterology. 2010;138:493.

    Article  CAS  PubMed  Google Scholar 

  20. Bialecki ES, Di Bisceglie AM. Diagnosis of hepatocellular carcinoma. HPB (Oxford). 2005;7:26.

    Article  Google Scholar 

  21. Marks PW. Hematologic manifestations of liver disease. Semin Hematol. 2013;50:216.

    Article  PubMed  Google Scholar 

  22. Johnston DG, Alberti KGMM, Binder C, Faber OK, Wright R, Orskov H. Hormonal and metabolic changes in hepatic cirrhosis. Horm Metab Res. 1982;14:34–9.

    Article  CAS  PubMed  Google Scholar 

  23. Megyesi C, Samols E, Marks V. Glucose tolerance and diabetes in chronic liver disease. Lancet. 1967;2:1051–6.

    Article  CAS  PubMed  Google Scholar 

  24. Ellis G, Goldberg DM, Spooner RJ, Ward AM. Serum enzyme tests in diseases of the liver and biliary tree. Am J Clin Pathol. 1978;70:248.

    Article  CAS  PubMed  Google Scholar 

  25. American College of Physicians. Gastroenterology and Hepatology. MKSAP: Medical Knowledge Self-Assessment 18. Philadelphia, PA: American College of Physicians. p. 50. isbn:978-1-938245-50-3 19881989.

    Google Scholar 

  26. Sahani DV, Sanjeeva PK. Imaging the liver. Oncologist. 2004;9:385–97.

    Article  PubMed  Google Scholar 

  27. Newsome PN, et al. Guidelines on the management of abnormal liver blood tests. Gut. 2018 Jan;67(1):6–19. https://doi.org/10.1136/gutjnl-2017-314924.

    Article  PubMed  Google Scholar 

  28. Matheny SC, Kingery JE. Hepatitis A. Am Fam Physician. 2012;86(11):1027–34. quiz 1010–1012

    PubMed  Google Scholar 

  29. Dienstag JL. Acute viral hepatitis. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J, editors. Harrison’s principles of internal medicine. 19th ed. New York, NY: McGraw-Hill; 2015. isbn:978-0-07-180215-4.

    Google Scholar 

  30. Liang TJ. Hepatitis B: the virus and disease. Hepatology (Baltimore, MD). 2009;49(5 Suppl):S13–21.

    Article  CAS  Google Scholar 

  31. Vos T, Allen C, Arora M, et al. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388:1545–602.

    Article  Google Scholar 

  32. Lok A, McMahon B, Brown R, Wong JB, Ahmed HT, Wigdan F, et al. Antiviral therapy for chronic hepatitis B virus infection in adults: a systematic review and meta-analysis. Hepatology. 2015;63:284–06.

    Article  PubMed  CAS  Google Scholar 

  33. CDC (2009) Guidelines for viral hepatitis surveillance and case management. http://www.cdc.gov/hepatitis/Statistics/SurveillanceGuidelines.htm. Accessed 26 Nov 2011

  34. Manns MP, Buti M, Gane E, Pawlotsky JM, Razavi H, Terrault N, et al. Hepatitis C virus infection. Nat Rev Dis Primers. 2017;3:17006.

    Article  PubMed  Google Scholar 

  35. Rutherford A, Dienstag JL. Viral hepatitis. In: Greenberger NJ, Blumberg RS, Burakoff R, editors. Current diagnosis & treatment: gastroenterology, hepatology, & endoscopy. 3rd ed. New York, NY: McGraw-Hill; 2016. isbn:978-0-07-183772-9.

    Google Scholar 

  36. Khalili M, Burman B. Liver disease. In: Hammer GD, McPhee SJ, editors. Pathophysiology of disease: an introduction to clinical medicine. 7th ed. New York, NY: McGraw-Hill; 2013.

    Google Scholar 

  37. Hsieh TH, Liu CJ, Chen DS, Chen PJ. Natural course and treatment of hepatitis D virus infection. J Formos Med Assoc. 2006;105:869–81.

    Article  CAS  PubMed  Google Scholar 

  38. Menon KV, Gores GJ, Shah VH. Pathogenesis, diagnosis, and treatment of alcoholic liver disease. Mayo Clin Proc. 2001;76(10):1021–9.

    Article  CAS  PubMed  Google Scholar 

  39. Osna NA, Donohue TM Jr, Kharbanda KK. Alcoholic liver disease: pathogenesis and current management. Alcohol Res. 2017;38(2):147–61.

    PubMed  PubMed Central  Google Scholar 

  40. Fontana R, Hayashi P. Clinical features, diagnosis, and natural history of drug-induced liver injury. Seminars in liver disease. 2014;34(2):134–44.

    Article  PubMed  Google Scholar 

  41. Bynum TE, Boitnott JK, Maddrey WC. Ischemic hepatitis. Dig Dis Sci. 1979;24:129–35.

    Article  CAS  PubMed  Google Scholar 

  42. Fuchs S, Bogomolski-Yahalom V, Paltiel O, Ackerman Z. Ischemic hepatitis: clinical and laboratory observations of 34 patients. J Clin Gastroenterol. 1998;26:183–6.

    Article  CAS  PubMed  Google Scholar 

  43. Bernal W, Wendon J. Acute liver failure. N Engl J Med. 2013;369:2525–34.

    Article  CAS  PubMed  Google Scholar 

  44. Czaja AJ. Diagnosis and management of autoimmune hepatitis: current status and future directions. Gut Liver. 2016;10:177–203.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. Benedict M, Zhang X. Non-alcoholic fatty liver disease: an expanded review. World J Hepatol. 2017;9:715–32.

    Article  PubMed  PubMed Central  Google Scholar 

  46. Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology. 2011;54(1):328–43.

    Article  PubMed  Google Scholar 

  47. Crownover BK, Covey CJ. Hereditary hemochromatosis. Am Fam Physician. 2013;87:183–90.

    PubMed  Google Scholar 

  48. Stoller JK, Aboussouan LS. A review of alpha1-antitrypsin deficiency. Am J Respir Crit Care Med. 2012;185:246–59.

    Article  CAS  PubMed  Google Scholar 

  49. Roberts EA, Schilsky ML. A practice guideline on Wilson disease. Hepatology. 2003;37:1475–92.

    Article  PubMed  Google Scholar 

  50. Lindor KD, Gershwin ME, Poupon R, Kaplan M, Bergasa NV, Heathcote EJ. Primary biliary cirrhosis. Hepatology. 2009;50:291–308.

    Article  PubMed  Google Scholar 

  51. Kaplan MM, Gershwin ME. Primary biliary cirrhosis. N Engl J Med. 2005;353:1261–73.

    Article  CAS  PubMed  Google Scholar 

  52. Rudic JS, Poropat G, Krstic MN, Bjelakovic G, Gluud C. Ursodeoxycholic acid for primary biliary cirrhosis. Cochrane Database Syst Rev. 2012;12:CD000551.

    PubMed  Google Scholar 

  53. Lazaridis KN, LaRusso NF. Primary sclerosing cholangitis. N Engl J Med. 2016;375:1161–70.

    Article  PubMed  PubMed Central  Google Scholar 

  54. Karlsen TH, Folseraas T, Thorburn D, Vesterhus M. Primary sclerosing cholangitis—a comprehensive review. J Hepatol. 2017;67(6):1298–323.

    Article  PubMed  Google Scholar 

  55. Tsochatzis EA, Bosch J, Burroughs AK. Liver cirrhosis. Lancet. 2014;383:1749–61.

    Article  PubMed  Google Scholar 

  56. Schuppan D, Afdhal NH. Liver cirrhosis. Lancet. 2008;371:838–51.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  57. Procopet B, Berzigotti A. Diagnosis of cirrhosis and portal hypertension: imaging, non-invasive markers of fibrosis and liver biopsy. Gastroenterol Rep. 2017;5(2):79–89.

    Article  Google Scholar 

  58. Ge PS, Runyon BA. Treatment of patients with cirrhosis. N Engl J Med. 2016;375:767–77.

    Article  CAS  PubMed  Google Scholar 

  59. Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010;362(9):823–32.

    Article  CAS  PubMed  Google Scholar 

  60. Haq I, Tripathi D. Recent advances in the management of variceal bleeding. Gastroenterol Rep. 2017;5:113–26.

    Article  Google Scholar 

  61. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368(1):11–21.

    Article  CAS  PubMed  Google Scholar 

  62. Ferenci P. Hepatic encephalopathy. Gastroenterol Rep. 2017;5(2):138–47.

    Article  Google Scholar 

  63. Sharma BC, et al. A randomized, double-blind, controlled trial comparing rifaximin plus lactulose with lactulose alone in treatment of overt hepatic encephalopathy. Am J Gastroenterol. 2013;108(9):1458–63.

    Article  CAS  PubMed  Google Scholar 

  64. Porres-Aguilar M, Altamirano JT, Torre-Delgadillo A, Charlton MR, Duarte-Rojo A. Portopulmonary hypertension and hepatopulmonary syndrome: a clinician-oriented overview. Eur Respir Rev. 2012;21:223–33.

    Article  PubMed  Google Scholar 

  65. Dever JB, Sheikh MY. Review article: spontaneous bacterial peritonitis—bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther. 2015;41:1116–31.

    Article  CAS  PubMed  Google Scholar 

  66. Sort P, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341(6):403–9.

    Article  CAS  PubMed  Google Scholar 

  67. Ng CKF, Chan MHM, Tai MHL, Lam CWK. Hepatorenal syndrome. Clin Biochem Rev. 2007;28:11–7.

    PubMed  PubMed Central  Google Scholar 

  68. Ferenci P, et al. Hepatocellular carcinoma (HCC): a global perspective. J Clin Gastroenterol. 2010;44:239–45.

    Article  PubMed  Google Scholar 

  69. Forner A, Llovet JM, Bruix J. Hepatocellular carcinoma. Lancet. 2012;379:1245–55.

    Article  PubMed  Google Scholar 

  70. Tangkijvanich P, Anukulkarnkusol N, Suwangool P, et al. Clinical characteristics and prognosis of hepatocellular carcinoma. Analysis based in serum αfetoprotein levels. J Clin Gastroenterol. 2000;31(4):302–8.

    Article  CAS  PubMed  Google Scholar 

  71. Hanazaki K, Kajikawa S, Koide N, Adachi W, Amano J. Prognostic factors after hepatic resection for hepatocellular carcinoma with hepatitis C viral infection: univariate and multivariate analysis. Am J Gastroenterol. 2001 Apr;96(4):1243–50.

    Article  CAS  PubMed  Google Scholar 

  72. Heimbach J, Kulik LM, Finn R, et al. AASLD guidelines for the treatment of hepatocellular carcinoma. Hepatology. 2018;67(1):358–80.

    Article  PubMed  Google Scholar 

  73. Malinchoc M, Kamath PS, Gordon FD, Peine CJ, Rank J, ter Borg PC. A model to predict poor survival in patients undergoing transjugular intrahepatic portosystemic shunts. Hepatology. 2000;31:864–71.

    Article  CAS  PubMed  Google Scholar 

  74. Wiesner R, Edwards E, Freeman R, et al. Model for end-stage liver disease (MELD) and allocation of donor livers. Gastroenterology. 2003;124:91–6.

    Article  PubMed  Google Scholar 

  75. Cholongitas E, Marelli L, Shusang V, Senzolo M, Rolles K, Patch D, et al. A systematic review of the performance of the model for end-stage liver disease (MELD) in the setting of liver transplantation. Liver Transpl. 2006;12:1049–61.

    Article  PubMed  Google Scholar 

  76. Cholongitas E, Papatheodoridis GV, Vangeli M, Terreni N, Patch D, Burroughs AK. Systematic review: the model for end-stage liver disease–should it replace Child-Pugh’s classification for assessing prognosis in cirrhosis? Aliment Pharmacol Ther. 2005;22(11–12):1079–89.

    Article  CAS  PubMed  Google Scholar 

  77. Child CG, Turcotte JG. Surgery and portal hypertension. Major Probl Clin Surg. 1964;1:1–85.

    CAS  PubMed  Google Scholar 

  78. Durand F, Valla D. Assessment of prognosis of cirrhosis. Semin Liver Dis. 2008;28:110–22.

    Article  CAS  PubMed  Google Scholar 

  79. Weng Y, Cui Y, Fang J. Biological functions of cytokeratin 18 in cancer. Mol Cancer Res. 2012;10:485–93.

    Article  CAS  PubMed  Google Scholar 

  80. Maher MM, Ibrahim WA, Saleh SA, Shash L, Abou Gabal H, Tarif M, et al. Cytokeratin 18 as a non invasive marker in diagnosis of NASH and its usefulness in correlation with disease severity in Egyptian patients. Egypt J Med Hum Genet. 2015;16(1):41–6. https://doi.org/10.1016/j.ejmhg.2014.11.003.

    Article  Google Scholar 

  81. Feldstein AE, Wieckowska A, Lopez AR, Liu YC, Zein NN, McCullough AJ. Cytokeratin-18 fragment levels as noninvasive biomarker for nonalcoholic steatohepatitis: A multicenter validation study. Hepatology. 2009;50:1072–8.

    Article  CAS  PubMed  Google Scholar 

  82. Wang K, Zhang S, Marzolf B, Troisch P, Brightman A, Hu Z, Hood LE, Galas DJ. Circulating microRNAs, potential biomarkers for drug-induced liver injury. Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4402–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  83. Cortez MA, Bueso-Ramos C, Ferdin J, Lopez-Berestein G, Sood AK, Calin GA. MicroRNAs in body fluids—the mix of hormones and biomarkers. Nat Rev Clin Oncol. 2011;8(8):467–77.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  84. Loosen SH, Schueller F, Trautwein C, et al. Role of circulating microRNAs in liver diseases. World J Hepatol. 2017;9:586–94.

    Article  PubMed  PubMed Central  Google Scholar 

  85. El-Ahwany E, Nagy F, Zoheiry M, Shemis M, Nosseir M, Taleb HA, El Ghannam M, Atta R, Zada S. Circulating miRNAs as predictor markers for activation of hepatic stellate cells and progression of HCV-induced liver fibrosis. Electr Phys. 2016;8(1):1804–10.

    Article  Google Scholar 

  86. Wu X, Wu S, Tong L, Luan T, Lin L, Lu S, et al. MiR-122 affects the viability and apoptosis of hepatocellular carcinoma cells. Sci J Gastroenterol. 2009;44:1332–9.

    Article  CAS  Google Scholar 

  87. Sato K, Meng F, Glaser S, Alpini G. Exosomes in liver pathology. J Hepatol. 2016;65:213–21.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  88. Li T, Yan Y, Wang B, Qian H, Zhang X, Shen L, et al. Exosomes derived from human umbilical cord mesenchymal stem cells alleviate liver fibrosis. Stem Cells Dev. 2013;22:845–54.

    Article  CAS  PubMed  Google Scholar 

  89. Tan CY, Lai RC, Wong W, Dan YY, Lim SK, Ho HK. Mesenchymal stem cell-derived exosomes promote hepatic regeneration in drug-induced liver injury models. Stem Cell Res Ther. 2014;5:76.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Zain Moosvi .

Editor information

Editors and Affiliations

Self Study

Self Study

1.1 Questions

  1. 1.

    Which statement is true?

    1. (a)

      Bilirubin is exclusively synthesized in the liver.

    2. (b)

      Unconjugated hyperbilirubinemia will result in bilirubin in the urine.

    3. (c)

      Hyperbilirubinemia is caused by overproduction of bilirubin, impaired uptake, conjugation, or excretion, or leakage from hepatocytes or bile ducts.

    4. (d)

      Hyperbilirubinemia is always accompanied by elevated transaminases.

  2. 2.

    Which statement is true?

    1. (a)

      An AST/ALT ratio of less than 2 is consistent with alcoholic liver disease.

    2. (b)

      ALP elevation in the setting of normal GGT level is suggestive of liver disease.

    3. (c)

      An elevated INR is suggestive of increased liver synthetic function.

    4. (d)

      While elevated serum AFP levels are suggestive of HCC, they can also be elevated in other malignancies as well as hepatitis.

  3. 3.

    Which statement is true?

    1. (a)

      Hepatitis A is treated with antiviral therapy.

    2. (b)

      Hepatitis C is the most prevalent of all viral hepatitides worldwide.

    3. (c)

      All patients with chronic hepatitis B should receive antiviral therapy.

    4. (d)

      Sustained virologic response (SVR) is defined as undetectable hepatitis C virus RNA 6 months after the completion of antiviral therapy.

  4. 4.

    Which statement is true?

    1. (a)

      Pentoxifylline is first-line treatment of alcoholic hepatitis.

    2. (b)

      Hepatic steatosis is reversible with cessation of alcohol consumption.

    3. (c)

      Five-year transplant-free survival rate is not affected by the cessation of alcohol consumption.

    4. (d)

      Patients with alcoholic hepatitis are usually asymptomatic.

  5. 5.

    Which statement is true?

    1. (a)

      Drug-induced liver injury is most commonly caused by antibiotics.

    2. (b)

      A serum ALT to LDH ratio of greater than 1.5 is suggestive of ischemic hepatitis.

    3. (c)

      Serum transferrin levels are elevated in hereditary hemochromatosis.

    4. (d)

      Antibodies to liver/kidney microsomes are suggestive of primary sclerosing cholangitis.

  6. 6.

    Which statement is true?

    1. (a)

      The presence of antimitochondrial antibodies are suggestive of primary biliary cholangitis.

    2. (b)

      Wilson’s disease is characterized by low ceruloplasmin levels.

    3. (c)

      Primary biliary cholangitis is strongly associated with inflammatory bowel disease.

    4. (d)

      The malignancy that is most strongly associated with primary sclerosing cholangitis is hepatocellular carcinoma.

1.2 Answers

  1. 1.

    Which statement is true?

    1. (a)

      Bilirubin is made both in the bone marrow and in the liver. It is exclusively conjugated in the liver.

    2. (b)

      Conjugated hyperbilirubinemia will result in bilirubin in the urine. Unconjugated bilirubin is bound to albumin, and is not filtered by the glomerulus into the urine.

    3. (c)

      Correct: Hyperbilirubinemia can be caused by a variety of pathologies but all are related to overproduction, reduced excretion, impaired conjugation, or leakage.

    4. (d)

      Hyperbilirubinemia can be caused by a multitude of etiologies. Only liver disease such as cirrhosis will cause elevated transaminases as well.

  2. 2.

    Which statement is true?

    1. (a)

      An AST to ALT ratio greater than 2 is consistent with alcoholic liver disease. An AST to ALT ratio less than 2 is suggestive of NASH and Wilson’s disease.

    2. (b)

      GGT is found in hepatocytes, in addition to a myriad of other cells. ALP is found in liver, bone, and placenta. Therefore, an elevated ALP in the setting of an elevated, not normal GGT, is suggestive of liver disease.

    3. (c)

      INR is a marker for coagulation function. It is affected by coagulation factors, which are made in the liver. Therefore, reduced, not elevated synthetic function, would cause an elevated INR.

    4. (d)

      Correct: AFP is not specific to HCC. It can also be elevated in gastric cancer, germ-cell tumors, and non-germ cell tumors.

  3. 3.

    Which statement is true?

    1. (a)

      Hepatitis A is a self-remitting illness and therefore should be treated with supportive care only.

    2. (b)

      Hepatitis B, not hepatitis C, is the most common of the viral hepatitides worldwide.

    3. (c)

      Patients with chronic hepatitis B should only receive antiviral treatment if serum ALT is elevated and HBV DNA is less than 10,000 IU/mL.

    4. (d)

      Correct: Sustained virologic response is a term used to define successful antiviral treatment of hepatitis C and is based on HCV viral load.

  4. 4.

    Which statement is true?

    1. (a)

      Prednisone, not pentoxifylline, is first-line treatment for alcoholic hepatitis. Pentoxifylline should be used in the setting of infection, variceal hemorrhage, or acute kidney injury.

    2. (b)

      Correct: Hepatic steatosis, the first stage of alcohol-induced liver disease, is reversible with cessation of alcohol consumption, as no fibrosis has occurred at this point.

    3. (c)

      Five-year transplant-free survival rate is doubled from 30% to 60% if patients cease alcohol consumption.

    4. (d)

      Patients with alcoholic hepatitis usually present with anorexia, jaundice, hepatomegaly, and abdominal pain. Patients with hepatic steatosis are usually asymptomatic.

  5. 5.

    Which statement is true?

    1. (a)

      Drug-induced liver injury is most commonly caused by acetaminophen, not antibiotics.

    2. (b)

      A serum ALT to LDH ratio of less than, not greater than 1.5 is suggestive of ischemic hepatitis.

    3. (c)

      Correct: Serum transferrin levels are the best initial screening test for hereditary hemochromatosis. Transferrin saturation values greater than 45% in men and 35% in premenopausal women necessitate further workup.

    4. (d)

      Antibodies to liver/kidney microsomes are suggestive of primary biliary cirrhosis, not primary sclerosing cholangitis.

  6. 6.

    Which statement is true?

    1. (a)

      Correct: Antimitochondrial antibodies are present in between 90% and 95% of patients with PBC.

    2. (b)

      Serum ceruloplasmin can be elevated or normal in Wilson’s disease. Serum copper levels will be low.

    3. (c)

      Primary sclerosing cholangitis, not primary biliary cholangitis, is strongly associated with inflammatory bowel disease.

    4. (d)

      The malignancy that is most strongly associated with primary sclerosing cholangitis is cholangiocarcinoma, not hepatocellular carcinoma.

Rights and permissions

Reprints and permissions

Copyright information

© 2020 Springer Nature Switzerland AG

About this chapter

Check for updates. Verify currency and authenticity via CrossMark

Cite this chapter

Moosvi, Z., Lui, F.H., Nguyen, D. (2020). Assessment of Liver Function. In: Radu-Ionita, F., Pyrsopoulos, N., Jinga, M., Tintoiu, I., Sun, Z., Bontas, E. (eds) Liver Diseases. Springer, Cham. https://doi.org/10.1007/978-3-030-24432-3_35

Download citation

  • DOI: https://doi.org/10.1007/978-3-030-24432-3_35

  • Published:

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-030-24431-6

  • Online ISBN: 978-3-030-24432-3

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics