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Approach to Elevated LFTs PowerPoint Presentation

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Description : Check out this medical presentation on Alanine Aminotransferase (alanine transaminase), which is titled "Approach to Elevated LFT’s", to know about the interpretation of abnormal liver enzymes, and an approach to managing elevated liver enzymes.

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Approach to Elevated LFT’s Miguel H. Malespin M.D. Assistant Professor, Department of Medicine Medical Director, Hepatology Department of Medicine, Division of Gastroenterology and Hepatology
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Disclosures Consultant for Gilead Pharmaceuticals
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Learning Objectives Describe the prevalence of liver disease within the United States Review interpretation of abnormal liver enzymes Develop an approach to managing elevated liver enzymes
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Critical Role of Primary Care Elevated liver transaminase levels are found in up to 8.9% of patients seen in primary care clinics 1,2 Approximately 9% of patients with elevated liver enzymes are asymptomatic 3,4
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Why is identification of patients with abnormal liver enzymes important?
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Peak of the Hepatitis C Epidemic Prevalence of HCV within the United States is ~1.6% 5 Making it the most common bloodborne pathogen in the United States Estimated 4 and 7 million persons 6,7
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Rising Prevalence of Elevated Liver Enzymes Nearly ½ of persons with chronic HCV are unidentified Normal liver enzymes are found in 25–30% of chronic HCV carriers 8 Institution of screening for baby boomers born between 1945-1965
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Currently at the peak of the HCV epidemic2
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Hepatitis C surpassed HIV as a cause of virus-related death in 2006
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Incidence of Hepatitis C8 http://www.cdc.gov/hepatitis/statistics/
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Second Culprit on the Loose…
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Insulin Resistance
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Diabetes is an important risk factor for progression of fibrosis11,12
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Obesity Epidemic Coincides with the rise in NAFLD
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Rising Prevalence of NAFLD10
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Epidemiology Related to Cirrhosis Prevalence of cirrhosis in the United States is estimated to be ~0.27 percent of the population 633,323 Adults 13 Nearly 2 million deaths annually are attributable to CLD and cirrhosis 14 12th leading cause of death
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Epidemiology of Cirrhosis Total number of persons with cirrhosis is estimated to peak at 1 million in 202015 Rates of hepatic decompensation and hepatocellular carcinoma are expected to increase for another 10 to 13 years15
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Over time, there has been an increase in mortality from liver disease2
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Normal transaminases do not exclude the presence of chronic liver disease Fluctuation in transaminase levels occur Particularly in patients with chronic HBV, HCV, and NASH “Burned out cirrhosis” Poor sensitivity/specificity 19,877 asymptomatic US Airforce basic trainees, 99 were found to have abnormal ALT elevation, 12 were positive for liver disease 16
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What are LFT’s? Serologic measurements ordered to evaluate for liver disease The term liver function tests are actually a misnomer Serum aminotransferases (ALT/AST) reflect inflammation Alkaline Phosphatase (AP) reflects biliary injury Bilirubin, albumin, and PT/INR more accurately reflect hepatic function
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Why are LFT’s ordered? Routine check-up Drug monitoring Symptoms Screen for liver disease
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General Approach What is the liver trying to tell me? Does this appear to be acute or chronic? If chronic, do findings exist that are concerning for advanced fibrosis/cirrhosis
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Elevated Aminotransferases Good indicators of hepatocellular injury Serum glutamic oxaloacetic transaminase (SGOT) AST is located in the cytosol and mitochondria Also present in striated muscle, the kidney, brain, pancreas, lung, leukocytes, and erythrocytes Serum glutamic pyruvic transaminases (SGPT) ALT lies in the cytosol More specific indicator of liver injury
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Normal Values AST <37 IU/L or ALT <40 IU/L for men AST or ALT <31 IU/L for women
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Elevated Aminotranferases Elevated aminotransferase levels are present in 7.9% of the population when sampling asymptomatic individuals 17 Some of the most common identifiable causes include: 18 alcohol use (13.5%) hepatitis C (7.0%) hemochromatosis (3.4%) hepatitis B (0.9%) combination of causes (6.1%)
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Table 1. Causes of elevated aminotransferases. a Aminotransferase level increase of 5-10 x upper limit of normal b Aminotransferase level increase of >10 x upper limit of normal cBilirubin increase of <5 x upper reference limit
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Clinical Case #1 45 year old male with a history of alcohol abuse and chronic back pain for which he takes 3 Norco tablets a day presents with jaundice, nausea, malaise and abdominal pain. Total bilirubin 3.5 ALT 5344 Direct bilirubin 2.7 AST 3923 Alkaline phosphatase 240 INR 1.3
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Clinical Case #1 RUQ US: normal liver contour Acetaminophen level: <1 ANA: Normal ASMA: Normal Hepatitis B surface antigen Positive Hepatitis B core IgM Positive
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Clinical Case #2 63 year old female with a history of obesity, hypertension, diabetes who presents for evaluation of elevated liver enzymes. ALT 64 Platelet Count 110 AST 53 INR 1.1 AP 90 TB 1.0 Physical Exam: Evidence of spider angiomas and palmar erythema
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Ultrasound splenomegaly, steatosis ANA normal ASMA normal Ferritin 500 Iron/TIBC 24 A1AT Normal HBsAg Negative Hepatitis C antibody positive Clinical Case #2
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General Approach Obtain baseline right upper quadrant ultrasound to evaluate for liver lesions, hepatic morphology, thrombus, splenomegaly Obtain baseline labs to evaluate for acute/chronic liver disease Referral to GI/Hepatology
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Alkaline Phosphatase/Gamma-glutamyl Transferase (GGT) ALP Produced predominantly in the liver and bone Can be found in renal, intestinal, placental tissue, or within leukocytes GGT/ALP Fractionation It has a high sensitivity for hepatobiliary disease Elevated GGT levels also occur in alcohol-related liver disease Most useful when elevated alkaline phosphatase levels occur with otherwise normal liver enzymes and bilirubin levels
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Clinical Case #3 45 year old female presents for evaluation of elevated liver enzymes. She denies abdominal pain. ALT 45 AST 39 ALP 650 TB .9 INR .8
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Clinical Case #3 Denies medication or recent antibiotic use Denies alcohol use RUQ US negative Hep b sAg negative HCV Ab negative ANA/ASMA negative AMA positive
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Real LFT’s Bilirubin PT/INR Albumin
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Bilirubin Metabolism
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Clinical Case #4 33 year old female with a BMI 32 presents to clinic for evaluation of jaundice and right upper quadrant pain. ALT 55 AST 49 AP 233 TB 3.5
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Clinical Case #4 RUQ US Dilated common bile duct to 20 mm, gallstones without evidence of cholecystitis
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Albumin Exclusively made by in the liver and accounts for 75% of the plasma colloid pressure. In chronic liver disease, hepatic synthesis of albumin is impaired Not specific to liver diseases
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Prothrombin Time Measurement of the rate at which prothrombin is converted to thrombin The extrinsic pathway depends on the activity of clotting factors II, V, VII, and X—all of which are synthesized in the liver Therefore, prothrombin time is a reflection of liver dysfunction In chronic liver diseases, prolonged prothrombin time is a sign of advanced liver disease In acute liver diseases, it is a more reliable indicator of immediate synthetic function given it’s shorter half life
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Conclusion Stable elevated liver enzymes DO NOT exist We are currently at the peak of HCV prevalence and there is a concomitant rise in the prevalence of NASH Screen patients born between 1945-1965 Cirrhosis is the greatest risk factor for hepatocellular carcinoma and hepatic decompensation
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Conclusion Interpretation of laboratory values in patients with abnormalities in liver panel testing is critical to developing a differential diagnosis and initiation an adequate work-up The initial step is determination of an acute, chronic, or acute-on-chronic process
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Conclusion Acquisition of histology can be used to confirm a suspected diagnosis, rule out hepatic disease, and stage the degree of fibrosis Upon establishment of chronicity, the role of the practitioner is to establish the severity of hepatic dysfunction, potential for reversibility, and the need for escalation of care
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References 1. Younossi ZM, Stepanova M, Afendy M, et al. Changes in the prevalence of the most common causes of chronic liver diseases in the United States from 1988 to 2008. Clin Gastroenterol Hepatol. 2011 Jun;9(6):524-530. 2. Udompap P, Kim D, Kim WR. Current and Future Burden of Chronic Nonmalignant Liver Disease. Clin Gastroenterol Hepatol. 2015 Nov;13(12):2031-41. Epub 2015 Aug 17. 3. Hultcrantz R, Glaumann H, Lindberg G, Nilsson LH. Liver investigation in 149 asymptomatic patients with moderately elevated activities of serum aminotransferases. Scand J Gastroenterol 1986; 21:109–113. 4. Ioanou GN, Boyko EJ, Lee SP. The prevalence and predictors of elevated serum aminotransferase activity in the United States in 1999-2002. Am J Gastroenterol 2006; 101:76–82. 5. Chou R et al. Agency for Healthcare Research and Quality; 2012. 6. Chak E et al. Liver Int. 2011 Sep;31(8):1090-101. 7. Lavanchy D. Liver Int. 2009 Jan;29 Suppl 1:74-81. 8. Puoti C, Castellacci R, Montagnese F et al. Histological and virological features and follow-up of hepatitis C virus carriers with normal aminotransferase levels: the Italian prospective study of the asymptomatic C carriers (ISACC). J Hepatol 2002; 37: 117–123. 9. Ly KN et al. Ann Intern Med. 2012;156:271-8. 10. Lazo M, Hernaez R, Eberhardt MS, et al. Prevalence of nonalcoholic fatty liver disease in the United States: the Third National Health and Nutrition Examination Survey, 1988-1994. Am J Epidemiol. 2013 Jul 1;178(1):38-45. 11. L.A. Adams, S. Sanderson, K.D. Lindor, P. Angulo. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. J Hepatol, 42 (2005), pp. 132–138. 12. McPherson S, Hardy T, Henderson E, et al. Evidence of NAFLD progression from steatosis to fibrosing-steatohepatitis using paired biopsies: implications for prognosis and clinical management. J Hepatol. 2015 May;62(5):1148-55. 13. Heron M. Natl Vital Stat Rep.2012;61:1–96. 14. Scaglione S et al. J Clin Gastroenterol. 2014 Oct 8. 15. Chou R et al. Agency for Healthcare Research and Quality; 2012. 16. Kundrotas LW; Clement DJ. Serum alanine aminotransferase (ALT) elevation in asymptomatic US Air Force basic trainee blood donors. Dig Dis Sci 1993; 38:2145-2150 17. Clark JM, Brancati FL, Diehl AM. The prevalence and etiology of elevated aminotransferase levels in the United States. Am J Gastroenterol. 2003 May;98(5):960–7. 18. Liangpunsakul S, Chalasani N. Unexplained Elevations in Alanine Aminotransferase in Individuals with the Metabolic Syndrome: Results from the Third National Health and Nutrition Survey (NHANES III). The American Journal of the Medical Sciences [Internet]. 2005;329(3).
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