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ASGE Annual GI Advanced Practice Provider Course ( ...
Decoding Abnormal LFTs: Interpretation and Action
Decoding Abnormal LFTs: Interpretation and Action
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This presentation reviews how to interpret abnormal “liver function tests” and what actions to take. It emphasizes that “liver tests” are broader than a single concept and that the term “LFTs” is often misused: AST and ALT primarily indicate hepatocellular injury (not function), while true synthetic function is reflected by albumin and PT/INR. Bilirubin is not an enzyme, but can reflect impaired hepatic uptake/conjugation/transport and often rises later in cholestasis. Cholestatic enzymes include alkaline phosphatase (ALP), GGT, and 5’-nucleotidase; ALP is not liver-specific and can rise in any cholestatic process, with GGT or 5’-nucleotidase helping confirm a hepatic source.<br /><br />The talk organizes liver test abnormalities into patterns. A hepatocellular pattern features AST/ALT elevations out of proportion to ALP, suggesting hepatitis or toxic/ischemic injury. A cholestatic pattern features ALP elevation out of proportion to AST/ALT, with bilirubin typically increasing later; early AST/ALT rises can occur with biliary obstruction. Additional recognizable scenarios include ultra-high aminotransferases in ischemic hepatopathy (“shock liver”), very high values in acute hepatitis, and acute liver failure when high aminotransferases are accompanied by elevated INR and encephalopathy. An AST:ALT ratio around 2:1 in the right context suggests alcohol-associated liver injury.<br /><br />Workup should begin with history and physical exam to assess acuity, symptoms (pain, pruritus, dark urine, weight loss, bruising, confusion), pregnancy status, medications/toxins (including acetaminophen), alcohol and drug use, viral risk/travel, comorbidities (e.g., diabetes, autoimmune disease), and exam signs (jaundice, ascites/portal hypertension, RUQ tenderness). Testing is then pattern-directed: hepatocellular injury prompts viral serologies, toxicology/acetaminophen levels, autoimmune and metabolic studies, and ultrasound with Dopplers; cholestasis prompts ultrasound to assess obstruction, followed by MRI/MRCP and possible ERCP. Cases illustrate classic management: supportive care for ischemic hepatopathy, antibiotics plus urgent biliary evaluation for suspected cholangitis, and emergent acetaminophen toxicity management with N-acetylcysteine and ICU/liver-unit care.
Asset Subtitle
John A. Martin, MD, FASGE
Keywords
abnormal liver function tests interpretation
AST ALT hepatocellular injury pattern
albumin PT INR synthetic liver function
bilirubin conjugation transport cholestasis
alkaline phosphatase GGT 5-nucleotidase
cholestatic liver enzyme pattern workup
ischemic hepatopathy shock liver ultra-high aminotransferases
acute hepatitis very high transaminases
acute liver failure elevated INR encephalopathy
acetaminophen toxicity N-acetylcysteine management
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