Clinical meaning
Liver function tests (LFTs) reflect distinct hepatic processes, and pattern recognition guides differential diagnosis. Aminotransferases (AST and ALT) are released from hepatocytes during cell injury or necrosis: ALT is predominantly cytoplasmic and liver-specific, while AST exists in both cytoplasmic and mitochondrial fractions and is found in liver, skeletal muscle, heart, and red blood cells. The AST:ALT ratio carries diagnostic significance — a ratio >2:1 is characteristic of alcoholic liver disease because alcohol-induced mitochondrial injury preferentially releases mitochondrial AST, and alcohol also depletes pyridoxal phosphate (vitamin B6), the cofactor required for ALT synthesis. Alkaline phosphatase (ALP) is concentrated on the canalicular membrane of hepatocytes and in bile duct epithelium; elevation indicates cholestatic injury (impaired bile flow), but ALP also originates from bone, placenta, and intestine. Gamma-glutamyl transferase (GGT) is co-elevated with ALP in hepatobiliary disease but NOT in bone disease, making it the confirmatory test for hepatobiliary origin of elevated ALP. The R-factor ([ALT/ULN] / [ALP/ULN]) rapidly classifies injury patterns: R >5 indicates hepatocellular injury, R <2 indicates cholestatic injury, and R 2-5 indicates mixed pattern. Synthetic function is assessed by albumin (half-life 21 days, reflecting chronic hepatic capacity) and INR/prothrombin time (factor VII half-life 6 hours, the most sensitive early marker of acute hepatic failure because it declines first). Bilirubin metabolism involves hepatocyte uptake of unconjugated (indirect) bilirubin, conjugation with glucuronic acid by UDP-glucuronosyltransferase, and excretion into bile canaliculi — defects at each step produce distinct patterns of hyperbilirubinemia.