Hepatitis

Hepatitis encompasses liver inflammation from multiple etiologies requiring systematic diagnostic differentiation. Viral hepatitis (A-E) must be distinguished from alcoholic hepatitis (AST:ALT ratio >2:1, typically with AST <300, GGT elevation), drug-induced liver injury (DILI — acetaminophen is the most common cause of acute liver failure in developed countries; N-acetylcysteine is the antidote), autoimmune hepatitis (positive ANA, anti-smooth muscle antibody, elevated IgG; treated with corticosteroids and azathioprine), and non-alcoholic steatohepatitis (NASH — associated with metabolic syndrome; diagnosed by liver biopsy showing steatosis, inflammation, and ballooning degeneration; managed with weight loss, exercise, and pioglitazone or vitamin E in select patients). The liver injury pattern guides workup: hepatocellular pattern (ALT/AST predominant elevation, R ratio >5) suggests viral hepatitis, DILI, autoimmune hepatitis, ischemic hepatitis, or Wilson disease; cholestatic pattern (ALP/GGT predominant elevation, R ratio <2) suggests biliary obstruction, primary biliary cholangitis (PBC — anti-mitochondrial antibody positive), primary sclerosing cholangitis (PSC — associated with ulcerative colitis, MRCP shows beading of bile ducts), or drug-induced cholestasis. The clinician evaluates acute versus chronic hepatitis, determines etiology through targeted serologic, autoimmune, metabolic (ceruloplasmin for Wilson, ferritin/transferrin saturation for hemochromatosis),...