TABLE 5.
Paradigm used for clinicopathologic evaluation of liver biopsies from long-term survivors
| Portal tract findings | Lobular findings | Vascular findings | Liver injury tests |
Clinical history | |
|---|---|---|---|---|---|
| Acute rejection | Mixed inflammation, more than an occasional damaged bile duct, “moth-eaten” limiting plate | Kupffer cell hypertrophy, mild sinusoidal lymphocytosis, minimal to no lobular disarray ± cholestasis | Perivenular inflammation, central dropout/congestion ± subendothelial inflammation | ↑ ALT/AST ↑ γGTP/ALP ↑→ TB |
Inadequate immunosuppression |
| Chronic rejection | Minimal/mild inflammation, chronic bile duct changes (see text), bile duct loss, “hyalinization” of connective tissue | Spotty necrosis, cholestasis, foam cell clusters; central hepatocyte ballooning/dropout | Foam cell obliterative arteriopathya, perivenular sclerosis, sinusoidal foam cell clusters | ↑ ↑ γGTP/ALP ↑ AST/ALT ↑→TB (early) ↑ ↑ TB (late) |
Inadequate immunosuppression, chronic rejection in previous graft, acute rejection unresponsive to treatment, positive crossmatch |
| Obstructive cholangiopathy | Intraepithelial neutrophilic/eosinophilic inflammation, periductal edema, duct/cholangiolar proliferation ± fibrosis | Sinusoidal neutrophil clusters ± cholestasis | None | ↑ ↑ γGTP/ALP →↑ AST/ALT ↑→TB |
“Difficult” biliary anastomosis, hepatic artery stenosis/thrombosis original disease; PSC |
| Viral hepatitis | Mononuclear/mixed inflammation piecemeal necrosis, cholangiolar proliferation, nodular lymphoid aggregates, only occasional damaged bile duct | Spotty necrosis, disarray, swelling: steatosis (periportal/midzonal): mononuclear inflammation/Kupffer’s cell hypertrophy | None | ↑ ↑ ALT/AST →→ γGTP/ALP ↑ ↑ γGTP/ALP in cholestatic form |
Original disease; HCV, HBV, cryptogenic, autoimmune cirrhosis; positive HCV, HBV serologic/PCR tests; biochemical response to α-interferon therapy |
| Alcohol abuseb | ± Mononuclear/mixed inflammation | Mixed steatosis (central predominant), “acute foamy degeneration” of hepatocytes, + Kupffer’s cells iron deposition | Perivenular sclerosis, sinusoidal fibrosis | ↑ γGTP, → ALP ↑→ AST/ALT ↑→ TB |
Original disease: alcohol abuse; imporved liver injury test on hospitalization w/o intervention: positive blood alcohol test; R/O other causes of steatohepatitis |
| Primary biliary cirrhosis (15,22,29) | Mononuclear inflammation, noncaseating granulomas, bile duct damage/loss, cholangiolar proliferation | Kupffer’s cell hypertrophy/granuloma, mild inflammation, periportal copper deposition (late) | +/− Focal arterial thickening | ↑ γGTP/ALP ↑→ ALT/AST → TB |
Original disease: PBC R/O other causes of granulomas |
ALT, alanine aminotransferase; AST, aspartate aminotransferase; ALP, alkaline phosphatase; γ-GTP, gamma glutamyl transpeptidase; TB, total bilirubin; PSC, primary sclerosing cholangitis; PBC, primary biliary cirrhosis; HCV, hepatitis C virus; HBV, hepatitis B virus; PCR, polymerase chain reaction; R/O, rule out.
a
Uncommonly detected in needle biopsies.
b
Other causes of nonalcoholic steatohepatitis, if present, should be excluded.