Post-transplant liver biopsies: a concise and practical approach for beginners

Abstract

Exposure to post-transplant liver biopsies varies among pathology residencies and largely depends on the institution's training program, particularly if the hospital has a liver transplant program. The interpretation of biopsies from transplanted livers presents its own set of challenges, even for those with a solid understanding of non-transplant medical liver biopsies. In this review, we aim to provide a succinct, step-by-step approach to help you interpret liver transplant biopsies. This article may be beneficial for residents interested in liver pathology, gastrointestinal and liver pathology fellows in the early stages of training, clinical gastroenterology and hepatology fellows, hepatologists and general pathologists who are curious about this niche.

Keywords: Graft rejection; Hepatitis, viral, human; Liver transplantation.

Fig. 1.

(A) Autoimmune hepatitis: plasma cell-rich infiltrate with periportal apoptotic hepatocytes (arrows). (B) Primary biliary cholangitis: lymphocyte-rich infiltrate with poorly formed granuloma (arrow). (C, D) Primary sclerosing cholangitis: concentric periductal fibrosis (arrow) (D, Trichrome).

Fig. 2.

(A) Steatohepatitis: macrovesicular steatosis with ballooned hepatocytes (black arrows) and Mallory-Denk bodies (red arrow). (B) Alpha-1 antitrypsin deficiency: intrahepatocytic alpha-1 antitrypsin globules (arrow) (periodic acid–Schiff–diastase). (C) Hemochromatosis: intrahepatocytic iron accumulation (arrow) (Perl’s stain). (D) Wilson’s disease: intrahepatocytic copper accumulation (arrow) (Rhodanine stain).

Fig. 3.

(A) Hepatitis B virus hepatitis: ground glass hepatocytic inclusion (arrows). (B) Hepatitis C virus hepatitis: lymphoid follicle formation in the portal tract (arrow).

Fig. 4.

(A) Acute cellular rejection: endothelitis (arrows). (B) Plasma cell-rich rejection: centrilobular plasma cell-rich inflammatory infiltrate (arrow) (Courtesy of Maria Isabel Fiel MD). (C) Chronic rejection with foam cell arteriopathy: foam cell accumulation in the arterial wall (arrows) (Courtesy of Maria Isabel Fiel MD). (D) Chronic ductopenic rejection: absence of native bile duct in a portal tract.

Fig. 5.

(A, B) Antibody-mediated rejection: C4d deposition in a hepatic arteriole (B, C4d immunostain).

Fig. 6.

(A) Hepatic artery thrombosis: centrilobular (black arrow) and periportal coagulative necrosis (red arrow). (B) Hepatic vein thrombosis: centrilobular congestion and necrosis (arrow). (C) Portal vein thrombosis: dystrophic (dilated) portal vein (arrow).

Fig. 7.

(A) Bile duct obstruction: portal edema neutrophils and bile ductular reaction (arrow). (B) Reperfusion injury: centrilobular cholestasis and hepatocyte ballooning (arrows).

Fig. 8.

(A) Herpes simplex virus hepatitis: nuclear inclusion (arrow) (Courtesy of Hwa Jeong Lee, MD). (B) Cytomegalovirus: neutrophilic microabscess (arrows). (C) Epstein-Barr virus hepatitis: sinusoidal mildly atypical lymphocytic infiltrate (arrows).

Fig. 9.

(A) Drug-induced liver injury: pseudo-ground-glass inclusion secondary to polypharmacy (arrows).