What are the definitions of interface hepatitis and bridging necrosis?

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Definitions of Interface Hepatitis and Bridging Necrosis

Interface Hepatitis

Interface hepatitis is the histological hallmark of autoimmune hepatitis, characterized by disruption of the limiting plate with portal inflammatory infiltrates extending into the hepatic lobule, destroying periportal hepatocytes. 1

Structural Features

  • The portal tract becomes expanded by mononuclear inflammatory infiltrates 1
  • The limiting plate (the boundary between portal tract and hepatic parenchyma) is disrupted 1
  • Inflammatory cells extend from the portal area into the hepatic acinus/lobule 1
  • Portal lymphocytic or lymphoplasmacytic cells infiltrate beyond the portal-parenchymal interface 1

Cellular Composition

  • Dense plasma cell-rich lymphoplasmocytic infiltrates are typical, though plasma cells are abundant in only 66% of cases 1
  • The paucity of plasma cells (occurring in 34% of cases) does not preclude the diagnosis 1
  • CD3+, CD4+, and CD8+ T cells infiltrate both the interface and hepatic lobules 2

Mechanism and Alternative Terminology

  • The process involves lymphocyte-hepatocyte binding followed by gradual endocytosis of hepatocyte cellular components by lymphocytes 3
  • This results in progressive "nibbling away" of hepatocyte cytoplasm, leading to gradual hepatocyte disappearance 3
  • Previously termed "piecemeal necrosis," though this terminology has been replaced by "interface hepatitis" 3

Clinical Context and Specificity

  • Interface hepatitis is not disease-specific and can occur in viral hepatitis, drug-induced liver injury, and other immune-mediated liver diseases 1
  • When present with >50% of portal tract circumference involvement and accompanied by plasma cell infiltration, emperipolesis, and rosettes, it becomes highly suggestive of autoimmune hepatitis 1

Bridging Necrosis

Bridging necrosis represents severe inflammatory activity characterized by confluent hepatocyte necrosis that connects (bridges) adjacent portal tracts, central veins, or portal tracts to central veins, indicating advanced hepatic injury. 1

Prognostic Significance

  • Bridging necrosis or multiacinar necrosis on histologic examination progresses to cirrhosis in 82% of patients within 5 years, with 45% mortality 1
  • Cirrhosis develops in 40% of adults with multilobular necrosis or bridging necrosis 1
  • This histological finding is a critical determinant of disease severity and treatment urgency 1

Relationship to Disease Spectrum

  • Bridging necrosis is part of the histological spectrum of autoimmune hepatitis but occurs less commonly than interface hepatitis 1
  • It represents panlobular hepatitis with parenchymal collapse, particularly in acute disease presentations 1
  • Along with massive necrosis, it indicates severe inflammatory activity requiring immediate therapeutic intervention 1

Clinical Implications

  • Patients with bridging necrosis require immediate treatment initiation, as untreated disease carries 45% mortality within 5 years 1
  • The presence of bridging necrosis should prompt aggressive immunosuppressive therapy regardless of autoantibody titers or other serological markers 1
  • Sequential biopsies may show transition from pericentral hepatitis to interface hepatitis, suggesting bridging necrosis may represent an early severe manifestation 1

Common Pitfall

Do not confuse bridging necrosis with bridging fibrosis—bridging necrosis is active inflammatory destruction of hepatocytes spanning anatomical zones, while bridging fibrosis represents established scar tissue connecting portal-portal or portal-central areas, indicating chronic injury and advanced fibrosis stage 1.

References

1
Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

3
Research

"Piecemeal" necrosis: renamed troxis necrosis.

Experimental and molecular pathology, 2001

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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