[Non-alcoholic steatohepatitis : pathology and pathogenesis]

Nihon Rinsho. 2006 Jun;64(6):1107-13.
[Article in Japanese]

Abstract

Nonalcoholic steatohepatitis (NASH) has become to be widely recognized as a significant cause of chronic liver injuries. Evidences suggest that development of NASH requires a double "hit". The "first hit" involves the accumulation of fat in the liver, and the "second hit" includes oxidative stress, cytokines, stellate cell activation, and fibrogenesis. Microscopically, some alcoholic hepatitis-like findings, hepatocellular steatosis, ballooning degeneration, Mallory body, acute and chronic lobular inflammation, and zone 3 perisinusoidal fibrosis are noted. Because ballooning degeneration and Mallory body denote progressive NASH, we should identify clearly these findings. The diagnosis of nonalcoholic steatohepatitis requires histopathologic evaluation, because the lesions of parenchymal injury and fibrosis cannot be detected by imaging studies or laboratory tests.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Antibodies
  • Cytokines / physiology
  • Fatty Liver / diagnosis
  • Fatty Liver / pathology*
  • Fatty Liver / physiopathology*
  • Fibrosis
  • Humans
  • Immunohistochemistry
  • Lipid Metabolism
  • Liver / metabolism
  • Liver / pathology*
  • Necrosis
  • Oxidative Stress
  • Proteins / immunology
  • Sequestosome-1 Protein
  • Ubiquitin / immunology

Substances

  • Adaptor Proteins, Signal Transducing
  • Antibodies
  • Cytokines
  • Proteins
  • SQSTM1 protein, human
  • Sequestosome-1 Protein
  • Ubiquitin