A new approach to drug therapy in non-alcoholic steatohepatitis (NASH)

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23 Citations (Scopus)

Abstract

Liver steatosis is a common human disease, most often caused by long-term alcohol consumption. Non-alcoholic steatohepatitis (NASH) is characterized by similar histopathological features to those observed in alcoholic liver disease, but occurs in the absence of significant alcohol consumption. Several aetiological factors contribute to NASH: obesity, type 2 diabetes mellitus, hyperlipidaemia, pregnancy, different chemical intoxications, parenteral nutrition, jejeuno-ileal bypass, chronic inflammatory bowel disease, nutritional protein deficiency and congenital metabolic disorders. Biochemically, oxidative stress and lipid peroxidation and their ensuing damage are implicated in the pathogenesis of NASH and alcoholic steatohepatitis (probably resulting from free fatty acids in the mitochondria, and induction of the cytochrome P450 isoform CYP2E1 in hepatocytes and Kupffer's cells). This paper deals with the pathomechanisms, clinical findings and currently available therapies for NASH. The potential use of metadoxine in the treatment of NASH is also discussed.

Original languageEnglish
Pages (from-to)537-551
Number of pages15
JournalJournal of International Medical Research
Volume31
Issue number6
Publication statusPublished - Nov 2003

Fingerprint

Drug therapy
Fatty Liver
Drug Therapy
Liver
Alcohols
Cytochrome P-450 CYP2E1
Mitochondria
Oxidative stress
Nutrition
Medical problems
Nonesterified Fatty Acids
Alcohol Drinking
Cytochrome P-450 Enzyme System
Protein Isoforms
Alcoholic Fatty Liver
Lipids
Protein Deficiency
Congenital, Hereditary, and Neonatal Diseases and Abnormalities
Alcoholic Liver Diseases
Kupffer Cells

Keywords

  • Metadoxine
  • Non-alcoholic steatohepatitis
  • Pathogenesis
  • Pathology
  • Therapy

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A new approach to drug therapy in non-alcoholic steatohepatitis (NASH). / Fehér, J.; Lengyel, G.

In: Journal of International Medical Research, Vol. 31, No. 6, 11.2003, p. 537-551.

Research output: Contribution to journalArticle

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