Adalimumab Could Suppress the Activity of Non Alcoholic Steatohepatitis (NASH)

Zusammenfassung

Die Prävalenz der nicht alkoholischen Steatohepatitis (NASH) nimmt zu. Derzeit steht keine medikamentöse Therapie der NASH zur Verfügung. Bei der Progression der Fettleber zur NASH scheint das Zytokin TNF-α eine wichtige Rolle zu spielen, indem es nicht nur proinflammatorisch und proapoptotisch wirkt, sondern auch die Insulinresistenz begünstigt. TNF-α könnte daher ein therapeutisches Ziel bei Patienten mit NASH darstellen. Eine anti-TNF-α-Therapie wurde jedoch bisher in der Therapie der NASH nicht evaluiert. Wir berichten hier über eine Patientin, die bei histologisch gesicherter NASH eine anhaltende Normalisierung der Leberwerte unter Therapie mit dem humanisierten anti-TNF-α-Antikörper Adalimumab zeigte. Pilotstudien sollten daher den möglichen Nutzen einer Therapie der NASH mit Adalimumab untersuchen.

Abstract

The prevalence of non-alcoholic steatohepatitis (NASH) is increasing. NASH confers an increased risk of liver-related morbidity and mortality with a substantial risk of developing liver cirrhosis. At present, there is no established medical treatment for NASH. The pathogenesis of NASH is incompletely understood. Several lines of evidence suggest that TNF-α may be involved in the pathogenesis of NASH by promoting liver inflammation, insulin resistance and hepatocyte apoptosis. Anti-TNF-α therapy has not been evaluated for the treatment of NASH. We report here on a patient with NASH who has experienced rapid normalization of liver biochemistry during treatment of an associated rheumatoid arthritis with the humanized anti-TNF-α antibody adalimumab. This observation suggests that pilot studies may be warranted to evaluate the role of adalimumab for the treatment of NASH.

Schlüsselwörter

Leber - TNF-α - NASH

Key words

liver - TNF-α - NASH

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