Diagnosis and Management of Autoimmune Hepatitis

Hepatology (Impact Factor: 11.19). 06/2010; 51(6):2193 - 2213. DOI: 10.1002/hep.23584
Source: PubMed


Available from: James D Gorham, May 30, 2015
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    ABSTRACT: Autoimmune hepatitis (AIH) is a chronic liver disease of unknown etiology. It is composed of immune-mediated liver injury and significant immunological aspects. Arthritis can be observed in patients with AIH before recognition of the disease, which can lead to a diagnostic challenge. Although there are few reported cases in literature, peripheral blood eosinophilia might also play a part in such diagnosis. We report an intriguing case of a 41-year-old man who presented to our service with arthritis and eosinophilia as initial manifestations and was eventually diagnosed with overlap syndrome: AIH and primary sclerosing cholangitis. The present report aims to include eosinophilia among the clinical features of AIH, highlighting the possibility of its detection before the onset of either articular or hepatic disturbances.
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    ABSTRACT: Astaxanthin, a potent antioxidant, exhibits a wide range of biological activities, including antioxidant, atherosclerosis and antitumor activities. However, its effect on concanavalin A (ConA)-induced autoimmune hepatitis remains unclear. The aim of this study was to investigate the protective effects of astaxanthin on ConA-induced hepatitis in mice, and to elucidate the mechanisms of regulation. Autoimmune hepatitis was induced in in Balb/C mice using ConA (25 mg/kg), and astaxanthin was orally administered daily at two doses (20 mg/kg and 40 mg/kg) for 14 days before ConA injection. Levels of serum liver enzymes and the histopathology of inflammatory cytokines and other maker proteins were determined at three time points (2, 8 and 24 h). Primary hepatocytes were pretreated with astaxanthin (80 μM) in vitro 24 h before stimulation with TNF-α (10 ng/ml). The apoptosis rate and related protein expression were determined 24 h after the administration of TNF-α. Astaxanthin attenuated serum liver enzymes and pathological damage by reducing the release of inflammatory factors. It performed anti-apoptotic effects via the descending phosphorylation of Bcl-2 through the down-regulation of the JNK/p-JNK pathway. This research firstly expounded that astaxanthin reduced immune liver injury in ConA-induced autoimmune hepatitis. The mode of action appears to be downregulation of JNK/p-JNK-mediated apoptosis and autophagy.
    PLoS ONE 03/2015; 10(3):e0120440. DOI:10.1371/journal.pone.0120440 · 3.53 Impact Factor
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