We previously reported that liver natural killer (NK) and NKT cells play a critical role in mouse model of acetaminophen (APAP)-induced liver injury by producing interferon gamma (IFN-gamma) and modulating chemokine production and subsequent recruitment of neutrophils into the liver. In this report,
Neutrophil depletion protects against murine acetaminophen hepatotoxicity: Another perspective
✍ Scribed by Hartmut Jaeschke; Jie Liu
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 83 KB
- Volume
- 45
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
M6 (182 Ϯ 58 ϫ 10 9 /l versus 187 Ϯ 60 ϫ 10 9 /l, P Ͻ 0.0001, paired t test). By contrast, the platelet counts at baseline and M6 were similar (166 Ϯ 64 ϫ 10 9 /l versus 165 Ϯ 62 ϫ 10 9 /l) among nonresponders. Thus, the platelet component of APRI may more closely reflect the ongoing change in hepatic fibrosis after interferon-based therapy than the present proposed scoring systems. Taken together, the APRI determined after interferon-based therapy may not only correlate well with SVR and sustained biochemical response, but also with the slow, but significant regression of hepatic fibrosis. All the factors have been important factors associated with long-term outcome of liver disease. 4,7 Because patients with cirrhosis with and without an SVR are at risk of HCC, universal close follow-up is recommended in clinical practice and may overcome the limitation of APRI-M6 prediction for the subgroup. Nevertheless, with optimized cut-off values of APRI-M6, we could identify patients at risk for HCC development in low-risk groups (sustained responders and patients without cirrhosis). These results could provide decision-making information for scheduling follow-up intervals to detect HCC early.
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