Serum osteopontin levels in patients with acute liver dysfunction
Serum osteopontin levels in patients with acute liver dysfunction
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DOI：
10.1080/00365520510024061
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发表时间：
2006-01-01
影响因子：
1.9
通讯作者：
Saisho, H
中科院分区：
文献类型：
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作者：
Arai, M;Yokosuka, O;Saisho, H
Objective.暴发性肝功能衰竭（FHF）是一种突发性严重肝功能障碍伴脑病的临床综合征。在FHF中，肝细胞严重受损，普通肝再生受损。我们证明了骨桥蛋白（OPN），一种多功能细胞因子，在小鼠卵圆细胞（干细胞祖细胞）诱导模型中表达上调。材料和方法。基于这一发现，检测了43例FHF患者和45例急性自限性肝炎（AH）患者的血清OPN水平。为了确定OPN的细胞来源，在来自FHF患者的肝标本中研究了OPN的表达。结果FHF患者的平均OPN水平为2.809 +/- 0.48 ng/ml（log（10），+/- SD），显著高于AH患者（2.429 +/- 0.39 ng/ml）（p=0.003，非配对t检验）。血清OPN水平升高的患者比血清OPN水平未升高的患者预后明显较差。在FHF患者的肝脏中，OPN蛋白不仅在炎症细胞中表达，而且在再生的肝细胞和胆管结构中表达。结论.我们目前的研究表明，FHF患者的血清OPN水平升高，并且OPN可能在肝脏干细胞激活导致的肝脏再生中发挥重要作用。
Objective. Fulminant hepatic failure (FHF) is a clinical syndrome of sudden and severe liver dysfunction accompanied by encephalopathy in a previously healthy person. In FHF, hepatocytes are severely damaged and ordinary liver regeneration is impaired. We demonstrated that the expression of osteopontin (OPN), a multifunctional cytokine, was up-regulated in mouse oval cell (a stem-cell progenitor) induction models. Material and methods. Based on this finding, serum OPN levels were examined in 43 patients with FHF and in 45 patients with acute self-limited hepatitis (AH). To determine the cellular source of OPN, the expression of OPN was studied in a liver specimen derived from an FHF patient. Results. The mean OPN level of patients with FHF was 2.809 +/- 0.48 ng/ml (log(10), +/- SD), which was significantly higher than that of the patients with AH (2.429 +/- 0.39 ng/ml) (p=0.003, unpaired t-test). Patients with elevated serum OPN levels had a significantly poorer prognosis than patients whose serum OPN levels were not elevated. In the FHF patient's liver, OPN protein was expressed not only in inflammatory cells but also in regenerating hepatocytes and bile ductular structures. Conclusions. Our current study indicates that serum OPN levels increased in patients with FHF and that OPN might play an important role in liver regeneration due to activation of hepatic stem cells.