Response to the letter by Dr. Naoya Yamada, and Dr. Koichi Mizuta regarding our manuscript: "Mac-2 binding protein glycan isomer (M2BPGi) is a new serum biomarker for assessing liver fibrosis: more than a biomarker of liver fibrosis".
Response to the letter by Dr. Naoya Yamada, and Dr. Koichi Mizuta regarding our manuscript: "Mac-2 binding protein glycan isomer (M2BPGi) is a new serum biomarker for assessing liver fibrosis: more than a biomarker of liver fibrosis".
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对 Naoya Yamada 博士和 Koichi Mizuta 博士关于我们手稿的信函的回应：“Mac-2 结合蛋白聚糖异构体 (M2BPGi) 是一种用于评估肝纤维化的新血清生物标志物：不仅仅是肝纤维化的生物标志物”。
DOI：
10.1007/s00535-018-1524-5
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发表时间：
2019
期刊：
影响因子：
6.3
通讯作者：
Mizokami M.
中科院分区：
文献类型：
--
作者：
Shirabe K;Bekki Y;Gantumur D;Araki K;Ishii N;Kuno A;Narimatsu H;Mizokami M.
尊敬的编辑：我们感谢Yamada和Mizuta博士对我们研究的兴趣，并分享他们治疗胆道闭锁（BA）患者的经验。BA患者的肝纤维化血清标志物非常有价值，因为患者通常是儿童，并且获得肝活检可能很困难。Yamada和Mizuta博士证明了Mac-2结合蛋白糖基化异构体（M2 BPGi）血清水平对评估BA患者肝纤维化的临床意义[1]。他们注意到患有BA的女婴的M2 BPGi血清水平的显著变化。在胆管炎期间，血清M2 BPGi水平较高，治疗后降至正常范围。尚未确定M2 BPGi在人血清中的半衰期。然而，在接受肝移植治疗终末期肝硬化的患者中，术前血清M2 BPGi水平通常较高，并在24小时内降至正常范围（未发表的数据）。因此，如果M2 BPGi的产生停止，其水平会迅速下降。显然，无法解释胆管炎期间M2 BPGi水平的升高。我们先前发现M2 BPGi的独特特征如下：（1）截止值不同，即使对于与原因无关的纤维化的相同阶段也是如此。(2)M2 BPGi的水平在达到对丙型肝炎病毒的持续抗病毒应答后迅速下降[2]。最近，Bekki Y et al. [3]发现肝星状细胞（HSC）是其他肝衍生细胞亚群（如枯否细胞、内皮细胞、胆管上皮细胞和肝细胞）中M2 BPGi的来源。如果M2 BPGi是由活化的HSC特异性产生的，则可以解释M2 BPGi的独特特征。因此，M2 BPGi水平可以反映肝纤维化的程度以及某些慢性肝病中肝纤维化的加速。
Dear Editor, We thank Drs. Yamada and Mizuta for their interest in our study and for sharing their experience with a patient with biliary atresia (BA). Serum markers of liver fibrosis in patients with BA are extremely valuable, because patients are typically children, and acquiring a liver biopsy may be difficult. Drs. Yamada and Mizuta demonstrated the clinical significance of serum levels of Mac-2 binding protein glycosylation isomer (M2BPGi) for assessing liver fibrosis in patients with BA [1]. They note the dramatic changes in serum levels of M2BPGi in their female infant with BA. During cholangitis, the serum level of M2BPGi was high and decreased to the normal range after treatment. The half-life of M2BPGi in human serum has not been established. Nevertheless, in patients who undergo liver transplantation for end-stage liver cirrhosis, preoperative serum levels of M2BPGi are typically high and decrease to the normal range within 24 h (unpublished data). Therefore, the levels of M2BPGi rapidly decrease if its production is stopped.There, apparently, is no explanation for the elevation of M2BPGi levels during cholangitis. We previously discovered the unique features of M2BPGi as follows:(1) The cut-off values differ, even for the same stage of fibrosis independent of cause.(2) The levels of M2BPGi rapidly decrease after achieving a sustained antiviral response to hepatitis C virus [2]. Recently, Bekki Y et al.[3] found that hepatic stellate cells (HSCs) are the source of M2BPGi in subpopulations of other liver-derived cells such as Kupffer cells, endothelial cells, biliary epithelial cells, and hepatocytes. The unique features of M2BPGi may be explained if it is specifically produced by activated HSCs. Therefore, M2BPGi levels may reflect the extent of liver fibrosis as well as the acceleration of liver fibrosis in certain chronic liver diseases.