核糖核苷酸还原酶M2亚基（RRM2）在细胞和乙型肝炎病毒（HBV）复制中发挥关键作用。然而，它在管理肝病方面的临床意义尚未得到充分研究。共有412名参与者被纳入研究，包括60名健康对照个体，55名慢性乙型肝炎（CHB）患者，173名肝硬化患者和124名肝细胞癌（HCC）患者。通过ELISA测量血清RRM2水平。CHB、肝硬化和HCC患者的血清RRM2水平均高于健康对照组（P < 0.05）。HBV相关和非HBV相关患者之间的血清RRM2水平在肝硬化组中存在明显差异（P < 0.001），而在HBV相关和非HBV相关HCC之间的差异则相对较小（P = 0.86）。在HBV相关肝硬化组中，血清RRM2水平与HBV DNA、乙型肝炎表面抗原、乙型肝炎e抗原、Child-Pugh评分和MELD评分有显著正相关，并在CHB中诊断HBV相关肝硬化方面发挥强大作用，相比于纤维化-4分数和天冬氨酸氨基转移酶与血小板比值指数。血清RRM2是准确诊断和评估HBV相关肝硬化的可靠生物标志物，并可以反映HBV相关肝硬化患者的HBV复制状态。©作者（2023）。由牛津大学出版社代表美国临床病理学会出版。保留所有权利。有关权限，请发送电子邮件至：journals.permissions@oup.com。

Ribonucleotide reductase subunit M2 (RRM2) plays a key role in cell and hepatitis B virus (HBV) replication. Nevertheless, its clinical implications for managing liver diseases have been inadequately studied.A total of 412 participants were enrolled, including 60 healthy control individuals, 55 patients with chronic hepatitis B (CHB), 173 patients with cirrhosis, and 124 patients with hepatocellular carcinoma (HCC). Serum RRM2 was measured via ELISA.The level of serum RRM2 in patients with CHB, cirrhosis, and HCC was higher than that in healthy controls (P < .05). A large difference in serum RRM2 was found between HBV-related and non-HBV-related patients in the cirrhosis group (P < .001), compared with the difference between HBV-related HCC and non-HBV-related HCC (P = .86). In the HBV-related cirrhosis group, the serum RRM2 level showed significant positive correlations with HBV DNA, hepatitis B surface antigen, hepatitis B e antigen, Child-Pugh scores, and MELD scores and played a strong role in diagnosing HBV-related cirrhosis in CHB, compared with fibrosis-4 score and aspartate aminotransferase-to-platelet ratio index.Serum RRM2 is a reliable biomarker for accurate HBV-related cirrhosis diagnosis and evaluation. Also, serum RRM2 could reflect the expression state of HBV replication in patients with HBV-related cirrhosis.© The Author(s) 2023. Published by Oxford University Press on behalf of American Society for Clinical Pathology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.