- 现金
- 62111 元
- 精华
- 26
- 帖子
- 30437
- 注册时间
- 2009-10-5
- 最后登录
- 2022-12-28
|
Aliment Pharmacol Ther. 2018 Oct 10. doi: 10.1111/apt.15006. [Epub ahead of print]
Serum M2BPGi level and risk of hepatocellular carcinoma after oral anti-viral therapy in patients with chronic hepatitis B.
Hsu YC1,2,3,4, Jun T5, Huang YT6, Yeh ML7, Lee CL8, Ogawa S9, Cho SH6, Lin JT1,2, Yu ML7, Nguyen MH10, Tanaka Y9.
Author information
1
Division of Gastroenterology and Hepatology, Fu-Jen Catholic University Hospital, New Taipei, Taiwan.
2
School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei, Taiwan.
3
Division of Gastroenterology and Hepatology, E-Da Hospital, Kaohsiung, Taiwan.
4
Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
5
Department of Medicine, Stanford University Medical Center, Palo Alto, California.
6
Institute of Statistical Science, Academia Sinica, Taipei, Taiwan.
7
Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
8
Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan.
9
Department of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
10
Division of Gastroenterology and Hepatology, Stanford University Medical Center, Palo Alto, California.
Abstract
BACKGROUND:
Mac-2 binding protein glycosylation isomer (M2BPGi) is an emerging biomarker for risk prediction of liver disease, but data remain sparse for patients with chronic hepatitis B (CHB) who are treated with nucleos(t)ide analogues (NA).
AIM:
To clarify serial changes in M2BPGi and its association with subsequent hepatocellular carcinoma (HCC) development in NA-treated CHB patients.
METHODS:
We enrolled 384 previously untreated CHB patients who received NAs. Among them, 195 had baseline cirrhosis (n = 142:48:5 for Child A:B:C). Sera were collected at NA initiation, and after 1 and 2 years. Serum M2BPGi levels were measured and expressed as cut-off index (COI) at different time points. The association between M2BPGi and HCC was evaluated by the Cox proportional hazard model.
RESULTS:
The median M2BPGi levels significantly decreased from 1.68 COI at baseline, to 1.0 at year 1, and 0.88 at year 2. During median follow-up of 72.7 months, HCC occurred in 37 patients, 36 of whom had cirrhosis. In patients with cirrhosis, baseline M2BPGi level was associated with HCC risk (adjusted hazard ratio, 1.07 per COI; 95% CI, 1.01-1.14) on the multivariable Cox analysis, whereas levels at year 1 or 2 were not independently predictive. A risk score for HCC was developed using baseline M2BPGi, age and body mass index with c statistics of 0.77, 0.79 and 0.87 at 3, 5 and 10 years, respectively.
CONCLUSIONS:
Serum M2BPGi level significantly decreases after NA treatment in CHB patients. Baseline level can be factored into the risk prediction of HCC in NA-treated patients with cirrhosis.
© 2018 John Wiley & Sons Ltd.
PMID:
30306612
DOI:
10.1111/apt.15006 |
|