瞬态弹性成像
医学
纤维化
胃肠病学
内科学
肝硬化
置信区间
慢性肝炎
脂肪变性
阶段(地层学)
肝纤维化
乙型肝炎
免疫学
病毒
生物
古生物学
作者
Lung‐Yi Mak,Wai‐Kay Seto,Rex Wan‐Hin Hui,James Fung,Danny Ka‐Ho Wong,Ching–Lung Lai,Man‐Fung Yuen
摘要
Summary The degree of liver fibrosis in chronic hepatitis B ( CHB ) infection influences outcome and management. Existing data describing the long‐term dynamic changes of liver fibrosis are limited. This study aimed to evaluate the evolution of liver fibrosis in CHB across a 10‐year period. CHB patients with liver stiffness measurement ( LSM ) by transient elastography 10 years ago were recruited for follow‐up LSM . Fibrosis stages were classified according to EASL ‐ ALEH guidelines. Fibrosis progression/regression was arbitrarily defined as ≥1 fibrosis stage change from baseline. A total of 459 hepatitis B e antigen ( HB eAg)‐negative patients (224 untreated, 235 treated with nucleos(t)ide analogues [ NA s]) were recruited. The mean age at baseline LSM was 41.7 ± 9.0 years (56.2% male). Over 10 years, the proportion of patients with advanced fibrosis/cirrhosis significantly reduced from 16.3% to 5.7% ( P < 0.001). Fibrosis progression and regression were observed in 8.7% and 37.5%, respectively. No treatment with NA s ( OR 2.259, 95% confidence interval [CI]: 1.032‐4.945), metabolic syndrome ( OR 4.379, 95% CI: 1.128‐16.999) and hepatic steatosis ( OR 7.799, 95% CI: 2.271‐26.776) was associated with fibrosis progression. Liver stiffness decline demonstrated positive correlation with the time after HB sAg seroclearance ( r = −0.50, P < 0.001). Median liver stiffness was higher both at baseline (14.0 vs 6 kPa, P < 0.001) and 10 years (9.1 vs 4.9 kPa, P < 0.001) in patients with cirrhosis‐related complications/hepatocellular carcinoma compared with those without. In conclusion, CHB ‐related liver fibrosis changed dynamically across 10 years. Metabolic syndrome and hepatic steatosis were associated with fibrosis progression, while antiviral therapy was associated with fibrosis regression. Patients with HB sAg seroclearance demonstrated time‐dependent decline in liver stiffness.
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