背景:慢性乙型肝炎(CHB)和代谢功能障碍相关的脂肪肝(MAFLD)的共同发生由于其对疾病结局的影响而引起了相当大的关注。本研究旨在探讨肝脂肪变性与乙型肝炎病毒(HBV)之间的关联,并分析肝脂肪变性对慢性乙型肝炎患者乙型肝炎病毒学的影响。
方法:在这项横断面研究中,272例感染HBV谁是治疗初治或已停止抗病毒治疗>6个月被分为CHB组(n=128)和CHB+MAFLD组(n=144)。此外,基于HBVDNA是否高于2000IU/mL,患者分为高水平HBVDNA组(n=129)和低水平HBVDNA组(n=143).在CHB队列中分析了肝脂肪变性对乙型肝炎病毒学的影响。多因素logistic回归分析用于确定影响CHB患者前基因组RNA(pgRNA)水平低于检测下限(LLD)的独立因素。
结果:在272名患者中,与CHB组相比,HBVDNA水平(4.11vs.3.62log10IU/mL,P=0.045),乙型肝炎表面抗原(HBsAg)水平(3.52vs.3.20log10IU/mL,P=0.008)和乙型肝炎e抗原(HBeAg)阳性率(33.6%vs.22.2%,P=0.036)在CHB+MAFLD组中显著降低;在143低水平HBVDNA患者中,与CHB组相比,CHB+MAFLD组的pgRNA和HBsAg水平降低。然而,在129个高水平的HBVDNA患者,在pgRNA中观察到更显著的下降(3.85vs3.35log10拷贝/mL,P=0.044)和HBsAg(3.85vs3.59log10IU/mL,P=0.033);Spearman相关分析显示肝脂肪变性与pgRNA呈负相关(r=-0.529,P<0.001),HBVDNA(r=-0.456,P<0.001),HBsAg(r=-0.465,P<0.001)和HBeAg(r=-0.339,P<0.001)水平;多变量逻辑回归分析确定HBVDNA(比值比[OR]=0.283,P<0.001),HBsAg(OR=0.300,P<0.001),和受控衰减参数(CAP)值(OR=1.013,P=0.038)是影响CHB患者低于LLD的pgRNA水平的独立因素。
结论:这项研究建立了肝脂肪变性和乙型肝炎病毒学之间的负相关,显示CHB+MAFLD患者HBV表达降低。
The co-occurrence of chronic hepatitis B (
CHB) and metabolic dysfunction-associated fatty liver disease (MAFLD) has drawn considerable attention due to its impact on disease outcomes. This study aimed to investigate the association between hepatic steatosis and hepatitis B virus (HBV) and analyzed the influence of hepatic steatosis on hepatitis B virology in patients with
CHB.
In this cross-sectional study, 272 patients infected with HBV who were treatment-naïve or had ceased antiviral treatment for > 6 months were categorized into the CHB group (n = 128) and
CHB + MAFLD group (n = 144). Furthermore, based on whether HBV DNA was higher than 2000 IU/mL, patients were categorized into the high-level HBV DNA group (n = 129) and the low-level HBV DNA group (n = 143). The impact of hepatic steatosis on hepatitis B virology was analyzed within the
CHB cohort. Multivariate logistic regression analysis was employed to identify independent factors influencing pre-genomic RNA (pgRNA) levels below the lower limit of detection (LLD) in patients with CHB.
Among the 272 patients, compared with CHB group, HBV DNA levels (4.11 vs. 3.62 log10 IU/mL, P = 0.045), hepatitis B surface antigen (HBsAg) levels (3.52 vs. 3.20 log10 IU/mL, P = 0.008) and the hepatitis B e antigen (HBeAg) positive rate (33.6% vs. 22.2%, P = 0.036) were significantly decreased in the CHB + MAFLD group; In 143 low-level HBV DNA patients, the CHB + MAFLD group exhibited decreased levels of pgRNA and HBsAg compared to the
CHB group. However, in 129 high-level HBV DNA patients, a more significant decrease was observed in pgRNA (3.85 vs 3.35 log10 copies/mL, P = 0.044) and HBsAg (3.85 vs 3.59 log10 IU/mL, P = 0.033); Spearman correlation analysis revealed a negative correlation between hepatic steatosis and pgRNA (r = - 0.529, P < 0.001), HBV DNA (r = - 0.456, P < 0.001), HBsAg (r = - 0.465, P < 0.001) and HBeAg (r = - 0.339, P < 0.001) levels; Multivariate logistic regression analysis identified HBV DNA (odds ratio [OR] = 0.283, P < 0.001), HBsAg (OR = 0.300, P < 0.001), and controlled attenuation parameter (CAP) values (OR = 1.013, P = 0.038) as independent factors influencing pgRNA levels below the LLD in patients with CHB.
This study establishes a negative correlation between hepatic steatosis and hepatitis B virology, demonstrating decreased HBV expression in patients with CHB + MAFLD.