Torgersen Jessie, Newcomb Craig W, Carbonari Dean M, Smith Shanae M, Brecker Katherine L, Rajapakse Chamith S, Jones Brandon C, Cottrell Christiana, Grewal Rasleen, Price Jennifer C, Baker Joshua F, Kostman Jay R, Trooskin Stacey, Hubbard Rebecca A, Zemel Babette S, Leonard Mary B, Lo Re Iii Vincent
Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Department of Biostatistics, Epidemiology, and Informatics, Center for Clinical Epidemiology and Biostatistics, Center for Real-world Effectiveness and Safety of Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
PLoS One. 2025 Jul 23;20(7):e0327668. doi: 10.1371/journal.pone.0327668. eCollection 2025.
Chronic hepatitis C virus (HCV) infection may influence cytokine and insulin-like growth factor (IGF-1) levels, which could contribute to increased hepatic steatosis. We utilized MRI to compare three-dimensional volumetric liver fat fraction by chronic HCV status and evaluated associations between liver fat fraction and inflammatory cytokines and IGF-1.
Participants with untreated, non-genotype 3 chronic HCV and participants without HCV were enrolled between 2019-2022 and underwent MRI to quantify three-dimensional volumetric liver fat fraction. Interleukin (IL)-6, IL-18, tumor necrosis factor (TNF)-α, and IGF-1 were also measured. Multivariable linear regression was used to determine associations between liver fat fraction, chronic HCV, and cytokine and IGF-1 levels.
Among 54 participants with HCV and 54 without HCV, median volumetric liver fat fraction was 12.4% (IQR: 9.3, 18.0%) and 10.9% (IQR: 8.7, 13.3%), respectively. After adjustment for age, sex, and body mass index, mean liver fat fraction was 2.28% (95% CI: 0.55, 4.02%) higher in participants with HCV. HCV was associated with higher mean log TNF-α (0.11 [95% CI: 0.06, 0.16]) and IL-18 (0.14 [95% CI: 0.05, 0.24]), but lower mean log IGF-1 (-0.18 [95% CI: -0.26, -0.11]) when compared to those without HCV. IL-6, IL-18, TNF-α, and IGF-1 were not associated with liver fat fraction.
Chronic HCV is associated with higher volumetric liver fat fraction by MRI. TNF-α and IL-18 levels were higher with chronic HCV but were not associated with liver fat fraction. Further research is needed to identify alternative mechanisms that potentiate liver fat deposition in chronic HCV.
慢性丙型肝炎病毒(HCV)感染可能影响细胞因子和胰岛素样生长因子(IGF-1)水平,这可能导致肝脂肪变性增加。我们利用磁共振成像(MRI)按慢性HCV状态比较三维肝脏脂肪体积分数,并评估肝脏脂肪分数与炎性细胞因子和IGF-1之间的关联。
2019年至2022年期间纳入未经治疗的非3型慢性HCV参与者和无HCV参与者,并进行MRI以量化三维肝脏脂肪体积分数。同时检测白细胞介素(IL)-6、IL-18、肿瘤坏死因子(TNF)-α和IGF-1。采用多变量线性回归确定肝脏脂肪分数、慢性HCV以及细胞因子和IGF-1水平之间的关联。
在54例HCV感染者和54例无HCV感染者中,肝脏脂肪体积分数中位数分别为12.4%(四分位间距:9.3,18.0%)和10.9%(四分位间距:8.7,13.3%)。在调整年龄、性别和体重指数后,HCV感染者的平均肝脏脂肪分数高2.28%(95%置信区间:0.55,4.02%)。与无HCV感染者相比,HCV感染者的平均log TNF-α(0.11 [95%置信区间:0.06,0.16])和IL-18(0.14 [95%置信区间:0.05,0.24])更高,但平均log IGF-1更低(-0.18 [95%置信区间:-0.26,-0.11])。IL-6、IL-18、TNF-α和IGF-1与肝脏脂肪分数无关。
通过MRI检查,慢性HCV与更高的肝脏脂肪体积分数相关。慢性HCV感染者的TNF-α和IL-18水平更高,但与肝脏脂肪分数无关。需要进一步研究以确定在慢性HCV中增强肝脏脂肪沉积的其他机制。