Hepatic stellate cells and fibrosis progression in patients with nonalcoholic fatty liver disease

2005 ◽  
Vol 3 (4) ◽  
pp. 384-389 ◽  
Author(s):  
Ariel E. Feldstein ◽  
Bettina G. Papouchado ◽  
Paul Angulo ◽  
Schyler Sanderson ◽  
Leon Adams ◽  
...  
2018 ◽  
Vol 11 ◽  
pp. 175628481881518 ◽  
Author(s):  
Wei Chen ◽  
Jing Zhang ◽  
Hui-Ning Fan ◽  
Jin-Shui Zhu

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of hepatic pathology, ranging from simple accumulation of fat in its most benign form, steatohepatitis, to cirrhosis in its most advanced form. The prevalence of NAFLD is 20–30% in adults, and 10–20% of patients with NAFLD progress to nonalcoholic steatohepatitis (NASH) which is predicted to be the leading cause of liver transplantation over the next 10 years. Therefore, it is essential to explore effective diagnostic and treatment strategies for NAFLD patients. Chemokines are a family of small and highly conserved proteins (molecular weight ranging from 8 to 12 kDa) involved in regulating the migration and activities of hepatocytes, Kupffer cells (KCs), hepatic stellate cells (HSCs), endothelial cells and circulating immune cells. Accumulating data show that chemokine and its receptor act vital roles in the pathogenesis of NAFLD. Herein, we summarize the involvement of the chemokine and its receptor in the pathogenesis of NAFLD and explore the novel pharmacotherapeutic avenues for patients with NAFLD.


2019 ◽  
Vol 17 (13) ◽  
pp. 2776-2784.e4 ◽  
Author(s):  
Tracey G. Simon ◽  
Jacqueline Henson ◽  
Stephanie Osganian ◽  
Ricard Masia ◽  
Andrew T. Chan ◽  
...  

Author(s):  
Lindsay T Fourman ◽  
Takara L Stanley ◽  
Isabel Zheng ◽  
Chelsea S Pan ◽  
Meghan N Feldpausch ◽  
...  

Abstract Background Nonalcoholic fatty liver disease (NAFLD) affects more than one-third of people living with human immunodeficiency virus (HIV). Nonetheless, its natural history is poorly understood, including which patients are most likely to have a progressive disease course. Methods We leveraged a randomized trial of the growth hormone–releasing hormone analogue tesamorelin to treat NAFLD in HIV. Sixty-one participants with HIV-associated NAFLD were randomized to tesamorelin or placebo for 12 months with serial biopsies. Results In all participants with baseline biopsies (n = 58), 43% had hepatic fibrosis. Individuals with fibrosis had higher NAFLD Activity Score (NAS) (mean ± standard deviation [SD], 3.6 ± 2.0 vs 2.0 ± 0.8; P < .0001) and visceral fat content (mean ± SD, 284 ± 91 cm2 vs 212 ± 95 cm2; P = .005), but no difference in hepatic fat or body mass index. Among placebo-treated participants with paired biopsies (n = 24), 38% had hepatic fibrosis progression over 12 months. For each 25 cm2 higher visceral fat at baseline, odds of fibrosis progression increased by 37% (odds ratio, 1.37 [95% confidence interval, 1.03–2.07]). There was no difference in baseline NAS between fibrosis progressors and nonprogressors, though NAS rose over time in the progressor group (mean ± SD, 1.1 ± 0.8 vs −0.5 ± 0.6; P < .0001). Conclusions In this longitudinal study of HIV-associated NAFLD, high rates of hepatic fibrosis and progression were observed. Visceral adiposity was identified as a novel predictor of worsening fibrosis. In contrast, baseline histologic characteristics did not relate to fibrosis progression.


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