Chronic HCV infection is a risk of atherosclerosis. Role of HCV and HCV-related steatosis

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• 作者：Luigi E. Adinolfi^a ; ^{luigielio.adinolfi@unina2.it} ; Luciano Restivo^a ; Rosa Zampino^a ; Barbara Guerrera^a ; Amedeo Lonardo^c ; Laura Ruggiero^a ; Francesco Riello^d ; Paola Loria^c ; Anna Florio^b
• 关键词：CHC ; chronic hepatitis C ; IMT ; carotid intima-media thickness ; HOMA-IR ; homeostatic model assessment ; IR ; insulin resistance ; HCV ; hepatitis C virus ; HCV RNA ; hepatitis C virus RNA ; HAI ; histological activity index ; CRP ; C reactive protein
• 刊名：Atherosclerosis
• 出版年：2012
• 期刊代码：28_00219150
• 类别：med
• 出版时间：April, 2012
• 卷：221
• 期：2
• 页码：496-502
• 文件大小：233 K

摘要

Objectives

HCV and NAFLD are associated with atherosclerosis in general population. The prevalence of atherosclerosis in chronic hepatitis C (CHC) patients is unknown. We hypothesized that HCV per se and HCV-related steatosis could favour atherosclerosis. Thus, in CHC patients we assessed: (a) the prevalence of atherosclerosis; (b) the role of HCV, cardio-metabolic risk factors and hepatic histology.

Methods

Overall, 803 subjects were enrolled: (A) 326 patients with liver biopsy-proven treatment naive CHC (175 with and 151 without steatosis); (B) 477 age and gender matched controls, including 292 healthy subjects without steatosis (B1) and 185 with NAFLD (B2). Carotid atherosclerosis (CA), assessed by high-resolution B-mode ultrasonography, was categorized as either intima-media thickness (IMT: >1 mm) or plaques (鈮?.5 mm).

Results

CHC patients had a higher prevalence of CA than controls (53.7%vs 34.3%; p < 0.0001). Younger CHC (<50 years) had a higher prevalence of CA than controls (34.0%vs 16.0%; p < 0.04). CHC patients without steatosis had a higher prevalence of CA than B1 controls (26.0%vs 14.8%; p < 0.02). CHC with steatosis had a higher prevalence of CA than NAFLD patients (77.7%vs 57.8%, p < 0.0001). Viral load was associated with serum CRP and fibrinogen levels; steatosis with metabolic syndrome, HOMA-IR, hyperhomocysteinemia and liver fibrosis. Viral load and steatosis were independently associated with CA. Diabetes and metabolic syndrome were associated with plaques.

Conclusion

HCV infection is a risk factor for earlier and facilitated occurrence of CA via viral load and steatosis which modulate atherogenic factors such as inflammation and dysmetabolic milieu.