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: >1mm) or plaques (≥ 1.5mm). 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.
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 CHCpatients 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: >1mm) or plaques (≥ 1.5mm). RESULTS:CHCpatients 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). CHCpatients 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.
Authors: Parag Mahale; Eric A Engels; Ruosha Li; Harrys A Torres; Lu-Yu Hwang; Eric L Brown; Jennifer R Kramer Journal: Gut Date: 2017-06-20 Impact factor: 23.059
Authors: Umberto Vespasiani-Gentilucci; Paolo Gallo; Antonio De Vincentis; Giovanni Galati; Antonio Picardi Journal: World J Gastroenterol Date: 2014-03-21 Impact factor: 5.742
Authors: Rosa Zampino; Aldo Marrone; Luciano Restivo; Barbara Guerrera; Ausilia Sellitto; Luca Rinaldi; Ciro Romano; Luigi E Adinolfi Journal: World J Hepatol Date: 2013-10-27
Authors: K W Chew; D Bhattacharya; T B Horwich; P Yan; K A McGinnis; C Tseng; M S Freiberg; J S Currier; A A Butt Journal: J Viral Hepat Date: 2017-04-10 Impact factor: 3.728