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% vs34.3%; p<0.0001). Younger CHC (<50 years) had a higher prevalence of CA thancontrols (34.0% vs 16.0%; p<0.04). CHC patients without steatosis had a higherprevalence of CA than B1 controls (26.0% vs 14.8%; p<0.02). CHC with steatosishad 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 withmetabolic 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.

Chronic HCV infection is a risk of atherosclerosis. Role ofHCV and HCV-related steatosis / Adinolfi, Le; Restivo, L; Zampino, R; Guerrera, B; Lonardo, A; Ruggiero, L; Riello, F; Loria, Paola; Florio, A.. - In: ATHEROSCLEROSIS. - ISSN 0021-9150. - STAMPA. - 221:(2012), pp. 496-502. [10.1016/j.atherosclerosis.2012.01.051]

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

LORIA, Paola;
2012

Abstract

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% vs34.3%; p<0.0001). Younger CHC (<50 years) had a higher prevalence of CA thancontrols (34.0% vs 16.0%; p<0.04). CHC patients without steatosis had a higherprevalence of CA than B1 controls (26.0% vs 14.8%; p<0.02). CHC with steatosishad 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 withmetabolic 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.
2012
221
496
502
Chronic HCV infection is a risk of atherosclerosis. Role ofHCV and HCV-related steatosis / Adinolfi, Le; Restivo, L; Zampino, R; Guerrera, B; Lonardo, A; Ruggiero, L; Riello, F; Loria, Paola; Florio, A.. - In: ATHEROSCLEROSIS. - ISSN 0021-9150. - STAMPA. - 221:(2012), pp. 496-502. [10.1016/j.atherosclerosis.2012.01.051]
Adinolfi, Le; Restivo, L; Zampino, R; Guerrera, B; Lonardo, A; Ruggiero, L; Riello, F; Loria, Paola; Florio, A.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/761073
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