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. - 221:2(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
2
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. - 221:2(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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