LDL particle size and antioxidant HDL function improve after sustained virological response in patients with chronic HCV

• Published in: Annals of hepatology Vol. 27; no. 1; p. 100555
• Main Authors: Vargas, Jose Ignacio, Rivera, Katherine, Arrese, Marco, Benitez, Carlos, Barrera, Francisco, Hugo, Monrroy, Arab, Juan Pablo, Pino, Karla, Barrera, Aldo, Lopez-Lastra, Marcelo, Rigotti, Attilio, Soza, Alejandro
• Format: Journal Article
• Language: English
• Published: Mexico Elsevier España, S.L.U 01.01.2022; Elsevier
• Subjects: Aged; Antioxidants - therapeutic use; Antiviral Agents - therapeutic use; Cardiovascular risk; Direct-acting antivirals; Female; Follow-Up Studies; HDL antioxidant capacity; HDL functionality; Hepacivirus - isolation & purification; Hepatitis C virus; Hepatitis C, Chronic - blood; Hepatitis C, Chronic - drug therapy; Humans; LDL particle size; Lipoproteins, HDL - metabolism; Lipoproteins, LDL - blood; Male; Middle Aged; Particle Size; Prospective Studies; Sustained Virologic Response; Sustained virological response; Treatment Outcome; HDL antioxidant capacity; Cardiovascular risk; HDL functionality; Sustained virological response; LDL particle size; Hepatitis C virus; Direct-acting antivirals
• ISSN: 1665-2681; 2659-5982
• DOI: 10.1016/j.aohep.2021.100555

HCV infection is associated with an increased incidence of cardiovascular (CV) events. Mechanisms underlying this association remain unknown. In our study, twenty HCV patients (median age 60.5 years, 65% male and 80% with cirrhosis) were evaluated prior, during and after direct-acting antiviral treatment. Ninety percent of patients achieved sustained virological response (SVR). Significant changes were observed in LDL particle size index, measured by LDL-C/apoB ratio, which increased after treatment (p = 0.023). In addition, HDL antioxidant capacity improved gradually from 34.4% at baseline to 42.4% at 4 weeks (p = 0.011), 65.9% at end of treatment EOT (p = 0.002) and remained elevated at 12-week (p = 0.001) after EOT compared to baseline values. Our findings suggest that a shift to a less atherogenic lipid profile may be a possible mechanism associated with CV risk reduction in patients with HCV infection achieving SVR.