Lipid profile changes after direct acting antiviral treatment in different genotypes of chronic hepatitis C virus‐infected patients

The fact that chronic hepatitis C (CHC) virus interacts with serum lipid metabolism is well‐known, and previous studies have demonstrated that hepatitis C virus (HCV) eradication using direct acting antivirals (DAAs) or interferon‐based therapy, can cause lipid levels to increase during treatment. The current study focused on HCV patients with different genotypes who had a sustained virological response (SVR); their lipid levels and metabolism changes after DAA treatment were investigated. The current study retrospectively included 394 patients who received DAAs treatment for CHC with SVR in Liouying Chi‐Mei Medical Center. Patients who accepted lipid‐lowering therapy within 6 months prior to the start of DAA treatment were excluded. The patient's lipid profiles and homeostasis model assessment‐insulin resistance (HOMA‐IR) index were measured and evaluated at baseline and after 12 weeks of treatment. The SVR rate was 96.2% across all patients. The mean triglyceride level was not significantly increased after SVR. The mean total cholesterol level was significantly increased from baseline 165.2 ± 33.6 mg/dL to after SVR 184.5 ± 36.0 mg/dL (P< .0001). The mean high‐density lipoprotein cholesterol (HDLC) was significantly increased from baseline level 45.9 ± 12.3 mg/dL to after SVR 49.0 ± 12.4 mg/dL (P< .0001). The mean low‐density lipoprotein cholesterol (LDLC) was significantly increased from baseline 95.2 ± 28.3 mg/dL to after SVR 111.7 ± 31.3 (P< .0001). The HOMA‐IR had no significant change in the 294 patients without diabetes. The subgroups analysis of genotypes 1a, 1b, 2, and 6 revealed a significant increase in total cholesterol and LDLC levels following treatment. In conclusion, it was found that lipid profiles, including total cholesterol, HDLC, and LDLC levels, were significantly increased after DAA treatment for CHC patients who achieved SVR 12 with genotypes 1a, 1b, 2, and 6.