# Longitudinal Changes in Lipid Profile After Sustained Virological Response in Patients with Chronic Hepatitis C Treated with Direct-Acting Antivirals

**Authors:** Oana Koppandi, Bogdan Miutescu, Iulia Ratiu, Alexandru Popa, Camelia Nica, Eyad Gadour, Bogdan Dan Totolici, Raluca Lupusoru, Ana Maria Ghiuchici, Eftimie Miutescu

PMC · DOI: 10.3390/healthcare14040486 · Healthcare · 2026-02-14

## TL;DR

Curing hepatitis C with direct-acting antivirals leads to long-term increases in cholesterol and LDL, which remain stable over time and are not linked to weight changes.

## Contribution

This study provides real-world evidence of sustained lipid changes after hepatitis C cure, independent of body mass index.

## Key findings

- Total cholesterol and LDL-C increased after HCV cure and stabilized over time.
- Lipid changes occurred regardless of significant BMI changes or fibrosis stage.
- HDL-C and triglycerides showed minimal or inconsistent changes.

## Abstract

What are the main findings?
Long-term follow-up after HCV cure revealed sustained increases in total cholesterol and LDL-C, with stabilization over time.Lipid changes after SVR occurred independently of major changes in body mass index and were consistent across fibrosis stages.

Long-term follow-up after HCV cure revealed sustained increases in total cholesterol and LDL-C, with stabilization over time.

Lipid changes after SVR occurred independently of major changes in body mass index and were consistent across fibrosis stages.

What are the implications of the main findings?
Metabolic monitoring should be considered an integral part of post-SVR follow-up in patients cured of chronic hepatitis C.Awareness of post-cure lipid changes may help optimize cardiovascular risk assessment in the growing population of HCV-cured patients.

Metabolic monitoring should be considered an integral part of post-SVR follow-up in patients cured of chronic hepatitis C.

Awareness of post-cure lipid changes may help optimize cardiovascular risk assessment in the growing population of HCV-cured patients.

Background: Direct-acting antiviral (DAA) therapy has transformed chronic hepatitis C virus (HCV) infection into a curable disease. Beyond viral eradication, increasing attention has been directed toward metabolic changes following sustained virological response (SVR), particularly alterations in lipid metabolism. This study aimed to assess the long-term evolution of lipid parameters after HCV cure in a real-world clinical cohort. Methods: We conducted a prospective, single-center observational study including 85 patients with chronic HCV infection who achieved SVR after DAA therapy. Lipid parameters, including total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides, were assessed at baseline and during post-SVR follow-up at 24, 48, and 96 weeks. Body mass index (BMI) and non-invasive fibrosis indices were also evaluated. Longitudinal changes were analyzed using mixed-effects models. Results: Total cholesterol increased from 157.7 ± 35.6 mg/dL at baseline to 179.6 ± 42.9 mg/dL at SVR 24 and further to 189.0 ± 40.3 mg/dL at SVR 48, stabilizing at 177.7 ± 38.3 mg/dL at SVR 96. LDL-C showed a similar trajectory from 94.6 ± 30.8 mg/dL at baseline to 107.5 ± 33.3 mg/dL at SVR 24, further raising to 115.7 ± 36.2 mg/dL at SVR48, and 111.8 ± 39.5 mg/dL at SVR 96. HDL-C showed minimal change, while triglycerides demonstrated greater interindividual variability without a consistent population-level trend. BMI remained stable over follow-up (26.6 ± 4.7 to 27.6 kg/m2). Linear mixed-effects models confirmed a significant effect of time after SVR on total cholesterol and LDL-C (p < 0.05). Conclusions: In this real-world cohort, HCV cure with DAA therapy was associated with sustained long-term changes in lipid metabolism, characterized by increases in total cholesterol and LDL-C independent of major weight changes. These findings support the importance of continued metabolic monitoring after SVR, particularly in patients with additional cardiometabolic risk factors.

## Full-text entities

- **Diseases:** metabolic dysfunction (MESH:D008659), chronic obstructive pulmonary disease (MESH:D029424), weight gain (MESH:D015430), Liver cirrhosis (MESH:D008103), chronic kidney disease (MESH:D051436), Chronic HCV infection (MESH:D019698), dyslipidemia (MESH:D050171), injury to (MESH:D014947), liver disease (MESH:D008107), hepatic inflammation (MESH:D007249), F4 fibrosis (MESH:D005355), Cardiometabolic Comorbidity (MESH:D024821), Chronic (MESH:D002908), HIV (MESH:D015658), HCC (MESH:D006528), type 2 diabetes mellitus (MESH:D003924), heart failure (MESH:D006333), infected (MESH:D007239), atrial fibrillation (MESH:D001281), ischemic heart disease (MESH:D017202), hypertension (MESH:D006973), co-infection with human immunodeficiency virus (MESH:D060085), HCV infection (MESH:D006526)
- **Chemicals:** Cholesterol (MESH:D002784), Triglyceride (MESH:D014280), alcohol (MESH:D000438), Lipid (MESH:D008055), DAAs (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC12940491/full.md

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Source: https://tomesphere.com/paper/PMC12940491