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Article

The Effects of Pangenotypic Direct-Acting Antiviral Therapy on Lipid Profiles and Insulin Resistance in Chronic Hepatitis C Patients

1
Division of Gastroenterology and Hepatology, Yuanlin Christian Hospital, Changhua 510012, Taiwan
2
Division of Gastroenterology and Hepatology, Changhua Christian Hospital, Changhua 500209, Taiwan
3
Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung 402202, Taiwan
*
Author to whom correspondence should be addressed.
Viruses 2025, 17(2), 263; https://doi.org/10.3390/v17020263
Submission received: 3 January 2025 / Revised: 10 February 2025 / Accepted: 12 February 2025 / Published: 14 February 2025
(This article belongs to the Special Issue Hepatitis Viral Infections, Pathogenesis and Therapeutics)

Abstract

:
Hepatitis C virus (HCV) eradication is usually associated with dyslipidemia. Most studies in this field have focused on genotype-specific direct-acting antivirals (DAAs), with research on pangenotypic DAAs being limited. This study examined how two pangenotypic DAA regimens, glecaprevir/pibrentasvir (GLE/PIB) and sofosbuvir/velpatasvir (SOF/VEL), affect lipid profiles and insulin resistance after viral eradication in chronic HCV patients. A total of 100 patients (57 with GLE/PIB and 43 with SOF/VEL) treated between September 2020 and January 2022 were included in the retrospective analysis. This study found a significant increase in LDL and TC levels after treatment (p < 0.001), but no significant changes in triglycerides, high-density lipoprotein, HbA1C, or the Homeostatic Model Assessment of Insulin Resistance. According to a logistic regression analysis, higher baseline LDL or TC and lower baseline glucose are predictors of the degree of increase in LDL or TC following a sustained virological response. Both pangenotypic DAA regimens significantly impact lipid profiles, particularly LDL and TC, but not insulin resistance. This study emphasizes the need for more research into the long-term metabolic effects of DAAs.

1. Introduction

Hepatitis C virus (HCV) infection can cause chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC), affecting approximately 50 million people worldwide. This infection is a major public health concern, putting a heavy disease burden on both individuals and healthcare systems [1]. HCV infection is frequently asymptomatic and progresses to a chronic condition in most patients, with diagnosis usually occurring only after the disease has advanced to more severe stages of fibrosis.
The treatment of chronic HCV infection has dramatically improved with the introduction of new direct-acting antivirals (DAAs). These DAAs have higher efficacy across all genotypes and fewer side effects than previous interferon (IFN)-based therapies. While HCV eradication significantly reduces the risk of cirrhosis and HCC, patients with advanced liver fibrosis or cirrhosis must continue to undergo regular HCC screenings even after achieving a sustained virologic response (SVR) [2,3].
Several studies have found that HCV infection causes metabolic changes such as insulin resistance (IR), metabolic syndrome, and diabetes via complex pathways [4,5]. Chronic HCV infections have been linked to hepatic steatosis and dyslipidemia [6]. According to research, eradicating HCV can improve fasting glucose, HbA1C, and IR [7]. Furthermore, studies have reported varying effects on lipid profiles: some found a decrease in total cholesterol (TC) and low-density lipoprotein (LDL) levels with an increase in triglycerides (TG) during treatment, while others found an increase in LDL and TC levels post treatment but no significant changes in TG levels [8].
Most studies exploring the effect of lipid homeostasis and IR following viral eradication have focused on genotype-specific DAAs, particularly between subgroups treated with sofosbuvir (SOF)-based versus non-SOF-based DAAs [9,10]. However, limited research has investigated the impact of lipid profiles after treatment with new pangenotypic DAAs. This study aimed to evaluate the impact of viral eradication on lipid levels and IR in HCV patients after receiving pangenotypic DAA antiviral therapy.

2. Materials and Methods

We retrospectively included patients with chronic HCV infection who received DAA therapy between September 2020 and January 2022 at Changhua Christian Hospital in Taiwan. All patients had routine outpatient follow-ups during the treatment and none were discontinued due to adverse events. Exclusion criteria included the following: (1) patients who did not complete the lipid profile or had insufficient clinical data before and after DAA therapy; and (2) incomplete DAA therapy or a lack of sustained virological response 12 weeks after treatment. The DAA regimens consisted of glecaprevir/pibrentasvir (GLE/PIB) and sofosbuvir/velpatasvir (SOF/VEL). (Figure 1).
Lipid profiles measured TC, LDL, and TG. HCV genotyping was performed on all patients. A complete blood count was taken, liver function tests were conducted, and HCV RNA levels were measured before and 12 weeks after treatment. The current study was authorized by the institutional review board (IRB No. 231011), and informed consent was waived due to the anonymization of all data.
Liver elastography, steatosis, lipid profile, fasting glucose, and insulin levels were measured before and 12 weeks after DAA therapy. The degree of liver fibrosis was determined using FibroScan® 530 compact (Echosens, Franceand) and the FIB-4 index, which was calculated from indirect serum markers. Advanced fibrosis was defined as an FIB-4 score above 3.25 [11]. Liver stiffness and steatosis were determined via transient elastography, with a measurement range of 2.5 kPa to 75 kPa, and the controlled attenuation parameter (CAP), which ranges from 100 to 400 decibels per meter (dB/m), with the FibroScan® compact 530 (Echosens, Paris, France). Insulin resistance was assessed using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), which is calculated as (fasting glucose level × fasting serum insulin level)/405 [12]. The percentage change in LDL and TC was calculated by subtracting the pretreatment value from the post-treatment value and dividing by the pretreatment value.

Statistical Analysis

Demographic and other clinical data for continuous variables are given as mean ± standard deviation, while categorical variables are given as numbers and percentages. Baseline data comparisons between the GLE/PIB and SOF/VEL groups were made using the Chi-square test or Fisher’s exact test for categorical variables, and Student’s t-test for continuous variables. The paired samples t-test was used to compare the mean values of continuous data at two different time points: baseline (T0) and 12 weeks after the completion of DAA therapy (SVR). Pearson’s correlation coefficient was used for correlation analysis. Logistic regression models were used in both univariate and multivariate analyses. Factors that were significantly associated in univariate analyses were included in the multivariate model through backward elimination. All statistical analyses were carried out using PASW Statistics version 18 (formerly SPSS; IBM, Hong Kong). A p-value below 0.05 was deemed statistically significant.

3. Results

3.1. Baseline Characteristics of Total and Subgroup Patients

Our study included 100 patients: 57 treated with GLE/PIB and 43 treated with SOF/VEL. Table 1 shows the baseline characteristics in detail. Of the 100 patients, 50 (50%) were male, with an average age of 58.6 ± 12.7 years. The majority of patients (49%) had genotype 2 HCV. The average HCV RNA level was 5.53 ± 1.2 log10 IU/mL. Additionally, 36 patients (36%) had hypertension, 12 (12%) had diabetes mellitus, and 12 (12%) had cancer, including oral cancer (n = 3), colon cancer (n = 3), breast cancer (n = 2), lung cancer (n = 2), hepatoma (n = 1), and lymphoma (n = 1). Nineteen patients (19%) had an FIB-4 score ≥ 3.25. When comparing the two subgroups (GLE/PIB and SOF/VEL), the SOF/VEL group had a higher proportion of males, higher Aspartate Transaminase (AST) levels, lower LDL and TC levels, and greater liver stiffness.

3.2. Results Before and After DAA Treatment of the Total Patients

The laboratory tests and elastography results for the 100 patients before and after HCV treatment are shown in Table 2. Liver stiffness and FIB-4 scores significantly decreased (p < 0.001), whereas CAP increased after DAA therapy (p = 0.007). After treatment, LDL and TC levels were significantly higher than before (p < 0.001). There were no significant differences in fasting glucose, insulin, HOMA-IR, HbA1c, or HDL before and after treatment. The TG level was slightly higher after treatment than before, but the difference was not statistically significant (p = 0.088).

3.3. Results Before and After DAA Treatment for Subgroups of Two Pangenotypic DAAs

Table 3 shows the analysis of the two subgroups, separated by their DAA regimens: 57 patients received glecaprevir/pibrentasvir (GLE/PIB), while 43 received sofosbuvir/velpatasvir (SOF/VEL). TC and LDL levels were significantly higher after treatment in both subgroups than before treatment, with the GLE/PIB group showing a more pronounced increase. While liver stiffness measurements significantly decreased in both groups following treatment, the controlled CAP only increased in the GLE/PIB group.

3.4. Factors Associated with the Change in LDL and TC in Entire Population

Only pretreatment fasting glucose and LDL were found to be negatively associated with the percentage change in LDL after treatment in both univariate and multivariate analyses (p = 0.005 and p = 0.007, respectively). (Table 4) The findings were similar for TC, with pretreatment fasting glucose and TC being negatively associated with the percentage change in total cholesterol after treatment in both univariate and multivariate analyses (p = 0.001 and p = 0.009, respectively) (Table 5). Figure 2 shows a negative correlation between baseline LDL and the percentage change in LDL (r = −0.273), as well as between baseline TC and the percentage change in TC (r = −0.301).

4. Discussion

This is the first study to look at the effects of two different pangenotypic DAA regimens, GLE/PIB and SOF/VEL, on lipid profiles and IR. Our results show that LDL and TC levels were increased after viral eradication by two pangenotypic DAAs, but there were no significant changes in fasting glucose, HbA1c, HOMA-IR, TG, or HDL.
HCV can increase lipid biosynthesis and lower the export of apolipoproteins via multiple mechanisms of lipid metabolism. This phenomenon is reversed after HCV is eradicated using DAAs [13]. There is some debate about which lipid profiles are affected by HCV infection. Most studies show that LDL and TC are the most commonly affected lipids following HCV eradication [6,7,8]. However, some studies show that HCV eradication by DAA therapy lowers triglycerides and raises HDL levels [14,15]. Our study found that LDL and TC levels increased after HCV eradication, which is consistent with most previous studies. Furthermore, the effects of various DAA regimens on lipid profiles have yielded inconsistent results. Inoue Takako et al. and Endo Daisuke et al. found that patients treated with sofosbuvir plus ledipasvir had higher LDL and TC levels than those treated with daclatasvir plus asunaprevir [10,16]. A review by YW Wang et al. discovered that SOF-based DAAs cause more significant increases in LDL than non-SOF-based DAAs [17]. However, our findings indicated that SOF-based (SOF/VEL) and non-SOF-based (GLE/PIB) DAAs have similar effects on lipid profiles after viral eradication. LDL and TC levels significantly increased following DAA therapy, while TG and HDL levels remained unchanged. This could be explained by the strong and comparable efficacy of both pangenotypic DAAs in eliminating HCV, resulting in similar effects on lipid profiles.
Several factors have been linked to increased levels of LDL and TC [7]. These include the absence of cirrhosis, hyperlipidemia, and a larger baseline waist circumference [18]. Additionally, higher HOMA-IR, lower AST, higher triglycerides, and a higher BMI at baseline were linked to changes in LDL levels [15,16]. In our study, the predictors of the degree of change in LDL and TC included fasting glucose and baseline LDL and TC levels. These findings are consistent with those of previous research, but more studies are needed to confirm them.
Previous research has shown that IR is closely associated with chronic hepatitis C infection, particularly in genotypes 1 and 4 [5]. DAA therapy can reverse IR in patients with chronic hepatitis C infection and improve hyperglycemia [19]. One mechanism linking HCV and IR is that the HCV core protein induces serine phosphorylation of the insulin receptor substrate protein. This process inhibits phosphatidylinositol-4,5-bisphosphate 3-kinase signaling, which is followed by a decrease in protein kinase B and tuberous sclerosis complex 1/2 signaling [20,21]. Our study found no significant difference in fasting glucose, HbA1C, or HOMA-IR levels between baseline and post-treatment. However, there was a trend of mild decreases in HbA1C and HOMA-IR following DAA treatment. One possible explanation is that our study’s baseline levels of fasting glucose, HbA1C, and HOMA-IR were lower than those in other studies, resulting in no significant differences [19,22].
This study has several limitations. First, the sample size was small because we only included patients who had complete data on fasting glucose, insulin, HbA1C, and lipid profiles before and after DAA treatment. Because this was a real-world retrospective study, less than half of the patients who were initially included were analyzed. Consequently, some older patients or those with multiple comorbidities were excluded, which could explain why some parameters showed no significant differences. Second, the follow-up period in our study was brief. Researchers discovered that LDL and TC levels remained elevated even two years after DAA therapy. However, most studies observed a reduction in carotid atherosclerosis after HCV eradication [7]. In addition, previous studies have shown that HCV infection can increase the risk of cardiovascular disease, while antiviral therapy can lower this risk [23,24]. The possible mechanism is multifactorial, involving lipid disturbances, vascular injury, oxidative stress, and endothelial dysfunction. Therefore, more research is needed to understand the long-term impact of pangenotypic DAAs and their influence on clinical outcomes.

5. Conclusions

Treatment with the two pangenotypic DAAs increased LDL and TC levels. Our study found no significant differences in glucose, HbA1c, HOMA-IR, or TG levels before or after DAA therapy. The only significant predictors of an increase in LDL or TC levels at SVR12 were lower baseline fasting glucose and lower LDL or TC levels.

Author Contributions

Conceptualization, H.-H.Y.; data curation, Y.-C.H.; formal analysis, Y.-C.H. and S.-P.H.; methodology, S.-P.H. and P.-Y.S.; supervision, P.-Y.S.; writing—original draft, M.-Y.K.; writing—review and editing, P.-Y.S. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by Changhua Christian Hospital (113-CCH-IRP-016).

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of Changhua Christian Hospital (IRB No. 231011).

Informed Consent Statement

Patient consent was waived because all the data were anonymized.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author (P.S) upon reasonable request.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

HCVHepatitis C virus
LDLLow-density lipoprotein
TCTotal cholesterol
DAADirect-acting antiviral
GLEGlecaprevir
PIBPibrentasvir
SOFSofosbuvir
VELVelpatasvir
HCCHepatocellular carcinoma
IFNInterferon
SVRSustained virologic response
IRInsulin resistance
TGTriglycerides
HOMA-IRHomeostatic model assessment of insulin resistance
ASTAspartate transaminase
ALTAlanine transferase
BMIBody mass index
HbHemoglobin
INRInternational normalized ratio
FIB-4Fibrosis-4
LSMLiver stiffness measurement
CAPControlled Attenuation Parameter
HDLHigh-density lipoprotein
GTGenotype

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Figure 1. The flowchart of participants included and excluded from the study.
Figure 1. The flowchart of participants included and excluded from the study.
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Figure 2. The correlation between pretreatment LDL and TC levels and the percentage change of (A) LDL (ΔLDL(%)) and (B) TC (ΔTC(%)).
Figure 2. The correlation between pretreatment LDL and TC levels and the percentage change of (A) LDL (ΔLDL(%)) and (B) TC (ΔTC(%)).
Viruses 17 00263 g002
Table 1. The baseline characteristics of the patients in the study group.
Table 1. The baseline characteristics of the patients in the study group.
VariableTotal (N = 100)GLE/PIB (N = 57)SOF/VEL (N = 43)p-Value
Age, yrs58.6 ± 12.757.1 ± 11.360.6 ± 14.20.173
Gender (Male), n (%)50 (50.0%)22 (38.6%)28 (65.1%)0.009
Height, cm160.6 ± 9159.9 ± 9.9161.4 ± 7.70.429
Body weight, kg64.6 ± 12.465.7 ± 14.163.2 ± 9.70.306
BMI, kg/m224.96 ± 3.6525.47 ± 3.724.29 ± 3.520.111
DM, n (%)12 (12.0%)6 (10.5%)6 (14.0%)0.602
Hypertension, n (%)36 (36.0%)18 (31.6%)18 (41.9%)0.289
HCV RNA, log10 IU/mL5.53 ± 1.25.74 ± 1.065.25 ± 1.340.055
Genotype, n (%) 0.566
1/1a/1b37 (37.0%)24 (42.1%)13 (30.2%)
249 (49.0%)24 (42.1%)25 (58.1%)
34 (4.0%)2 (3.5%)2 (4.7%)
64 (4.0%)3 (5.3%)1 (2.3%)
Indeterminate6 (6.0%)4 (7.0%)2 (4.7%)
GOT (AST), U/L69.2 ± 94.447.1 ± 27.898.5 ± 135.70.018
GPT (ALT), U/L95.8 ± 198.564.1 ± 44.8137.9 ± 2950.111
Platelet count, 109/L 203.8 ± 63.6208.6 ± 62.8197.4 ± 64.70.386
Hb, g/dl13.9 ± 1.714 ± 1.513.8 ± 1.80.514
INR1 ± 0.150.99 ± 0.191 ± 0.070.664
Bilirubin-T, mg/dl0.72 ± 0.360.69 ± 0.210.77 ± 0.490.309
Creatinine, mg/dl0.99 ± 0.940.91 ± 0.841.09 ± 1.060.345
Albumin, g/dl4.2 ± 0.34.2 ± 0.34.1 ± 0.30.146
FIB-42.78 ± 3.732.43 ± 4.173.23 ± 3.030.293
Glucose (AC), mg/dL103.5 ± 21.6104.3 ± 19.6102.4 ± 24.10.665
Insulin (AC), μIU/mL9.79 ± 8.958.9 ± 7.8411.57 ± 10.780.215
HOMA-IR2.69 ± 3.22.3 ± 2.123.47 ± 4.620.228
HbA1c, %5.8 ± 0.85.7 ± 0.95.8 ± 0.80.65
HDL-cholesterol, mg/dL47.2 ± 15.548.5 ± 16.445.4 ± 14.30.318
LDL-cholesterol, mg/dL93.4 ± 29.398.8 ± 3286.7 ± 24.30.044
Total cholesterol, mg/dL163 ± 36.9171.3 ± 38.2152 ± 32.50.009
Triglyceride, mg/dL118.7 ± 81.2126.4 ± 99.6108.5 ± 46.20.234
Baseline Fibrosis (FIB-4), n (%) 0.003
F0-281 (81.0%)52 (91.2%)29 (67.4%)
F3-4 (FIB-4 ≥ 3.25)19 (19.0%)5 (8.8%)14 (32.6%)
LSM using FibroScan, kPa8.8 ± 77.2 ± 311.5 ± 10.40.037
CAP using FibroScan, dB/m228 ± 43233 ± 46221 ± 380.225
Table 2. The results of 100 patients before and after HCV treatment with direct-acting antivirals. (Data are expressed as mean ± standard deviation.).
Table 2. The results of 100 patients before and after HCV treatment with direct-acting antivirals. (Data are expressed as mean ± standard deviation.).
VariableTime PointValuep-Value
LSM using FibroScan, kPaT08.699 ± 6.289<0.001
SVR6.561 ± 4.026
CAP using FibroScan, dB/mT0227.522 ± 39.1260.007
SVR241.657 ± 50.303
FIB-4T02.776 ± 3.7290.021
SVR2.024 ± 1.424
Fasting glucose, mg/dLT0103.5 ± 21.5680.251
SVR109.65 ± 49.937
Fasting insulin, μIU/mLT010.06 ± 9.070.719
SVR9.66 ± 6.43
HOMA-IRT02.77 ± 3.260.571
SVR2.56 ± 1.83
HbA1c, %T05.779 ± 0.8410.162
SVR5.711 ± 0.761
HDL-cholesterol, mg/dLT047.19 ± 15.5390.440
SVR48 ± 13.924
LDL-cholesterol, mg/dLT093.41 ± 29.343<0.001
SVR106.777 ± 36.472
Total cholesterol, mg/dLT0163.02 ± 36.93<0.001
SVR177.33 ± 41.738
Triglyceride, mg/dLT0118.7 ± 81.240.088
SVR129.83 ± 98.46
Body weight, kgT065.1 ± 13.40.288
SVR64.7 ± 13.3
BMI, kg/m2T025.07 ± 3.570.192
SVR24.88 ± 3.63
Table 3. Results before and after DAA treatment for subgroups of two pangenotypic DAAs (GLE/PIB and SOF/VEL).
Table 3. Results before and after DAA treatment for subgroups of two pangenotypic DAAs (GLE/PIB and SOF/VEL).
GLE/PIB (N = 57)SOF/VEL (N = 43)
VariableTime PointValuep-ValueVariableTime PointValuep-Value
LSM using FibroScan,
kPa
T07.467 ± 3.141<0.001LSM using FibroScan,
kPa
T010.904 ± 9.3580.001
SVR5.802 ± 2.058SVR7.921 ± 5.981
CAP using FibroScan, dB/mT0230.186 ± 40.90.014CAP using FibroScan, dB/mT0222.75 ± 36.0710.241
SVR246.605 ± 53.344SVR232.792 ± 44.014
FIB-4T02.434 ± 4.1740.215FIB-4T03.23 ± 3.0290.001
SVR1.77 ± 1.032SVR2.361 ± 1.776
Glucose (AC), mg/dLT0104.316 ± 19.6240.953Glucose (AC), mg/dLT0102.419 ± 24.1020.250
SVR104.421 ± 15.004SVR116.581 ± 74.106
Insulin (AC), μIU/mLT09.08 ± 7.990.793Insulin (AC)T011.97 ± 10.810.437
SVR9.4 ± 6.36SVR10.18 ± 6.67
HOMA-IRT02.35 ± 2.170.717HOMA-IRT03.6 ± 4.670.353
SVR2.47 ± 1.8SVR2.73 ± 1.9
HbA1c, %T05.746 ± 0.8630.199HbA1c, %T05.823 ± 0.8180.46
SVR5.675 ± 0.613SVR5.758 ± 0.927
HDL-cholesterol, mg/dLT048.544 ± 16.3840.487HDL-cholesterol, mg/dLT045.395 ± 14.3330.715
SVR49.526 ± 12.696SVR45.977 ± 15.321
LDL-cholesterol, mg/dLT098.8 ± 32<0.001LDL-cholesterol, mg/dLT086.698 ± 24.340.042
SVR116.5 ± 38SVR94.53 ± 30.768
Total cholesterol, mg/dLT0171.3 ± 38.2<0.001Total cholesterol, mg/dLT0152.047 ± 32.4670.025
SVR188.9 ± 42.8SVR161.977 ± 35.242
Triglyceride, mg/dLT0126.404 ± 99.630.306Triglyceride, mg/dLT0108.488 ± 46.2030.109
SVR136.579 ± 113.994SVR120.884 ± 73.355
Body weight, kgT066.482 ± 14.7730.578Body weight, kgT062.5 ± 10.40.361
SVR66.271 ± 14.879SVR61.8 ± 9.6
BMI, kg/m2T025.485 ± 3.7620.773BMI, kg/m2T024.33 ± 3.120.098
SVR25.436 ± 3.801SVR23.89 ± 3.13
Table 4. Univariate and multivariate analyses of factors associated with the percentage of change in LDL-cholesterol.
Table 4. Univariate and multivariate analyses of factors associated with the percentage of change in LDL-cholesterol.
VariablesUnivariateMultivariate
B95% CI for Bp-ValueB95% CI for Bp-Value
LowerUpperLowerUpper
Age−0.004 −0.009 0.000 0.068
Gender−0.044 −0.160 0.071 0.449
BMI−0.008 −0.025 0.008 0.335
DM−0.036 −0.212 0.140 0.687
HT−0.088 −0.207 0.031 0.145
CANCER−0.057 −0.240 0.126 0.536
HCV RNA (log10)0.021 −0.027 0.069 0.396
Genotype
Non-GT1--------
GT1−0.004 −0.125 0.116 0.942
GOT (AST)0.0001 −0.001 0.001 0.797
GPT (ALT)0.0001 0.000 0.000 0.575
Platelet count−0.001 −0.001 0.000 0.251
Hb−0.004 −0.038 0.031 0.842
I.N.R.−0.218 −0.605 0.169 0.267
Bilirubin-T−0.168 −0.325 −0.010 0.037
Creatinine0.026 −0.035 0.087 0.397
Albumin−0.088 −0.256 0.081 0.305
Glucose (AC)−0.004 −0.007 −0.002 0.002 −0.004−0.006−0.0010.005
Insulin (AC)−0.002 −0.009 0.006 0.635
HbA1c, %−0.024 −0.093 0.044 0.480
Cholesterol−0.001 −0.003 0.000 0.171
LDL-cholesterol−0.003 −0.005 −0.001 0.007 −0.003−0.004−0.0010.007
HDL-cholesterol0.003 −0.001 0.006 0.150
Triglyceride0.00004 −0.001 0.001 0.942
DAA regimen
GLE/PIB--------
SOF/VEL−0.093 −0.208 0.023 0.113
LSM0.0001 −0.009 0.009 0.985
CAP−0.001 −0.003 0.001 0.194
FIB-40.003 −0.012 0.019 0.677
Table 5. Univariate and multivariate analyses of factors associated with the percentage change in total cholesterol.
Table 5. Univariate and multivariate analyses of factors associated with the percentage change in total cholesterol.
VariablesUnivariateMultivariate
B95% CI for Bp-ValueB95% CI for Bp-Value
LowerUpperLowerUpper
Age−0.0004 −0.003 0.002 0.784
Gender−0.014 −0.084 0.056 0.686
BMI−0.005 −0.014 0.005 0.352
DM−0.009 −0.117 0.098 0.865
HT−0.025 −0.098 0.047 0.487
CANCER−0.026 −0.133 0.082 0.637
HCV RNA(log10)0.009 −0.020 0.038 0.537
Genotype
Non-GT1--------
GT10.036 −0.036 0.108 0.327
GOT (AST)−0.00001 0.000 0.000 0.974
GPT (ALT)0.00002 0.000 0.000 0.857
Platelet count−0.00027 −0.001 0.000 0.323
Hb−0.001 −0.022 0.020 0.937
I.N.R.−0.327 −0.555 −0.099 0.005
Bilirubin-T−0.070 −0.167 0.028 0.159
Creatinine0.016 −0.022 0.053 0.409
Albumin−0.026 −0.129 0.077 0.614
Glucose (AC)−0.003 −0.004 −0.001 <0.001−0.002−0.004−0.0010.001
Insulin (AC)−0.001 −0.005 0.003 0.487
HbA1c, %−0.026 −0.067 0.016 0.222
Cholesterol−0.001 −0.002 −0.001 0.002 −0.001−0.0020.0000.009
LDL-cholesterol−0.001 −0.002 0.000 0.126
HDL-cholesterol−0.002 −0.004 0.001 0.138
Triglyceride−0.0004 −0.001 0.000 0.039
DAA regimen
GLE/PIB--------
SOF/VEL−0.034 −0.104 0.036 0.339
LSM0.001 −0.004 0.007 0.584
CAP−0.001 −0.001 0.000 0.197
FIB-40.003 −0.006 0.012 0.532
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Ko, M.-Y.; Hsu, Y.-C.; Yen, H.-H.; Huang, S.-P.; Su, P.-Y. The Effects of Pangenotypic Direct-Acting Antiviral Therapy on Lipid Profiles and Insulin Resistance in Chronic Hepatitis C Patients. Viruses 2025, 17, 263. https://doi.org/10.3390/v17020263

AMA Style

Ko M-Y, Hsu Y-C, Yen H-H, Huang S-P, Su P-Y. The Effects of Pangenotypic Direct-Acting Antiviral Therapy on Lipid Profiles and Insulin Resistance in Chronic Hepatitis C Patients. Viruses. 2025; 17(2):263. https://doi.org/10.3390/v17020263

Chicago/Turabian Style

Ko, Meng-Yu, Yu-Chung Hsu, Hsu-Heng Yen, Siou-Ping Huang, and Pei-Yuan Su. 2025. "The Effects of Pangenotypic Direct-Acting Antiviral Therapy on Lipid Profiles and Insulin Resistance in Chronic Hepatitis C Patients" Viruses 17, no. 2: 263. https://doi.org/10.3390/v17020263

APA Style

Ko, M.-Y., Hsu, Y.-C., Yen, H.-H., Huang, S.-P., & Su, P.-Y. (2025). The Effects of Pangenotypic Direct-Acting Antiviral Therapy on Lipid Profiles and Insulin Resistance in Chronic Hepatitis C Patients. Viruses, 17(2), 263. https://doi.org/10.3390/v17020263

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