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Dynamic change of metabolic dysfunction-associated steatotic liver disease in patients with hepatitis C virus infection after achieving sustained virologic response with direct-acting antivirals

  • Original Article―Liver, Pancreas, and Biliary Tract
  • Published:
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Abstract

Background

Information on the dynamics of metabolic dysfunction-associated steatotic liver disease (MASLD) among hepatitis C virus patients achieving sustained virologic response (SVR12) with direct-acting antivirals (DAAs) is limited.

Methods

We enrolled 1512 eligible participants in this prospective study. MASLD was defined by a controlled attenuation parameter (CAP) of ≥248 dB/m utilizing vibration-controlled transient elastography in conjunction with presence of  ≥1 cardiometabolic risk factor. The distribution of MASLD and the changes in CAP were evaluated before treatment and at SVR12. Forward stepwise logistic regression analyses were performed to determine factors significantly associated with the regression or emergence of MASLD.

Results

The prevalence of MASLD decreased from 45.0% before treatment to 36.1% at SVR12. Among 681 participants with MASLD before treatment, 144 (21%) exhibited MASLD regression at SVR12. Conversely, among 831 participants without MASLD before treatment, 9 (1.1%) developed MASLD at SVR12. Absence of type 2 diabetes (T2D) [odds ratio (OR): 1.73, 95% confidence interval (CI): 1.13–2.65, p = 0.011], age > 50 years (OR: 1.73, 95% CI: 1.11–2.68, p = 0.015), and alanine transaminase (ALT) ≤ 2 times the upper limit of normal (ULN) (OR: 1.56; 95% CI: 1.03–2.37, p = 0.035) were associated with the regression of MASLD. Presence of T2D was associated with the emergence of MASLD (OR: 5.83, 95% CI: 1.51–22.56, p = 0.011).

Conclusions

The prevalence of MASLD decreased after achieving SVR12 with DAAs. Patients with pre-existing T2D showed a diminished probability of MASLD regression and a heightened risk of MASLD emergence post-SVR12.

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Abbreviations

DAA:

Direct-acting antiviral

HCV:

Hepatitis C virus

SVR12 :

Sustained virologic response

NAFLD:

Non-alcoholic fatty liver disease

NASH:

Non-alcoholic steatohepatitis

IR:

Insulin resistance

T2D:

Type 2 diabetes

HCC:

Hepatocellular carcinoma

MASLD:

Metabolic dysfunction-associated steatotic liver disease

MASH:

Metabolic dysfunction-associated steatohepatitis

MS:

Metabolic syndrome

NIT:

Noninvasive test

VCTE:

Vibration-controlled transient elastography

CAP:

Controlled attenuation parameter

MRI:

Magnetic resonance imaging

PDFF:

Proton density fat fraction

IFN:

Interferon

RNA:

Ribonucleic acid

LLOQ:

Lower limit of quantification

dB:

Decibel

CMRF:

Cardiometabolic risk factor

BMI:

Body mass index

HbA1c:

Glycosylated hemoglobin

HTN:

Hypertension

HDL-C:

High-density lipoprotein-cholesterol

HBV:

Hepatitis B virus

HIV:

Human immunodeficiency virus

LSM:

Liver stiffness measurement

SLD:

Steatotic liver disease

INR:

International normalized ratio

AST:

Aspartate transaminase

ALT:

Alanine transaminase

FIB-4:

Fibrosis index based on four parameters

HBsAg:

Hepatitis B surface antigen

kPa:

Kilo Pascal

ULN:

Upper limit of normal

IQR:

Interquartile range

OR:

Odds ratio

CI:

Confidence interval

SREBP:

Sterol regulatory element-binding protein

LDL-C:

Low-density lipoprotein-cholesterol

VLDL-C:

Very low-density lipoprotein-cholesterol

MTP:

Microsomal triglyceride transport protein

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Acknowledgements

The authors thank Hui-Ju Lin and Pin-Chin Huang for clinical data management; the 7th Core Lab of the National Taiwan University Hospital, and the 1st Common Laboratory of the National Taiwan University Hospital, Yun-Lin Branch, for the instrumental and technical support.

Funding

The study was supported by National Science and Technology Council, Taiwan (NSTC 112-2314-B-002-131-MY3) and National Taiwan University Hospital (112-IF0004).

Author information

Author notes

  1. Chen-Hua Liu and Yu-Ping Chang contributed equally to this work.

Authors and Affiliations

  1. Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan

    Chen-Hua Liu, Yu-Ping Chang, Tung-Hung Su, Tai-Chung Tseng, Chun-Jen Liu, Pei-Jer Chen & Jia-Horng Kao

  2. Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan

    Chen-Hua Liu, Tung-Hung Su, Tai-Chung Tseng, Chun-Jen Liu, Pei-Jer Chen & Jia-Horng Kao

  3. Department of Internal Medicine, National Taiwan University Hospital, Yun-Lin Branch, Yunlin, Taiwan

    Chen-Hua Liu & Yu-Jen Fang

  4. Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan

    Pin-Nan Cheng

  5. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Ditmanson Medical Foundation Chiayi Christian Hospital, Chiayi, Taiwan

    Chi-Yi Chen

  6. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan

    Wei-Yu Kao

  7. Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

    Wei-Yu Kao

  8. TMU Research Center for Digestive Medicine, Taipei Medical University, Taipei, Taiwan

    Wei-Yu Kao

  9. Taipei Cancer Center, Taipei Medical University, Taipei, Taiwan

    Wei-Yu Kao

  10. Department of Gastroenterology, Taipei City Hospital, Ren-Ai Branch, Taipei, Taiwan

    Chih-Lin Lin

  11. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan

    Sheng-Shun Yang

  12. School of Medicine, Chung Shan Medical University, Taichung, Taiwan

    Sheng-Shun Yang

  13. Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan

    Sheng-Shun Yang

  14. Division of Gastroenterology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan

    Yu-Lueng Shih

  15. Center for Digestive Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan

    Cheng-Yuan Peng

  16. School of Medicine, China Medical University, Taichung, Taiwan

    Cheng-Yuan Peng

  17. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan

    Ming-Chang Tsai

  18. Institute of Medicine, School of Medicine, Chung Shan Medical University, Taichung, Taiwan

    Ming-Chang Tsai

  19. Department of Internal Medicine, National Taiwan University Hospital Bei-Hu Branch, Taipei, Taiwan

    Shang-Chin Huang

  20. Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan

    Tai-Chung Tseng & Jia-Horng Kao

  21. Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, 7 Chung-Shan South Road, Taipei, 10002, Taiwan

    Chun-Jen Liu, Pei-Jer Chen & Jia-Horng Kao

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  1. Chen-Hua Liu
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  2. Yu-Ping Chang
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  3. Yu-Jen Fang
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Contributions

Conceptualization: Chen-Hua Liu, Jia-Horng Kao; Data curation: Chen-Hua Liu; Formal analysis: Chen-Hua Liu, Yu-Ping Chang, Jia-Horng Kao; Funding acquisition: Chen-Hua Liu; Investigation: Chen-Hua Liu, Yu-Ping Chang, Yu-Jen Fang, Pin-Nan Cheng, Chi-Yi Chen, Wei-Yu Kao, Chih-Lin Lin, Sheng-Shun Yang, Yu-Lueng Shih, Cheng-Yuan Peng, Ming-Chang Tsai, Shang-Chin Huang, Tung-Hung Su, Tai-Chung Tseng, Chun-Jen Liu, Pei-Jer Chen, Jia-Horng Kao; Methodology: Chen-Hua Liu, Yu-Ping Chang; Project administration: Chen-Hua Liu, Yu-Ping Chang, Jia-Horng Kao; Resources: Chen-Hua Liu, Yu-Ping Chang, Yu-Jen Fang, Pin-Nan Cheng, Chi-Yi Chen, Wei-Yu Kao, Chih-Lin Lin, Sheng-Shun Yang, Yu-Lueng Shih, Cheng-Yuan Peng, Ming-Chang Tsai, Shang-Chin Huang, Tung-Hung Su, Tai-Chung Tseng, Chun-Jen Liu, Pei-Jer Chen, Jia-Horng Kao; Software: Chen-Hua Liu; Supervision: Jia-Horng Kao; Validation: Chen-Hua Liu, Yu-Ping Chang; Visualization: Chen-Hua Liu, Yu-Ping Chang; Writing – original draft: Chen-Hua Liu, Yu-Ping Chang, Jia-Horng Kao; Writing – review & editing: Chen-Hua Liu, Yu-Ping Chang, Yu-Jen Fang, Pin-Nan Cheng, Chi-Yi Chen, Wei-Yu Kao, Chih-Lin Lin, Sheng-Shun Yang, Yu-Lueng Shih, Cheng-Yuan Peng, Ming-Chang Tsai, Shang-Chin Huang, Tung-Hung Su, Tai-Chung Tseng, Chun-Jen Liu, Pei-Jer Chen, Jia-Horng Kao.

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Supplementary file1 (DOCX 97 KB)

535_2024_2101_MOESM2_ESM.jpg

Supplementary Figure 1. Change in CAP level before treatment and at SVR12. The horizontal lines within the boxes are the median levels. The tops and bottoms of the boxes are the first and the third quartiles. The tops and the bottoms of the horizontal lines are the upper and lower whiskers. The circles denote mild outliers and the asterisks denote extreme outliers. The median levels of change in CAP from pre-treatment to SVR12 were (A) −8 dB/m (IQR: −14 to −2 dB/m) in the entire study population; (B) −8 dB/m (IQR: −15 to −3 dB/m) in participants with MASLD before treatment; (C) −8 dB/m (IQR: −13 to −2 dB/m) in participants without MASLD before treatment. CAP, controlled attenuation parameter, IQR, interquartile range; dB, decibel (JPG 381 KB)

535_2024_2101_MOESM3_ESM.jpg

Supplementary Figure 2. Change in CAP level among participants with different patterns of MASLD evolution before and after treatment. The horizontal lines within the boxes are the median levels. The tops and the bottoms of the boxes are the first and the third quartiles. The tops and the bottoms of the horizontal lines are the upper and the lower whiskers. The circles denote mild outliers and the asterisks denote extreme outliers. The median levels of change in CAP from pre-treatment to SVR12 were (A) −6 dB/m (IQR: −13 to −2 dB/m) in Group 1; (B) −16 dB/m (IQR: −32 to 11 dB/m) in Group 2; (C) −8 dB/m (IQR: −13 to −2 dB/m) in Group 3; (D) 31 dB/m (IQR: 7–64 dB/m) in Group 4. The p values were < 0.001 between Group 1 and Group 2, and between Group 3 and Group 4. CAP, controlled attenuation parameter, IQR, interquartile range; dB, decibel (JPG 54 KB)

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Liu, CH., Chang, YP., Fang, YJ. et al. Dynamic change of metabolic dysfunction-associated steatotic liver disease in patients with hepatitis C virus infection after achieving sustained virologic response with direct-acting antivirals. J Gastroenterol (2024). https://doi.org/10.1007/s00535-024-02101-2

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