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Inducing and Characterizing Vesicular Steatosis in Differentiated HepaRG Cells
Published on: July 18, 2019
The Prevalence and Determinants of Hepatic Steatosis Assessed by Controlled Attenuation Parameter in Thai Chronic
A Sirinawasatien1, T Techasirioangkun1
1Division of Gastroenterology, Department of Medicine, Rajavithi Hospital, College of Medicine, Rangsit University, Bangkok, Thailand.
Aims:
To describe the prevalence of hepatic steatosis using a controlled attenuation parameter (CAP) and to identify the determinants associated with steatosis in Thai chronic hepatitis C patients. Patients and Methods. An observational study was conducted among consecutive chronic hepatitis C patients who underwent vibration-controlled transient elastography (VCTE, FibroScan®) with CAP and followed up at Rajavithi Hospital, Bangkok, Thailand, between June 2018 and May 2019. Hepatic steatosis (i.e., steatosis grades S1-3) was defined by the CAP cutoff value of ≥248 (dB/m). VCTE with CAP assessments and medical records were retrospectively reviewed, and the prevalence and determinants of hepatic steatosis were analyzed.
Results:
A total of 197 eligible patients, of whom 127 (64.5%) were male, were included. The mean age was 54.52 years (SD 9.49 years), and 41.1% of subjects had a body mass index ≥ 25. The prevalence of hepatic steatosis was 26.9%. The mean liver stiffness measurement (LSM) was 21.50 kPa (SD 15.58 kPa), and 61.9% of the study population had cirrhosis, which was defined as LSM ≥ 12.5 kPa. Genotype (GT) 3 was predominant at 40.1%, followed by GT1 at 38.1% and GT6 at 21.8%. The median serum hepatitis C virus viral load was 1,100,000 IU/mL (range 5,824-20,436,840). The significant determinants of hepatic steatosis were obesity (aOR 8.58 (95% CI: 3.41-21.54)) and diabetes mellitus (aOR 3.30 (95% CI: 1.24-8.78)).
Conclusion:
A large proportion of these Thai chronic hepatitis C patients (26.9%) had hepatic steatosis, which was strongly associated with host metabolic factors, e.g., obesity (BMI ≥ 25) and diabetes mellitus. These cofactors contributed to the progression of liver disease to cirrhosis and required concurrent management with antiviral therapy.
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