Abstract

Backgrounds The aim of this study was to appraise the relationship between serum fragmented cytokeratin-18(CK-18), controlled attenuation parameter (CAP), and liver steatosis assessed by ultrasound (US) in nonalcoholic fatty liver disease (NAFLD) patients. Methods Patients who underwent abdominal US were recruited, followed with measurement of CAP using Fibroscan® and serum fragmented CK-18 using enzyme-linked immunosorbent assay. The degree of liver steatosis assessed by US was categorized into mild (S1), moderate (S2), and severe (S3). Results A total of 109 patients were included in our study. CAP and fragmented CK-18 level were significantly correlated with liver steatosis grade with rs = 0.56 and 0.68, p=0.001, respectively. NAFLD Fibrosis Score was poorly correlated with liver steatosis grade (rs=-0.096, p=0.318). Using fragmented CK-18 level, area under receiver operating characteristic (AUROC) curves for S≥2 and S≥3 were excellent (0.82 and 0.84, respectively). Using CAP, AUROC curves for detection of S≥2 and S≥3 were good (0.76, 0.77, respectively). We also proposed cut-off value of CAP to detect S≥2 and S≥3 to be 263 and 319db/m, respectively, and fragmented CK-18 level to detect S≥2 and S≥3 (194 and 294 U/L, respectively). Conclusions Both the fragmented CK-18 level and the CAP, but not NAFLD Fibrosis Score, were well correlated with hepatic steatosis grade as assessed by US.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) is the liver pandemic in this 21st century, affecting 20-45% population around the world [1,2,3,4,5]

  • We found that NAFLD fibrosis score (NFS) was poorly correlated with liver steatosis grade

  • We found that higher Body mass index (BMI), waist circumference (Table 2), and liver biochemistry (ALT, AST≥35U/L) (Table 3) are associated with increased severity of liver steatosis, as assessed by US

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is the liver pandemic in this 21st century, affecting 20-45% population around the world [1,2,3,4,5]. NAFLD has been proven to cause liver fibrosis, liver cirrhosis, and hepatocellular carcinoma [6,7,8,9]. NAFLD is usually benign, it may be associated with inflammation and hepatocyte apoptosis resulting in nonalcoholic steatohepatitis (NASH) of 20–30% of subjects. One-fifth of these NASH subjects will progress to develop liver cirrhosis [13]. Liver biopsy is still the gold standard to stage liver fibrosis as it provides a multitude of information on the inflammation activity. The NAFLD fibrosis score (NFS) developed by Angulo et al utilizes six variables (age, body mass index (BMI), diabetes, aspartatetransaminase (AST), alaninetransaminase (ALT), and albumin) which are commonly available in patient’s assessment. In NASH, liver cell apoptosis and necroinflammation play a major role. Serum caspase-cleaved fragmented cytokeratin-18(CK-18) reflects the degree of apoptosis and has been shown as an independent predictor in diagnosis of International Journal of Hepatology

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