Abstract
Sustained virological response (SVR) rates have increased remarkably since the introduction of direct-acting antiviral agents (DAAs) for chronic hepatitis C. Autotaxin (ATX) is a secreted enzyme converting lysophosphatidylcholine to lysophosphatidic acid and a newly established biomarker for liver fibrosis. Interferon-free DAA regimens for chronic hepatitis C could improve liver stiffness in SVR patients according to several non-invasive evaluation methods, but the clinical response and significance of ATX in this context have not yet been defined. We therefore investigated sequential serum ATX levels at baseline, 4 weeks after the start of treatment, and 24 weeks after treatment in 159 hepatitis C virus (HCV)-infected patients who received DAA therapy. Other non-invasive fibrosis markers (aspartate aminotransferase-to-platelet ratio and FIB-4 index) were examined as well. Baseline median ATX levels were comparable between the 144 patients who achieved a SVR and the 15 who did not (1.54 vs. 1.62 mg/L), but median ATX levels became significantly decreased during and after DAA therapy in the SVR group only (from 1.54 to 1.40 and 1.31 mg/L, respectively; P < 0.001). ATX was significantly decreased between baseline and 4 weeks of treatment in overall, male, and female SVR patients (all P < 0.001). In subjects with low necroinflammatory activity in the liver (i.e., alanine aminotransferase < 30 U/L), ATX levels were significantly reduced from baseline to 4 weeks of treatment and remained low (P < 0.001) in patients with a SVR. Thus, interferon-free DAA therapy was associated with a significant decrease in serum ATX levels in patients achieving a SVR, suggesting early regression of liver fibrosis in addition to inflammation treatment.
Highlights
Persistent hepatitis C virus (HCV) infection develops into chronic hepatitis and leads to cirrhosis and hepatocellular carcinoma (HCC) [1, 2]
We detected no significant differences between patients with and without a Sustained virological response (SVR) in relation to clinical background (Table 2)
Baseline serum ATX levels did not differ between the SVR and non-SVR groups (1.54 vs. 1.62 mg/L; P = 0.967), nor were remarkable differences seen for FIB-4 index or APRI
Summary
Persistent hepatitis C virus (HCV) infection develops into chronic hepatitis and leads to cirrhosis and hepatocellular carcinoma (HCC) [1, 2]. Accumulating evidence has indicated that IFN-free DAA therapy improves liver fibrosis according to several non-invasive evaluation methods [7,8,9,10,11,12]. Serum ATX is correlated with liver fibrosis and represents a new non-invasive indicator of hepatic status [18,19,20,21,22,23]. Changes in ATX have been studied in small cohorts of HCV-infected patients receiving IFN-free DAA therapy [24], its ability to reflect fibrosis improvement remains unknown. This study assessed the sequential changes in serum ATX levels for evaluating liver fibrosis in patients with chronic hepatitis C before, during, and after IFNfree DAA therapy
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