Angiotensin-converting enzyme for noninvasive assessment of liver fibrosis in autoimmune hepatitis.

There are no validated noninvasive markers of liver fibrosis in autoimmune hepatitis (AIH). An activated renin-angiotensin system (RAS) and its key element angiotensin-converting enzyme (ACE) have been implicated in the pathogenesis of hepatic fibrogenesis. We aimed to study the assumed role of activated RAS in the fibrogenic process and whether the serum concentration of ACE can predict different fibrosis stages in AIH. Serum samples of 73 consecutive patients who were diagnosed with AIH were analysed for ACE concentration. All patients underwent a liver biopsy. Serum ACE levels increased significantly for each fibrosis score. The median ACE was 45 U/l in patients with fibrosis score I, 54 U/l in patients with fibrosis score II, 68 U/l in patients with fibrosis score III and 87 U/l in patients with fibrosis score IV. For significant fibrosis (≤F2), a 56 U/l cut-off value of ACE had 95.5% sensitivity and 74.5% specificity, and receiver-operating characteristic curves showed an area under the curve (AUC) of 0.89. For advanced fibrosis (≤F3), a 64 U/l cut-off level of ACE had 85.2% sensitivity and 94.8% specificity, and AUC was 0.91. For cirrhosis, a 68 U/l cut-off level of ACE had 100% sensitivity and 84.4% specificity, and AUC was 0.95. Our results suggest that activated RAS may sustain hepatic fibrogenesis in AIH. Measurement of serum ACE offers an easy, accurate and inexpensive noninvasive method that differentiates significant from nonsignificant liver fibrosis in AIH. Blockade of RAS may exert beneficial effects on fibrosis progression in AIH.