Clinicopathological characteristics of serum amyloid A‐positive hepatocellular neoplasms/nodules arising in alcoholic cirrhosis

Aims To characterize serum amyloid A ( SAA )‐positive hepatocellular neoplasms/nodules arising in alcoholic cirrhosis, which are detected as hypervascular hepatocellular nodules resembling hepatocellular carcinoma on imaging. Methods and results Fifty‐three hepatocellular nodules were examined with immunostaining for SAA , glutamine synthetase and glypican‐3 in 23 patients (four women and 19 men) with alcoholic cirrhosis. Sixteen nodules were examined with magnetic resonance imaging with gadolinium ethoxybenzyl diethylenetriaminepentaacetic acid enhancement ( EOB ‐ MRI ). Somatic mutations in IL 6 ST , GNAS and STAT 3 were examined in 19 nodules. Thirty‐six nodules in 18 patients were diagnosed as SAA ‐positive hepatocellular neoplasms/nodules, and the remaining 17 nodules in eight patients were SAA ‐negative focal nodular hyperplasia ( FNH )‐like nodules. SAA ‐positive hepatocellular neoplasms/nodules showed significantly more extensive sinusoidal dilatation, inflammatory reaction, abnormally thick arteries and cellular atypia than FNH ‐like nodules ( P  < 0.05). Eight SAA ‐positive hepatocellular neoplasms/nodules (67%) showed slight hypointensity in the hepatobiliary phase on EOB ‐ MRI , whereas all four FNH ‐like nodules showed iso‐intensity ( P  < 0.05). STAT 3 mutations were detected in two of 17 SAA ‐positive hepatocellular neoplasms/nodules. Conclusions This study showed that approximately two‐thirds of hypervascular hepatocellular nodules arising in alcoholic cirrhosis were SAA ‐positive hepatocellular neoplasms/nodules, which show different findings on the EOB ‐ MRI . STAT 3 mutations were detected in 11.8% of SAA ‐positive hepatocellular neoplasms/nodules, supporting a neoplastic nature.