Pathological Study on Differences in Growth Patterns Between Hepatic Alveolar Echinococcosis and Hepatocellular...

Hepatic alveolar echinococcosis (HAE) is frequently described as a "parasitic cancer" because of its tumor-like growth characteristics; however, whether it truly exhibits carcinoma-like invasive behavior remains unclear. In this study, we performed a systematic histopathological comparison of HAE and hepatocellular carcinoma (HCC) to delineate differences in their growth patterns. Our findings provide a new theoretical basis for optimizing clinical management strategies for HAE.

Lesional tissue samples were obtained from patients with HAE and HCC for histological slide preparation. The pathological features of both conditions were then systematically examined by light microscopy to assess differences in their growth patterns.

(1) Within lesional tissues, vascular structures in HAE were predominantly residual vessels that were encased and compressed by the advancing lesion, rather than newly formed vessels; in contrast, clustered neovascularization predominated in HCC. Similarly, in HAE, bile ducts represent residual normal bile duct structures rather than newly formed bile ducts. In HCC, only a small percentage of cases show subtle proliferation of small bile ducts within the tumor stroma. Neural involvement was comparable between the two conditions: perineural encasement was observed in 12.6% of HAE cases versus 8.4% of HCC cases (P = 0.319), and neural invasion occurred in 3.9% and 1.9% of cases, respectively (P = 0.644). (2) At the interface between lesional and hepatic tissues, the fibrous capsule remained intact without evidence of infiltration in HAE. In contrast, cancer cell infiltration was observed in 80.4% of HCC cases (P < 0.05). HAE showed no direct invasion of the hepatic parenchyma, consistent with preservation of fibrous septa, whereas septal disruption with direct parenchymal invasion along sinusoids was identified in 17.8% of HCC cases (P < 0.05). The incidence of vascular compression was comparable between the two groups (HAE: 20.4% vs. HCC: 16.8%; P = 0.507). However, vascular invasion was rare in HAE (1.9%) but occurred in 31.8% of HCC cases (P < 0.05). No significant differences were observed in bile duct compression (HAE: 16.5% vs. HCC: 10.3%; P = 0.185) or bile duct invasion (HAE: 1.9% vs. HCC: 3.7%; P = 0.714). (3) At the lesional surface, HAE lesions adjacent to the hepatic capsule were consistently covered by dense fibrous tissue, with no evidence of capsular invasion. In contrast, direct capsular invasion was observed in 17.8% of HCC cases (P < 0.05).

From a pathological perspective, the growth pattern of HAE differs markedly from the invasive growth of HCC. HAE exhibits an expansive growth pattern, always encased by a fibrous capsule, which provides a theoretical foundation for the complete surgical resection of the lesion.