Abstract
BACKGROUND: While hepatic cystic echinococcosis (CE) has been extensively studied in animal models, its impact on the human liver microenvironment remains unclear. Elucidating its pathogenic mechanisms in humans may reveal novel prognostic biomarkers and potential therapeutic targets. We aimed to investigate the impact of CE on the glycogen content of hepatocytes, CD10 expression in the bile canaliculi, and the profibrotic α-smooth muscle actin (α-SMA) in the adjacent portal areas. METHODS: The study involved 20 cases with hepatic hydatid cysts and 20 controls. Histopathological and viability assessments were done for the surgically obtained samples. Glycogen storage was evaluated using periodic acid-Schiff (PAS) special staining. Expressions of α-SMA and CD10 were investigated using immunohistochemistry. RESULTS: Biochemical tests and eosin staining confirmed high viability of the metacestodes, and histopathology showed distorted portal tracts. In hydatid cases, 85% (17/20) exhibited mild PAS staining of the hepatocytes, whereas control liver tissues were intensely in 65% (13/20) of the cases (p < 0.001). The laminated layer of the metacestode showed a strong positive PAS staining. In hydatid cases, α-SMA expression in the portal connective tissue exhibited a score of 2 in 45% (9/20) of cases, versus a score of 0 in 85% (17/20) of the control (P < 0.001). Increased α-SMA was also observed in the adventitial layer of the cyst. CD10 expression in pericystic liver tissue was absent in 25% (5/20) of hydatid cases, while mild to moderate canalicular expression was recorded in 65% (13/20) of cases. Nevertheless, marked expression was detected in 80% (16/20) of the controls (P < 0.001). CONCLUSION: As a preliminary report, hepatic hydatidosis may lead to glycogen depletion and α-SMA induction, suggesting potential therapeutic targets. CD10 may serve as a prognostic and post-treatment monitoring marker. Larger studies with multi-center design are recommended.