Risk factors for post-hepatectomy liver dysfunction in primary liver cancer patients with concurrent hepatic schistosomiasis and chronic hepatitis

Objective:The purpose of this study was to analyze risk factors for development of post-hepatectomy liver dysfunction in primary liver cancer(PLC)patients with concurrent hepatic schistosomiasis and chronic hepatitis.Methods:A retrospective analysis of 73 PLC patients with concurrent hepatic schistosomiasis and chronic hepatitis,of which 16 patients developed liver dysfunction(persistent ascites or pleural effusion or occurrence of liver-related potentially fatal complications)following hepatectomy,was performed.After clinical characteristics were recorded,preoperative liver function parameters and surgery-related parameters in these patients were assessed.Seventeen potential risk factors for post-hepatectomy liver dysfunction were identified.The association between these potential risk factors and post-hepatectomy liver dysfunction then was analyzed.Results:Univariate analysis showed that liver cirrhosis,intraoperative blood loss,and preoperative total bilirubin were associated with the development of post-hepatectomy liver dysfunction.Multivariate logistic regression analysis of these three factors revealed that intraoperative blood loss≥600 mL and cirrhosis were two independent risk factors for post-hepatectomy liver dysfunction in PLC patients with concurrent hepatic schistosomiasis and chronic hepatitis.Conclusion:Keeping intraoperative blood loss below 600 mL can help avoid the development of post-hepatectomy liver dysfunction in liver cancer patients with concurrent hepatic schistosomiasis and chronic hepatitis.For patients with concomitant liver cirrhosis,every effort should be made to minimize potential liver function impairment induced by other adverse factors.

Pentoxifylline Inhibits Liver Fibrosis via Hedgehog Signaling Pathway

Infection of schistosomiasis japonica may eventually lead to liver fibrosis, and no effective antifibrotic therapies are available but liver transplantation. Hedgehog（HH） signaling pathway has been involved in the process and is a promising target for treating liver fibrosis. This study aimed to explore the effects of pentoxifylline（PTX） on liver fibrosis induced by schistosoma japonicum infection by inhibiting the HH signaling pathway. Phorbol12-myristate13-acetate（PMA） was used to induce human acute mononuclear leukemia cells THP-1 to differentiate into macrophages. The THP-1-derived macrophages were stimulated by soluble egg antigen（SEA）, and the culture supernatants were collected for detection of activation of macrophages. Cell Counting Kit-8（CCK-8） was used to detect the cytotoxicity of the culture supernatant and PTX on the LX-2 cells. The LX-2 cells were administered with activated culture supernatant from macrophages and（or） PTX to detect the transforming growth factor-β gene expression. The m RNA expression of shh and gli-1, key parts in HH signaling pathway, was detected. The m RNA expression of shh and gli-1 was increased in LX-2 cells treated with activated macrophages-derived culture supernatant, suggesting HH signaling pathway may play a key role in the activation process of hepatic stellate cells（HSCs）. The expression of these genes decreased in LX-2 cells co-cultured with both activated macrophages-derived culture supernatant and PTX, indicating PTX could suppress the activation process of HSCs. In conclusion, these data provide evidence that PTX prevents liver fibrogenesis in vitro by the suppression of HH signaling pathway.