Ex Vivo Liver Resection and Autotransplantation for End-Stage Alveolar Echinococcosis: A Case Series.

The role of autotransplantation in end-stage hepatic alveolar echinococcosis (AE) is unclear. We aimed to present our 15-case experience and propose selection criteria for autotransplantation. All patients were considered to have unresectable hepatic AE by conventional resection due to critical invasion to retrohepatic vena cava, hepatocaval region along with three hepatic veins, and the tertiary portal and arterial branches. All patients successfully underwent ex vivo extended right hepatectomy and autotransplantation without intraoperative mortality. The median autograft weight was 706 g (380-1000 g); operative time was 15.5 hours (11.5-20.5 hours); and anhepatic time was 283.8 minutes (180-435 min). Postoperative hospital stay was 32.3 days (12-60 days). Postoperative complication Clavien-Dindo grade IIIa or higher occurred in three patients including one death that occurred 12 days after the surgery due to acute liver failure. One patient was lost to follow-up after the sixth month. Thirteen patients were followed for a median of 21.6 months with no relapse. This is the largest reported series of patients with end-stage hepatic AE treated with liver autotransplantation. The technique requires neither organ donor nor postoperative immunosuppressant. The early postoperative mortality was low with acceptable morbidity. Preoperative precise assessment and strict patient selection are of utmost importance.

Th17/Treg imbalance in patients with liver cystic echinococcosis.

Echinococcosis is a chronic parasitic infectious disease regulated by T-cell subsets. CD4(+) CD25(+) FoxP3 (+) regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effect on inflammation. Th17/Treg balance controls inflammation and may play an important role in the pathogenesis of immune evasion. To assess whether this balance was broken, we detected Th17/Treg functions in different levels including cell frequencies, related cytokines secretion and key transcription factors in patients with cystic echincoccosis and healthy controls. The results demonstrated that patients with cystic echinococcosis revealed significant increase in peripheral Treg number, related cytokines (IL-10 and TGF-ß1) and transcription factor (Foxp3) levels and moderate decrease in Th17 number, related cytokines (IL-17 and IL-23) and transcription factor (RORγt) levels as compared with controls. Results indicated that Th17/Treg functional imbalance exists in patients with chronic cystic echinococcosis, suggesting a potential role for Th17/Treg imbalance in the pathogenesis of immune evasion in echinococcosis.

TLR2 and TLR4 expression in peripheral blood mononuclear cells of patients with chronic cystic echinococcosis and its relationship with IL-10.

This study aims at relating Toll-like receptors (TLR) and human systemic cytokines in patients with chronic cystic echinococcosis (CE). By real-time fluorescent quantitative reverse-transcription polymerase chain reaction, we measured the expression level of TLR2 and TLR4 mRNA in peripheral blood mononuclear cells (PBMCs), and using ELISA, we detected the cytokines IFN-γ, IL-12p70, IL-10, IL-4 and IL-17A from 34 chronic CE cases (four patients with biliary leakage; four patients with secondary location including three in lung and one in bone) and 22 healthy controls (HC). TLR2 and TLR4 mRNA expression were significantly higher in the CE group (P<0·05); levels of serum IL-10, IL-4 and IL-12p70 in patients with CE were significantly higher than those in controls (P<0·05). There were no differences in IFN-γ and IL-17A levels between the CE group and the HC group (P>0·05). In the patients with CE, positive correlations were noted between the expression of TLR2 and the serum level of IL-10, as well as between the expression of TLR4 and the serum level of IL-10. Our findings supported the hypothesis that during chronic CE infection, altered TLR expression might be involved in the cytokine modulation, which allowed the parasite to escape host immunosurveillance and promoted chronic infection.