Use of the hilar plate looping technique for bile duct dissection in living donor liver transplantation significantly reduces recipient biliary complications.

Biliary complications remain a major cause of morbidity after liver transplantation, especially in living donor liver transplantation (LDLT). Maintaining adequate blood supply to the bile duct is important for the prevention of biliary complications. The objective of this study was to analyze the effects of different techniques for bile duct anastomosis on posttransplantation biliary complications. From August 2005 to August 2008, 121 liver transplantations were performed at our center. Among the total 121 liver transplant recipients, 68 patients underwent a LDLT using a right lobe graft and were enrolled in this study. We used classic dissection for the first 38 recipients and the hilar plate looping technique for the next 30 patients. The hilar plate looping technique involves the looping of the complete hilar plate and Glissonian sheath around the hepatic duct after full dissection of the right hepatic artery and portal vein. Biliary complications were defined as bilomas or strictures that developed within 6 months after transplantation and required surgical or radiological intervention. There were no significant demographic differences between the 2 groups. The incidence of complications was 15 (39.5%) for classic dissection and 3 (18.8%) for hilar plate looping. Furthermore, there were no biliary strictures in the hilar plate looping group, and there was a significant difference in the complication rate between the 2 groups (P = .011). In conclusion, the hilar plate looping technique during LDLT significantly reduces recipient biliary complications.

Impact of graft type on remnant liver regeneration: right hepatectomy versus extended right hepatectomy.

Right hepatectomy with the middle hepatic vein (MHV) affects venous return and function of the remaining liver. We compared the remnant liver volume in the donors of resection with or without the MHV on the remnant liver volume regeneration. Living donors who had undergone right hepatectomy without MHV (RH group; n = 36) and those with MHV (ERH group; n = 19) were reviewed. Volume regeneration of segments I-III, segment IV, and total remnant liver volume was assessed at postoperative day (POD) 7 and 30 using a computed tomography-based volumetry program. According to the measured volume data, we calculated the liver remnant volume and the rate of liver remnant volume increase. The regeneration rate of segment IV was significantly low in the ERH group compared with that in the RH group at POD 7 and POD 30 (160% vs 141%; P = .018 and 189% vs 154%; P = .007). In contrast, the regeneration rate of the total remnant liver volume was not significantly different between the 2 groups (173% vs 175%; P = .758 and 199% vs 198%; P = .880). In conclusion, extended right hepatectomy can be safely performed with careful preoperative evaluation without significant impairment of remnant liver regeneration.

Up-regulated macrophage migration inhibitory factor protects apoptosis of dermal fibroblasts in patients with systemic sclerosis.

Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that has been demonstrated to regulate the apoptosis of several cell types. Dysregulated apoptosis of fibroblasts has been implicated in a variety of fibrotic diseases, including systemic sclerosis (SSc). In this study, we investigated the role of MIF in the apoptosis of dermal fibroblasts. The concentrations of MIF were measured in sera and in culture supernatants of peripheral blood mononuclear cells (PBMCs) and dermal fibroblasts by enzyme-linked immunosorbent assay. The degree of apoptosis was determined by colorimetric assay, and signalling pathways were examined by Western blot. The results showed that serum levels of MIF were significantly higher in patients with SSc (n = 47) than in healthy controls (n = 56). Stimulation of PBMCs by anti-CD3 and anti-CD28 increased the production of MIF by fourfold over the constitutive levels. SSc dermal fibroblasts produced higher amounts of MIF than normal dermal fibroblasts. When treated with sodium nitroprusside (SNP), SSc dermal fibroblasts showed a lower degree of apoptosis compared with normal dermal fibroblasts. Exogenous MIF (1-100 ng/ml) inhibited SNP-induced apoptosis of dermal fibroblasts dose-dependently. Both extracellular regulated kinase (ERK) inhibitor (PD98059) and protein kinase B (Akt) inhibitor (LY294002) almost completely blocked the inhibitory effect of MIF on apoptosis. Furthermore, MIF increased the expression of Bcl-2, phospho-ERK and phospho-Akt activity in dermal fibroblasts. Taken together, our data suggest that MIF released by activated T cells and dermal fibroblasts decreases the apoptosis of dermal fibroblasts through activation of ERK, Akt and Bcl-2 signalling pathways, which might be associated with excessive fibrosis in SSc.