Active behavior of triple-negative breast cancer with adipose tissue invasion: a single center and retrospective review.

BACKGROUND: Interactions between adipocyte and breast cancer (BC) cells have yet to be fully elucidated. Here we investigated the prognostic impact of marginal adipose tissue invasion in both luminal breast cancer (HR+/HER2-) and triple-negative breast cancer (TNBC) (HR-/HER2-). METHODS: A total of 735 patients with early-stage invasive BC (1999-2014) were retrospectively registered. Median length of patient follow-up was 8.9 years. Survival curves were calculated using a Kaplan-Meier cumulative survival plot. The prognostic difference between two groups were assessed by the univariate Cox-proportional hazard regression model. RESULTS: Patients with adipose tissue invasion (n = 614) had a significantly poorer prognosis than those without adipose tissue invasion (n = 121) in overall survival (OS) (hazard ratio, 2.1; 95% Confidence interval [CI], 1.1 to 4.0; P = 0.025). While a poorer prognosis was observed in TNBC (n = 137) than in luminal BC patients (n = 496) (hazard ratio, 0.45; 95% CI, 0.30 to 0.68, P < 0.001), this aggressive nature of TNBC was noted in node-positive disease (hazard ratio, 0.3; 95% CI, 0.18 to 0.5, P < 0.001) but not in node-negative disease (hazard ratio, 0.78; 95% CI, 0.39 to 1.55, P = 0.472), and also noted in adipose tissue invasion-positive patients (hazard ratio, 0.4; 95% CI, 0.26 to 0.6, P < 0.001) but not in adipose tissue invasion-negative patients (hazard ratio, 0.73; 95% CI, 0.16 to 3.24, P = 0.675). In addition, although patients suffering from TNBC with adipose tissue invasion had a poorer outcome than those without adipose tissue invasion (hazard ratio, 3.63; 95% CI, 1.11 to 11.84; P = 0.033), the difference was not observed in luminal BC (hazard ratio, 1.75; 95% CI, 0.64 to 4.82; P = 0.277). CONCLUSIONS: Adipose tissue invasion was correlated with poor survival in TNBC. Cancer cell invasion into local fat may be a first step on cancer progression and systemic disease in TNBC.

Clinical Evaluation of Hepatic Portal Venous Gas after Abdominal Surgery.

Hepatic portal venous gas (HPVG) is induced by various abdominal diseases. Since HPVG is accompanied by bowel ischemia, intestinal infection and hypovolemia, various modes of critical management are needed to treat the underlying conditions. HPVG associated with abdominal complications after surgery has rarely been reported. We present 4 patients with HPVG after abdominal surgery: 2 of the 4 patients died of multiple organ failure, and the other 2 recovered with solely conservative therapy. Although postoperative HPVG is a severe and life-threatening condition, early detection and systemic treatment lead to a better patient outcome.

Review to better understand the macroscopic subtypes and histogenesis of intrahepatic cholangiocarcinoma.

Intrahepatic cholangiocarcinoma is macroscopically classified into three subtypes, mass-forming-type, periductal infiltrating-type, and intraductal growth-type. Each subtype should be preoperatively differentiated to perform the valid surgical resection. Recent researches have revealed the clinical, radiologic, pathobiological characteristics of each subtype. We reviewed recently published studies covering various aspects of intrahepatic cholangiocarcinoma (ICC), focusing especially on the macroscopic subtypes and stem cell features to better understand the pathophysiology of ICC and to establish the valid therapeutic strategy.

An autologous in situ tumor vaccination approach for hepatocellular carcinoma. 2. Tumor-specific immunity and cure after radio-inducible suicide gene therapy and systemic CD40-ligand and Flt3-ligand gene therapy in an orthotopic tumor model.

Diffuse hepatocellular carcinoma (HCC) is a lethal disease that radiation therapy (RT) currently has a limited role in treating because of the potential for developing fatal radiation-induced liver disease. However, recently diffuse HCC, "radio-inducible suicide gene therapy" has been shown to enhance local tumor control and residual microscopic disease within the liver for diffuse HCC, by using a combination of chemoactivation and molecular radiosensitization. We have demonstrated that the addition of recombinant adenovirus-expressing human Flt3 ligand (Adeno-Flt3L) after radio-inducible suicide gene therapy induced a Th1-biased, immune response and enhanced tumor control in an ectopic model of HCC. We hypothesized that sequential administration of recombinant adenovirus-expressing CD40L (Adeno-CD40L) could further potentiate the efficacy of our trimodal therapy with RT + HSV-TK + Adeno-Flt3L. We examined our hypothesis in an orthotopic model of diffuse HCC using BNL1ME A.7R.1 (BNL) cells in Balb/c mice. BNL murine hepatoma cells (5 × 10(4)) transfected with an expression vector of HSV-TK under the control of a radiation-inducible promoter were injected intraportally into BALB/cJ mice. Fourteen days after the HCC injection, mice were treated with a 25 Gy dose of radiation to the whole liver, followed by ganciclovir (GCV) treatment and systemic adenoviral cytokine gene therapy (Flt3L or CD40L or both). Untreated mice died in 27 ± 4 days. Radiation therapy alone had a marginal effect on survival (median = 35 ± 7 days) and the addition of HSV-TK/GCV gene therapy improved the median survival to 47 ± 6 days. However, the addition of Adeno-Flt3L to radiation therapy and HSV-TK/GCV therapy significantly (P = 0.0005) increased survival to a median of 63 ± 20 days with 44% (7/16) of the animals still alive 116 days after tumor implantation. The curative effect of Flt3L was completely abolished when using immunodeficient nude mice or mice depleted for CD4, CD8 and natural killer cells. The addition of Adeno-CD40L further improved the median survival of animals to 80 ± 15 days and this effect was abolished only when using anti-CD8 antibodies. Chromium-51 (51Cr) release assay showed cytotoxic T lymphocyte (CTL) activation, suggesting efficient dendritic cell (DC) activation with CTL activation after the treatment. Furthermore, when surviving mice were rechallenged with BNL-ETK cells on the foot pad, RT + HSV-TK/GCV + Flt3L + CD40L-treated mice developed a small tumor on day 56 but the tumor eventually disappeared after 105 days. Mice treated with RT + HSV-TK/GCV + Flt3L showed a slowed tumor growth curve compared with untreated mice. Therefore, combination therapy using Flt3L to induce DC proliferation and CD40L to enhance DC maturation holds great promise for immunomodulation of radiation therapy to enhance HCC tumor control and prevent progression of disease in patients with diffuse HCC.

An autologous in situ tumor vaccination approach for hepatocellular carcinoma. 1. Flt3 ligand gene transfer increases antitumor effects of a radio-inducible suicide gene therapy in an ectopic tumor model.

Hepatocellular carcinoma (HCC) often presents as a diffuse or multifocal tumor making it difficult to control by surgery or radiation. Radio-inducible herpes simplex virus thymidine kinase (HSV-TK) gene therapy has been shown to enhance local tumor control after radiation therapy (RT), while limiting the expression of the transgene in the irradiated tumor tissues. To prevent liver tumor recurrence and control systemic disease while limiting the potential bystander toxicity of HSV-TK therapy, we proposed to stimulate endogenous dendritic cell (DC) proliferation with systemic adenovirus Flt3 ligand (Adeno-Flt3L) gene therapy, followed by primary tumor radiation therapy combined with a radio-inducible HSV-TK gene therapy. We hypothesized that adenovirus-expressing Flt3L gene therapy will stimulate DC proliferation, allowing the upregulated DCs to locally harness tumor antigens released from HSV-TK/RT-treated HCC cells, thereby converting irradiated tumors to an autologous in situ tumor vaccine in mice with primary liver tumors. To test this hypothesis, an expression vector of HSV-TK was constructed under the control of a radio-inducible promoter early-growth response (Egr-TK) and a recombinant adenovirus-expressing human Flt3L was constructed. The Adeno-Flt3L [10(9) plaque forming units (pfu)] was administered intravenously on days 1 and 8 after radiation therapy. The murine hepatoma cell line (BNL1ME) was stably transfected by Egr-TK or Egr-Null (encoding no therapeutic gene). Palpable tumors in BALB/c mice were treated with a localized dose of 25 Gy of radiation followed by ganciclovir (GCV, 100 mg/kg, 14 days). Four treatment cohorts were compared: Egr-Null/GCV + RT + Adeno-LacZ; Egr-Null/GCV + RT + Adeno-Flt3L; Egr-TK/GCV + RT + Adeno-LacZ; and Egr-TK/GCV + RT + Adeno-Flt3L. There was no primary tumor regression in the Egr-Null tumors after radiation therapy alone. In contrast, Egr-TK tumors had nearly complete tumor regression for 3 weeks after radiation therapy (P < 0.01), however, long-term follow-up demonstrated primary tumor recurrence and death secondary to pulmonary metastasis. Flt3L expression was confirmed by serum bioassay (mean = 88 ng/mL) in these animals and Western blotting of tissue culture medium in Adeno-Flt3L-infected BaF/huFlt3L cells. Radiation therapy with Adeno-Flt3L gene therapy effectively retarded primary tumor growth when compared to radiation therapy alone. The trimodality therapy (Egr-TK/GCV + RT + Adeno-Flt3L) was the most efficacious with 40% complete tumor regression (>100 days) and <20% pulmonary metastases, indicating the development of sustained antitumor immune response. These studies provide a rationale for triple modality therapies with radiation-inducible HSV-TK gene therapy and Adeno-Flt3L when used in combination with primary tumor radiation therapy for improved local and systemic control of HCC.

A large hepatic cyst with obstructive jaundice successfully treated with single-incision laparoscopic deroofing.

We herein present a case of hepatic cysts causing obstructive jaundice that was treated with single-incision laparoscopic deroofing. A 72-year-old female patient was referred to hospital due to a large hepatic cyst that compressed the intrahepatic bile ducts. The patient was scheduled to undergo single-incision laparoscopic deroofing. The EZ ACCESS(TM) oval type (Hakko Co. Ltd.) was placed at the umbilicus using a 25-mm incision with two 5-mm trocars. An additional 12-mm port was placed at the left epigastric region. We unroofed and excised the cyst wall using a vessel sealing system in liver segment 4. After surgery, the patient was found to be asymptomatic. The unroofed cysts were completely diminished. Notably, the remnant liver had fairly regenerated. The estimated regeneration volume of the normal liver was 153 cm(3). To prevent surgical complications, clinicians should perform adequate management and use of devices. To prevent postoperative recurrence of cysts, performing complete deroofing is essential. Single-incision laparoscopic deroofing contributes to improving the quality of life of patients and should be considered a standard treatment.

The impact of hepatic denervation on the accumulation of hepatic progenitor cells during liver regeneration in rats.

BACKGROUND/AIMS: All autonomic hepatic nerves are transected following liver transplantation. Recent studies have shown the relationship between an inhibition of autonomic nerves and the accumulation of hepatic progenitor cells (HPC). This study aims to elucidate the influence of hepatic denervation on the accumulation of HPC in the process of liver regeneration. METHODOLOGY: Male Sprague-Dawley rats underwent hepatic denervation. Immediately after either denervation (DN group, n=30) or a sham operation (control group, n=30), a two-thirds hepatectomy was performed, and these were sacrificed chronologically. An immunohistochemical analysis of HPC was performed with a mouse monoclonal OV6 type antibody. RESULTS: The liver per body weight ratio gradually increased in both groups. On postoperative day (POD) 7, the DN group showed a significantly higher ratio. The HPC expression gradually increased in both groups. The maximal HPC number was observed on POD 7 in the DN group and on POD 3 in the control group. Although there was no significant difference in the HPC numbers between the DN and control group until POD 3, the number of HPC were significantly higher in livers of the denervated rats than in those of the sham operated rats between POD 5 and 14. CONCLUSIONS: The hepatic autonomic nerves were thus suggested to play an important role in the accumulation of HPC during liver regeneration in rats.

Complete dissection of a hepatic segment after blunt abdominal injury successfully treated by anatomical hepatic lobectomy: report of a case.

A 21-year-old male patient was transferred to the emergency room of our hospital after suffering seat belt abdominal injury in a traffic accident. Abdominal computed tomography revealed a massive hematoma in the abdominal cavity associated with deep hepatic lacerations in the right lobe. The presence of a solid tissue possibly containing pneumobilia was observed above the greater omentum. These findings were consistent with a tentative diagnosis of hepatic laceration due to blunt trauma; therefore, this prompted us to perform emergency laparotomy. The operative findings revealed a massive hematoma and pulsatile bleeding from the lacerated liver and a retroperitoneal hepatoma, which was most likely due to subcapsular injury of the right kidney. In accordance with the preoperative imaging studies, a pale liver fragment on the greater omentum was observed, which was morphologically consistent with the defect in the posterior segment of the liver. Since the damaged area of the liver broadly followed the course of the middle hepatic vein, we carefully inspected and isolated the inflow vessels and eventually performed a right hepatic lobectomy. The patient's postoperative course was uneventful, and he was doing well at 10 months after surgery.

Laparoscopy-assisted right hepatectomy in a case of Fasciola hepatica.

Laparoscopic hepatectomy provides the usual advantages of a minimally invasive surgery. This study presents a case of Fasciola hepatica infection that was successfully treated with laparoscopic hepatectomy. The patient was referred because of persistent fever and right hypochondralgia with a huge mass occupying the right lobe of the liver, which was detected by imaging analysis. Serologic tests indicated an F. hepatica infection. The patient underwent a laparoscopic resection because the anthelmintic agent, triclabendazole was not effective. During the surgical technique, 5 trocars were inserted. After liver mobilization, the Glissonian pedicles and right hepatic veins were safely taped. A Penrose drain was placed behind the liver for a liver-hanging maneuver. A liver parenchymal transection was performed through an 8 cm handport site using a dissecting sealer (TissueLink Medical) after precoagulating its superficial layer by microtaze. Glissonian pedicles and the right hepatic vein were divided using an endolinear stapler (endcutter 45, Ethicon). Finally, the resected specimen was extracted from the handport. The surgical time was 450 minutes and the surgical blood loss was 370 mL. The patient was discharged 10 days after the surgery with an uneventful postoperative course. The laparoscopy-assisted hepatectomy in this case was beneficial for the patient's quality of life as a minimally invasive operation with a high degree of safety.

Liver repopulation by transplanted hepatocytes in a rat model of acute liver failure induced by carbon tetrachloride and a partial hepatectomy.

BACKGROUND: Although hepatocyte transplantation holds great promise, most of the transplanted hepatocytes fail to proliferate in the liver without any manipulation of the host. Previous studies have shown that the replacement of the host liver cells with transplanted hepatocytes, called "liver repopulation", requires a combination of proliferative stimuli to the transplanted hepatocytes and suppression of the host hepatocytes. This study explored whether liver repopulation could be achieved by hepatocyte transplantation in a chemically and surgically induced-liver failure model in the rat. MATERIAL/METHODS: Dipeptidyl peptidase IV-positive (DPPIV +) Fisher rats were used as donor and syngeneic DPPIV-deficient (DPPIV-) rats served as recipient. The recipient rats were treated with carbon tetrachloride (CCl4) for 4 weeks followed by a 68% partial hepatectomy (PH) and transplantation of the hepatocytes (HT). Five groups were established based on the influence of specific factors including CCl4, PH, and HT. The liver regeneration rates were evaluated by the liver weight/body weight (LW/BW) ratio. The liver repopulation rates were determined by the formula; (DPPIV+ cell counts/all cell counts) ×100%. RESULTS: The liver regeneration rates were 3.5 and 2.6 in the rats with CCl4+PH, and PH alone, respectively (P<0.01). In the rats with CCl4+PH, DPPIV positive cell clusters appeared in the host liver parenchyma 7 days after HT (day 7), exhibiting continuous proliferation up to day 28 (The liver repopulation rates were 1.1% and 13.4%, respectively, p<0.05). CONCLUSIONS: Liver repopulation by hepatocyte transplantation was therefore found to be possible in partially hepatectomized rats under the continuous exposure to regulated doses of CCl4.

Successful laparoscopic repair of a lumbar hernia occurring after iliac bone harvest.

INTRODUCTION: Many techniques have been described for the surgical repair of lumbar hernias, including primary repair, local tissue flaps, and conventional mesh repair. All these open techniques require a large incision plus extensive dissection to expose the hernia ring. This report presents a case of a recurrent lumbar hernia, which was successfully repaired using a laparoscopic approach. CASE REPORT: A 75-year-old female presented with a symptomatic right lumbar hernia, 1-year after an iliac bone harvest for knee surgery. Under general anesthesia, the patient was placed in a lateral decubitus position. A 3 trocar technique was used to do adhesiolysis of the surrounding tissues, to provide an ample working space to identify the hernia. A composix dual mesh (bard) was tailored so that it would overlap the defect with intermittent fixation by a spiral tacker (protac). No hernia recurrence occurred over 2 years after surgery. CONCLUSION: The laparoscopic approach has significant advantages for the repair a lumbar hernia: it enables the exact localization of the anatomic defect, and the mesh can be placed deep into the defect, thus allowing the intraabdominal pressure to hold it in position.

Low-dose recombinant human hepatocyte growth factor enhances effect of hepatocyte transplantation in rats treated with retrorsine.

BACKGROUND/AIMS: The aim of this study was to regenerate transplanted hepatocytes selectively in a recipient using retrorsine and recombinant human hepatocyte growth factor (rhHGF). METHODOLOGY: Nagase analbuminemic rats (NARs) received pretreatment with retrosine and were divided into three experimental groups. Group1: Hepatocyte transplantation (HcTx) + 50 microg/kg/day rhHGF. Group2: HcTx + 250 microg/kg/day rhHGF. Group3: HcTx + normal saline. The serum levels of albumin and the albumin-positive hepatocytes in the liver were investigated. The rat endogenous HGF of the rats given only retrorsine was measured. RESULTS: The serum albumin levels of Group11 were higher than those of Group2, while there was no significant difference between Group2 and GroupS. Histological examination of Group1 and 3 showed the presence of a large number of albumin-positive hepatocytes, which frequently consisted of large clusters and occupied 53.90 +/- 2.31% and 31.25 +/- 5.36% of host liver, respectively. The liver sections of Group2 showed numerous albumin-positive hepatocyte, which were not seen as clusters. The rat endogenous HGF concentration was extremely high. CONCLUSION: Low-dose rhHGF enhances the effect of HcTx under the suppressive state of proliferation of host hepatocytes. Because of the high endogenous HGF, the administration of a high concentration of rhHGF suppressed the regenerative activity of the transplanted hepatocytes.

Efficacy and limitation of bone marrow transplantation in the treatment of acute and subacute liver failure in rats.

AIM: Recent reports have shown that bone marrow cells (BMC) retain the potential to differentiate into hepatocytes. Thus, the BMC have been recognized as an attractive source for liver regenerative medicine. However, it has not been clarified whether BMC transplantation can be used to treat liver damage in vivo. In the present study, we explored whether BMC possess therapeutic potential to treat acute and/or subacute liver failure. METHODS: Fulminant hepatic failure (FHF) was induced by 70% hepatectomy with ligation of the right lobe pedicle (24% liver mass), followed by transplantation of BMC into the spleen. Dipeptidyl peptidase IV-positive (DPPIV(+)) BMC were then transplanted into DPPIV-negative (DPPIV(-)) recipients following hepatic irradiation (HIR) in which 70% of the liver was resected and the remnant liver irradiated. RESULTS: There was no benefit of BMC transplantation towards survival in the FHF model. DPPIV(+) hepatocytes appeared in the liver tissues of the DPPIV(-) HIR model rats, but DPPIV(+) hepatocytes replaced less than 13% of the recipient liver. CONCLUSION: BMC transplantation may have limitations in the treatment of fulminant or acute liver failure because they do not have sufficient time to develop into functional hepatocytes. Preparative HIR may be beneficial in help to convert the transplanted BMC into host hepatocytes, and provide a survival benefit. Although, However, the precise mechanism warrants further studies.

Metabolism for cyclosporin A during liver regeneration after partial hepatectomy in rats.

AIM: To elucidate the metabolism and the effect of the cyclosporin A (CyA) as a representative immunosuppressive drug used in transplantation in a partially hepatectomized rat model. METHODS: CyA was administered to rats that underwent a 70% hepatectomy. These rats were randomly assigned into three groups according to the dose of CyA administration as follows; (group 1) water, (group 2) 5 mg/kg CyA, (group 3) 10 mg/kg CyA. On postoperative days-1, 3, 7 and 14, the rats were killed to analyze the serum concentration of CyA, the liver regeneration ratio, biochemical or histological markers, and mRNA expression using reverse transcriptase-polymerase chain reaction method to determine albumin and cytochrome p450 expression. RESULTS: The serum concentration of CyA in group 3 was significantly higher than group 2 during liver regeneration. CyA enhanced the liver regeneration in a dose dependent manner. The mRNA expression associated with CyA metabolism was significantly decreased on day 14, while preserving the albumin producing activity. CONCLUSION: These data indicate that the p-450 activity required to metabolize the CyA may be reduced during regeneration of the remnant liver after a hepatectomy, which may, therefore, be linked to difficulty in controlling the optimal dose of CyA during early period of LDLT.

Compressive stenosis of the inferior vena cava due to localized ascites after living-donor liver transplantation.

A 54-year-old woman was admitted to our hospital following the diagnosis of decompensated liver cirrhosis with hepatitis C. She underwent living-donor liver transplantation, performed using the left hepatic lobe with the middle hepatic vein donated by her husband. After the transplantation, the patient suffered from massive ascites with liver dysfunction. Computed tomography demonstrated stenosis of the suprahepatic inferior vena cava (IVC) with focal collection of fluid. A second laparotomy was performed 19 days after the transplantation. When the encapsulated localized ascites on both sides of the IVC was opened, the ascites was flushed away. Subsequently, the grafted liver was easily mobilized and it was placed in the natural position without any tension, and the pressure gradient of the IVC was improved. Herein, we report a very rare case of compression stenosis of the IVC resulting in Budd-Chiari syndrome caused by localized encapsulated ascites.

Significance of the serum level of soluble E-cadherin in patients with HCC.

BACKGROUND/AIMS: E-cadherin (E-cad) is a type of adhesion molecule, and recent studies have demonstrated a correlation between its expression in tumor lesions and the recurrence of HCC. Serum levels of soluble E-cad are significantly elevated in patients with several types of cancer. The authors evaluated the significance of the serum level of soluble E-cad as a predictor of early recurrences (intrahepatic or extrahepatic metastasis) of HCC after a curative resection. METHODOLOGY: The concentrations of soluble E-cad in the serum of 25 HCC patients before surgery and 12 healthy subjects were measured using a sandwich enzyme-linked immunosorbent assay. The hepatic expression of E-cad was examined by immunohistochemical staining. RESULTS: The median serum soluble E-cad levels were significantly elevated in HCC patients before surgery in comparison to those in healthy subjects (10,759 ng/mL vs. 5,798 ng/mL, p < 0.05). The patients in the high serum soluble E-cad group experienced a higher incidence of early recurrence (p < 0.05). The levels of expression of E-cad in HCC lesions were not related to the serum levels of soluble E-cadherin. CONCLUSIONS: The study demonstrated that serum soluble E-cad levels were elevated in patients with HCC, and high serum soluble E-cadherin (> or = 8,000 ng/ml) was associated with early recurrence or extrahepatic metastasis. Serum soluble E-cad may therefore be a potential prognostic marker for HCC.

Hepatic repopulation with stably transduced conditionally immortalized hepatocytes in the Gunn rat.

BACKGROUND/AIMS: Conditionally immortalized hepatocytes offer a renewable source of hepatocytes, but although preparative maneuvers have been developed for hepatic repopulation with primary hepatocytes, extensive proliferation of transplanted immortalized hepatocytes has not been accomplished heretofore. Our aim was to achieve ex vivo gene therapy of uridinediphosphoglucuronate glucuronosyltransferase-1A1 (UGT1A1)-deficient jaundiced Gunn rats (model of Crigler-Najjar syndrome type-1) by hepatic repopulation with genetically modified and conditionally immortalized hepatocytes. METHODS: Gunn rat hepatocytes were conditionally immortalized by stable transduction with a thermolabile mutant simian virus 40 T-antigen ((ts)Tag(A58)) and further transduced with UGT1A1. These hepatocytes proliferate at 33 degrees C, but at 37 degrees C the (ts)Tag(A58) is degraded and the cells become quiescent. The cells were transplanted into Gunn rat livers after preparative hepatic irradiation (50 Gy) and 66% hepatectomy. RESULTS: The engrafted UGT1A1-positive immortalized hepatocytes replaced approximately 80% of the host hepatocytes in 20 weeks, leading to normalization of hyperbilirubinemia. Liver histology, and serum albumin and alanine aminotransferase levels remained normal. CONCLUSIONS: We achieved complete cure of hyperbilirubinemia in Gunn rats by ex vivo gene therapy via genetically modified and conditionally immortalized hepatocytes.

Tape-guided living donor left hepatectomy.

A procedure of tape-guided living donor left hepatectomy is described. A tape was placed along the anterior wall of the inferior vena cava for left liver with caudate lobe, and along Arantius' ligament for left liver without caudate lobe. The final step of liver transection was applied by dividing the liver parenchyma under tape guidance. This procedure contributed to safe and accurate anatomic procurement of left liver grafts in living donor hepatectomy.

Application of endovascular stapler in living-donor liver transplantation.

We used an endovascular stapler in recipients of living-donor liver transplantation (LDLT). Hepatic veins were transected in 10 recent LDLTs (6 right-lobe and 4 left-lobe grafts), and the portocaval shunt was transected in 5 of these 10 LDLTs. Median operative time with the vascular stapler was 861 minutes (range 675 to 932), whereas the median time to liver explantation was 292 minutes (range 200 to 461) (both with P < or = .05 vs vascular stapler use). To our knowledge, this is the first report on the use of an endovascular stapler device in LDLT.

Biliary complications in recipients of living-donor liver transplantation.

The key points of the management of biliary complications in recipients of living-donor liver transplantation are described. The characteristics of these complications are somewhat different from those in deceased-donor liver transplantation, mainly due to the technical difficulties. Appropriate prevention, diagnosis, and treatment are essential for successful transplants, to avoid the development of secondary biliary cirrhosis when complication occurs.