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Sheung Tat Fan

Publications and source records attributed to Sheung Tat Fan.

At least 91 records · Page 5Linked to original sources

Decreased expression of cytochrome P450 2E1 is associated with poor prognosis of hepatocellular carcinoma.

Cytochrome P450-2E1 (CYP2E1) is one of the major hepatic enzymes involved in the metabolism of procarcinogen. Our study aimed to investigate the differential expression level of CYP2E1 and its clinicopathological significance in hepatocellular carcinoma (HCC). CYP2E1 revealed low level of expression in 70% of the tumor tissues, when compared to the adjacent nontumor tissues, at both mRNA and protein levels. The low expression of CYP2E1 was significantly correlated with the aggressive tumor phenotype, including poor differentiation status (by the Edmondson grading system) (p=0.038), absence of tumor capsule (p=0.030) and younger age of the patients (p=0.002). Multivariate analysis indicated that CYP2E1 expression level and pTNM stage were independent prognostic factors for disease-free survival. CYP2E1 was also shown to have a differential expression level in different liver tissues. The level of CYP2E1 was significantly higher in nontumor tissues from HCC patients compared to the intermediate level in cirrhosis livers from noncancer patients and normal livers from healthy persons. Tumor tissues were shown to have the lowest expression level. In conclusion, our results have shown that CYP2E1 is upregulated in the nontumor tissue and downregulated in tumor tissue, which is associated with aggressive tumor type and poor prognosis of the patients. It suggested that the differential expression of CYP2E1 may play an important role in HCC tumorigenesis.

Adult↗

Management of hepatocellular carcinoma in renal transplant recipients.

BACKGROUND AND OBJECTIVE: In Hong Kong where hepatitis B virus (HBV) infection is endemic, hepatocellular carcinoma (HCC) accounts for 20% of all malignant transformations in renal transplant recipients. The aim of the present study was to review the management and outcome of HCC in renal transplant recipients at a specialized surgical center. METHOD: A retrospective analysis on the data collected prospectively in a tertiary referral center. RESULTS: From January 1991 to December 2002, five renal transplant recipients were diagnosed to have primary HCC and received treatment in our center. There were four men and one woman with a median age of 47 (range, 38-68) years. Four of them had cadaveric renal transplantation whereas one had live donor transplantation. All of them were HBV carriers. The median tumor size was 3.5 cm (range, 1.8-8 cm). All tumors, except one, were diagnosed in sub-clinical stage by surveillance serum alpha-fetoprotein assay and percutaneous ultrasonography. Four patients were treated with surgical resection and one received transarterial oily chemoembolization (TOCE) as their primary treatments. There was one peri-operative death and the remaining three surgically treated patients were alive 4, 62, and 64 months after the resection. One patient developed recurrence 18 months after curative resection and was treated with TOCE. The patient with unresectable disease was alive for 50 months after the initial diagnosis. The surgical resection and overall survival rates of these patients were better than the published results. CONCLUSION: Early detection with regular serum alpha-fetoprotein assay and ultrasonographic study, vigilant care in the peri-operative period, long-term follow-up for detection and treatment of recurrence, as well as close collaboration between renal physicians and liver surgeons may improve the outcome of treatment of HCC in renal transplant recipients.

Adult↗

Up-regulation of vascular endothelial growth factor (VEGF) in small-for-size liver grafts enhances macrophage activities through VEGF receptor 2-dependent pathway.

This study aims to investigate the potential role of vascular endothelial growth factor (VEGF) and VEGF-R2 (fetal liver kinase (Flk)-1) in mediating macrophage activities in small-for-size liver transplantation. A rat orthotopic liver transplantation model was performed using either whole, 50, or 30% liver grafts (both 50 and 30% were regarded as small-for-size) in syngeneic or allogeneic combinations, respectively. Firstly, the mRNA and protein levels of VEGF and Flk-1 in liver grafts were detected by RT-PCR and Western blot, and the number of Flk-1(+) macrophages (labeled by ED1) was determined by flow cytometry. It was found that the small-for-size isografts and allografts presented higher levels of VEGF and Flk-1 expression than the whole isograft and allograft. In addition, a higher number of Flk-1(+)ED1(+) cells were detected in the small-for-size isografts and allografts than the whole isograft and allograft. Secondly, our study revealed that macrophage cell lines did not initially express detectable Flk-1, but could be induced by VEGF, and the inducible expression of Flk-1 in macrophages was related to their migration and proliferation activities. Finally, our study demonstrated that the induction of Flk-1 expression on macrophages by VEGF was associated with the expression of NF-kappaB and heat shock protein 90. In conclusion, the present study showed that the up-regulated expression of VEGF and its interaction with Flk-1 in small-for-size liver grafts might facilitate the activities of macrophages.

Animals↗

FTY720 induces apoptosis of human hepatoma cell lines through PI3-K-mediated Akt dephosphorylation.

Our aim was to study the anticancer effect of the novel immunomodulator FTY720 in vitro and in vivo by investigation of cell cycle entry, cell cycle regulation, cell survival and apoptosis pathways. Three hepatoma cell lines with different p53 statuses (HepG2, Huh-7 and Hep3B) and one non-tumorigenic immortalized liver cell line (MIHA) were used for an in vitro study. The in vivo effects of FTY720 were evaluated in a nude mouse tumor model. Cell cycle distribution and cell cycle regulator proteins p27(Kip1) and cyclin D1, together with the PI3-K/Akt pathway, mitogen-activated protein kinases and cleaved caspase-3 and caspase-9, were evaluated. FTY720 selectively induced cell apoptosis in hepatoma cell lines with overexpression of cleaved caspase-3 and caspase-9, but the same phenomena were not found in MIHA cells. FTY720 induced Akt dephosphorylation at Ser473 mediated by phosphoinositide 3-kinase (PI3-K) inhibition. Dephosphorylation led to down-regulation of p42/p44 and dephosphorylation of Forkhead transcription factor and GSK-3beta and, subsequently, up-regulation of p27(Kip1) and down-regulation of cyclin D1. In our in vivo model FTY720 induced apoptosis of tumor cells by down-regulation of the Akt pathway. FTY720 suppressed tumor growth without notable side-effects in normal liver. In conclusion, FTY720 is a novel anticancer agent that induces apoptosis of hepatoma cell lines both in vitro and in vivo through PI3-K-mediated Akt dephosphorylation in a p53-independent manner.

Apoptosis↗

The potential role of hypoxia inducible factor 1alpha in tumor progression after hypoxia and chemotherapy in hepatocellular carcinoma.

This study investigates the possible molecular basis leading to failure in a treatment that is composed of hypoxia and chemotherapy in a rat orthotopic hepatoma model. Hypoxia was induced by hepatic artery ligation, whereas chemotherapeutic effect was achieved by intraportal injection of cisplatin. High-dose sodium salicylate was administered to achieve transcriptional blockade. Significant prolongation of animal survival was observed in the groups receiving hepatic artery ligation with cisplatin or sodium salicylate. Massive tumor cell necrosis and apoptosis were found in the ligation and all of the combined treatment groups. Up-regulation of hypoxia inducible factor 1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) at both mRNA and protein levels were detected in the groups receiving ligation and ligation with cisplatin, whereas a decreased level of von Hippel-Lindau tumor suppressor protein was identified in the group receiving ligation with cisplatin. Sodium salicylate enhanced expression of von Hippel-Lindau tumor suppressor protein but down-regulated HIF-1alpha and VEGF levels after ligation with or without cisplatin. An increased number of activated hepatic stellate cells in the tumors were observed in the ligation and ligation with cisplatin groups, whereas they were greatly reduced by sodium salicylate. In vitro study revealed that under hypoxic condition, both cisplatin and sodium salicylate could remarkably augment P53 and caspase 3 levels. Cisplatin stimulated HIF-1alpha up-regulation, whereas sodium salicylate suppressed HIF-1alpha expression. In conclusion, tumor progression after hypoxia and chemotherapy might be related to up-regulation of HIF-1alpha and subsequent VEGF production, and transcriptional blockade by sodium salicylate could enhance the therapeutic efficacy of hypoxia and chemotherapy.

Animals↗

Expression of hepatocyte-like phenotypes in bone marrow stromal cells after HGF induction.

Bone marrow comprises heterogeneous cell populations, of which certain progenitors have demonstrated the ability to differentiate into multiple mesenchymal cell lineages. This study demonstrates the bone marrow stromal cells (BMSCs) with intrinsic plasticity to differentiate into hepatocyte-like phenotypes under in vitro induction of hepatocyte growth factor (HGF). BMSCs isolated from rat femurs and tibias were cultured and passaged 3-4 times in the presence of HGF. Cells were harvested on days 0, 10, and 20 and subjected to examination of any hepatocyte characteristics by flow cytometry, RT-PCR, Western blot, and immunocytochemistry. Expression of albumin and alpha-fetoprotein at both mRNA and protein levels was detectable on day 10. By contrast, c-Met mRNA was significantly decreased in BMSC in the course of HGF induction. Here BMSC was shown to differentiate into hepatocyte-like phenotypes given the HGF induction, as an alternative source for adult stem cell transplantation in liver repair.

Albumins↗

Clinical significance of thrombospondin 1 expression in hepatocellular carcinoma.

PURPOSE: Thrombospondin 1 (THBS 1) is a matricellular protein capable of modulating angiogenesis. However, the actual role of THBS 1 in angiogenesis and tumor progression remains controversial. Hepatocellular carcinoma (HCC) is a hypervascular tumor characterized by neovascularization. The significance of THBS 1 in HCC remains unknown. In this study, the significance of THBS 1 in HCC was evaluated by correlating its expression with clinicopathological data. The possible role of THBS 1 in the angiogenesis of HCC was also studied by correlating its expression with vascular endothelial growth factor (VEGF) expression. EXPERIMENTAL DESIGN: Sixty HCC patients were recruited in this study. THBS 1 and VEGF protein expression in tumorous livers were localized by immunohistochemical staining and quantified by ELISA. THBS 1 mRNA was quantified by quantitative reverse transcription-PCR. RESULTS: Immunohistochemical staining of THBS 1 was positive in HCC cells in 51.7% of patients and in stromal cells in 65% of patients. Tumor THBS 1 protein level was significantly correlated with its mRNA expression (P = 0.001) and was significantly correlated with tumor VEGF protein levels (P = 0.001). Its expression was significantly associated with the presence of venous invasion (P = 0.008) and advanced tumor stage (P = 0.049). High THBS 1 expression was also a prognostic marker of poor survival in HCC patients. CONCLUSIONS: This study shows that high expression of THBS 1 is associated with tumor invasiveness and progression in HCC. THBS 1 appears to be a proangiogenic factor that stimulates angiogenesis in HCC in view of its positive correlation with VEGF expression.

Aged↗

PIN1 overexpression and beta-catenin gene mutations are distinct oncogenic events in human hepatocellular carcinoma.

The peptidyl-proplyl-isomerase, PIN1, upregulates beta-catenin by inhibiting its interaction with APC. beta-catenin accumulation occurs in about 70% of hepatocellular carcinoma (HCC), of which only 20% are due to beta-catenin mutations. The role of PIN1 in beta-catenin upregulation in HCC was investigated. PIN1 was shown to be overexpressed in more than 50% of HCC. All cases with PIN1 overexpression also showed beta-catenin accumulation, with 68% of cases showing concomitant beta-catenin and cyclin D1 accumulation. PIN1 was shown to contribute to beta-catenin and cyclin D1 overexpression directly by in vitro cell-line transfection experiments. Finally, we showed that PIN1 overexpression and beta-catenin gene mutations appeared to be mutually exclusive events, leading to beta-catenin accumulation in HCC. These results showed that PIN1 overexpression leading to beta-catenin accumulation might be a critical event in hepatocarcinogenesis, and that PIN1 is a potential target for therapeutic intervention in HCC.

Carcinoma, Hepatocellular↗

Regulatory role of vHL/HIF-1alpha in hypoxia-induced VEGF production in hepatic stellate cells.

Activated hepatic stellate cells (HSCs) produce cyclooxygenase-2 (COX-2) protein to induce vascular endothelial growth factor (VEGF) production that participates in angiogenesis in injured liver. To reveal the unknown regulatory mechanism, we used hypoxic atmosphere mimicking injured-tissue microenvironment to induce VEGF expression in a rat hepatic stellate cell line (T6-HSCs). The present study showed that hypoxia up-regulated the protein levels of COX-2 and hypoxia-inducible factor-1-alpha (HIF-1alpha), but rapidly effected degradation of von Hippel-Lindau (vHL) protein. As a result, expression of VEGF in HSCs was markedly elevated; and pretreatment with COX-2 inhibitors (nimesulide or indomethacin) could significantly ameliorate the angiogenic event. Collectively, hypoxic HSCs increased accumulation of HIF-1alpha protein and induced VEGF expression in a time-dependent manner. Inhibition of COX-2 activities would prevent vHL protein from degradation and suppress HIF-1alpha up-regulation. Thus, vHL/HIF-1alpha has a regulatory role in COX-2-mediated VEGF production in hypoxic stellate cells in injured liver.

Animals↗

Risk factors for biliary complications after liver transplantation.

HYPOTHESIS: Biliary complications after liver transplantation can be predicted from perioperative factors. DESIGN: Retrospective analysis of data collected prospectively. SETTING: Tertiary referral center. PATIENTS: From October 5, 1991, through June 22, 2002, 230 patients received 241 consecutive orthotopic liver transplants. Patients were divided into those with (group 1) and those without (group 2) biliary complications. MAIN OUTCOME MEASURES: Postoperative outcomes, biliary leakage, and anastomotic stricture. RESULTS: The overall biliary complication rate was 20.7%, including bile leakage rate of 7.1% and anastomotic stricture rate of 16.2%. By means of univariate analysis, risk factors associated with biliary complications were preoperative serum bilirubin level (P = .003), international normalized ratio (P = .04), the use of stent or T-tube splinting of the anastomosis (P = .02), and the use of live-donor liver graft (P = .03). Stepwise logistic regression analysis demonstrated that the preoperative serum bilirubin level (relative risk [RR], 1.00), use of stent or T-tube splinting of the anastomosis (RR, 2.10), and use of live-donor liver graft (RR, 2.01) were independent risk factors predicting biliary complications after liver transplantation. Graft survival rates at 1, 3, and 5 years were 89.5%, 84.7%, and 79.7%, respectively, in group 1 and 84.7%, 78.4%, and 75.1%, respectively, in group 2 (P>.05). Patient survival rates at 1, 3, and 5 years were 89.1%, 86.5%, and 86.5%, respectively, in group 1, and 86.1%, 82.8%, and 81.0%, respectively, in group 2 (P>.05). CONCLUSIONS: Preoperative serum bilirubin level and the use of stent or T-tube splinting of the anastomosis and live-donor liver grafts were independent risk factors for biliary complications after liver transplantation. We postulated that high preoperative serum bilirubin level reflected severe liver disease and difficult hemostasis, leading to inadvertent injury to the anastomosis during graft rotation or manipulation for hemostasis. The use of a stent or a T tube predisposes to more complications. Further technical refinement is necessary for biliary reconstruction in live-donor liver transplantation.

Adolescent↗

Tailoring donor hepatectomy per segment 4 venous drainage in right lobe live donor liver transplantation.

Including the middle hepatic vein (MHV) in the right lobe liver graft for adult-to-adult live donor liver transplantation provides more functional liver by securing adequate venous drainage. Donor outcome of this procedure in relation to different venous drainage patterns of segment 4 is unknown. Modification of graft harvesting technique by preserving segment 4b hepatic vein (V4b) in theory compensates for unfavorable venous drainage patterns. Consecutive 120 right lobe live donors were included. Computed tomography was studied in detail to assign each donor to one of the three types of the Nakamura classification of venous drainage pattern of segment 4. Type I drainage was mainly via the left hepatic vein (LHV), type II drainage was equally into the MHV and LHV, and type III drainage was predominantly into the MHV. Any distinct umbilical vein was also noted. In the early part of the series, the V4b draining into the MHV was divided to provide a long MHV stump in the graft. In the later part of the series, prominent V4b draining into the MHV was preserved in the donor as far as possible. Donor outcomes were measured by peak values of prothrombin time (PT), serum bilirubin and transaminases levels. There was no donor mortality. Type I donors (n=69) had the best outcome with peak PT of 17.9 sec (range 12.3-23.3 sec). Type II donors (n=44) had peak PT of 18.5 sec (range 15.4-24.4 sec). When V4b was preserved in type II donors (n=19), the peak PT (18.0 sec, range 15.4-20.7 sec) became significantly lower than that of type II donors who had V4b sacrificed (20.3 sec, range 16.2-24.4 sec) (P=0.001). A distinct umbilical vein (n=91, 75.8%) was insignificant for donor outcome measured by peak PT. Multivariate analysis identified that type II donors with V4b sacrificed (n=25), type III donors (n=7), and the first 50 cases had less favorable outcomes. In conclusion, unfavorable venous drainage patterns were one of the independent factors compromising postoperative donor liver function, but was circumvented by preservation of V4b.

Adult↗

Interleukin-2 receptor antibody (basiliximab) for immunosuppressive induction therapy after liver transplantation: a protocol with early elimination of steroids and reduction of tacrolimus dosage.

A prospective evaluation was performed to study the potential benefits of the use of interleukin-2 receptor antibody (IL-2Rab) in the induction therapy with early elimination of steroid and reduction of tacrolimus dosage in liver transplant recipients among whom 94% had chronic hepatitis B infection. Thirty-one liver transplant recipients who underwent right-lobe live donor (n = 19) or cadaveric (n = 12) liver transplantation received IL-2Rab, basiliximab 20 mg intravenously within 6 hours of graft reperfusion and on postoperative day 4 (IL-2ab group). Two doses of steroid injection were given intraoperatively and on postoperative day 1. Postoperative immunosuppression was maintained with oral tacrolimus and mycophenolate mofetil without the use of steroids. The operative outcomes were compared with those of 49 patients who received standard immunosuppressive regimen consisting of tacrolimus and corticosteroid (steroid group). The overall postoperative morbidity and hospital stay were comparable between the 2 groups. There were significantly lower incidences of postoperative new-onset diabetes (0% vs 28%, P =.011), acute cellular rejection (6% vs 27%, P =.038), and cytomegalovirus (CMV) antigenemia (0% vs 18%, P =.011) in the IL-2Rab group compared with the steroid group. The blood cholesterol level at 6 months after transplantation was significantly lower in the IL-2Rab group (median, 4.0 vs 4.4 mmol/L, P =.007). On follow-up, none of the patients in the IL-2Rab group had hepatitis B viral breakthrough or hepatocellular carcinoma (HCC) recurrence, whereas 1 and 3 patients in the steroid group developed these complications, respectively. In conclusion, treatment of liver transplant recipients with IL-2Rab with early withdrawal of steroids and reduction of tacrolimus dosage is associated with lower incidences of postoperative new-onset diabetes, acute cellular rejection, and CMV antigenemia, as well as a lower serum cholesterol level. Further studies and long-term follow-up are required to document their potential benefits on hepatitis B and HCC recurrences.

Adrenal Cortex Hormones↗

Insulin in UW solution exacerbates hepatic ischemia / reperfusion injury by energy depletion through the IRS-2 / SREBP-1c pathway.

Ischemia / reperfusion (I / R) injury is related to tissue graft energy status. Insulin, which is currently used in the University of Wisconsin (UW) preservation solution with insulin (UWI), is an anabolic hormone and was shown to exacerbate the hepatic I / R injury in our previous study. In this study, the energy status and regulation of metabolism genes by insulin were investigated in liver grafts preserved by UW solution. Insulin could significantly decrease adenosine triphosphate (ATP) level after 3 hours of preservation, as well as total adenine nucleotides (TANs) and energy charge (EC) levels. Energy regeneration deteriorated in the grafts preserved by insulin in terms of ATP and EC levels at 24 hours after transplantation. The insulin signal was transduced through the insulin receptor substrate-2 (IRS-2) pathway and the activity of IRS-2 was decreased gradually at the messenger ribonucleic acid (mRNA) level during cold preservation. Downstream targeting genes such as sterol regulatory element-binding protein-1c (SREBP-1c), glucokinase (GKC), and fatty acid synthase (FAS) genes, as well as phospho-glycogen synthase kinase-3beta (GSK-3beta) were activated and they showed the similar expression profiles during cold preservation. Lipoprotein metabolism was accelerated by insulin through upregulation of the activity of apolipoprotein C-III (Apo C-III) during cold preservation. The insulin-like growth factor-binding protein-1 pathway was inhibited during cold preservation. In conclusion, insulin in UW solution exacerbates hepatic I / R injury by energy depletion as the graft maintains its anabolic activity. The key enzyme activities of the energy-consuming process of glycogen and fatty acid synthesis as well as lipoprotein metabolism were accelerated by insulin through the IRS-2 / SREBP-1c pathway.

Adenosine↗

Applicability of histidine-tryptophan-ketoglutarate solution in right lobe adult-to-adult live donor liver transplantation.

In a consecutive series of 60 right lobe adult-to-adult live donor liver transplantations (ALDLTs), safety and efficacy of the University of Wisconsin (UW) and histidine-tryptophan-ketoglutarate (HTK) solution were evaluated. The first 30 liver grafts were perfused with UW solution and the subsequent 30 by HTK solution. Donor and recipient characteristics of both groups were comparable. All liver graft implantations were performed with cross-clamping of the inferior vena cava (IVC) and without veno-venous bypass. Main outcome measures were posttransplantation liver biochemistry, prothrombin time, and recipient morbidity, as well as graft and recipient survival. There were no significant differences of the outcome measures between the 2 groups. The low potassium content of the HTK solution nonetheless offered logistic advantages. In 25 of the 30 recipients of the HTK group, portal vein anastomosis was performed with a clamp on the donor portal vein while the clamps on the IVC were already released. This shortened the period during which the IVC was being cross-clamped. HTK solution was as safe and effective as a cold storage solution as UW solution in ALDLT. Its low potassium content has advantage of earlier restoration of patency of the IVC and thus hemodynamic stability. The cost of using HTK solution was also lower.

Adenosine↗

Pancreaticoduodenectomy with en bloc portal vein resection for pancreatic carcinoma with suspected portal vein involvement.

Pancreaticoduodenectomy combined with portal vein resection is increasingly accepted as a viable treatment option for pancreatic carcinoma with suspected involvement of the portal vein.However, its clinical benefit remains controversial. This study evaluated the outcomes of pancreaticoduodenectomy with portal vein resection for pancreatic carcinoma in a group of Chinese patients operated on by a specialized team in a center with a low case volume of pancreatic cancer. The perioperative and long-term outcomes of 12 patients with portal vein resection for suspected involvement of the portal vein and 38 patients who underwent pancreaticoduodenectomy without portal vein resection during the same period were compared. In the former group, eight patients underwent segmental resection, and four patients underwent wedge resection of the portal vein. There were no significant differences in operative blood loss (median 0.8 vs. 0.8 liter, p = 0.313), hospital mortality (0% vs. 2.6%, p = 1.000), or operative morbidity (41.7% vs. 42.1%, p = 0.979) between the two groups. Patients who required portal vein resection had higher frequencies of microscopic lymphatic permeation (58.3% vs. 18.4%, p = 0.023) and vascular invasion (50.0% vs. 15.8%, p = 0.025). Long-term survival was comparable between patients with portal vein resection and those without it (median 19.5 vs. 20.7 months,p = 0.769). These findings suggest that pancreaticoduodenectomy combined with portal vein resection can be performed safely by a specialized team in a center with a low case volume of pancreatic carcinoma and that it may offer survival benefit in patients with suspected portal vein involvement.

Adenocarcinoma↗

Hepatic resection for incidentaloma.

The study goal was to review a single-center experience in hepatic resection for patients who presented with incidental liver tumors. With recent advances in diagnostic imaging techniques, incidental finding of liver tumors, or "incidentalomas," is increasing in asymptomatic and healthy individuals. However, little information is available in the literature regarding the underlying pathology and operative outcomes after hepatic resection. Between January 1989 and December 2002, 1011 patients underwent hepatic resection for liver tumors; of these patients, 107 (11%) were asymptomatic individuals who presented with incidentalomas. Incidentalomas were first detected on percutaneous ultrasonography (n = 83), computed tomography (n = 23), or magnetic resonance imaging (n = 1). Fifteen (14%) patients had preoperative aspiration for cytology or biopsy for histology, and the results correlated with the final pathology in 12 patients. Fifty-six (52%) patients underwent major hepatic resection with resection of three or more Coiunaud's segments. Median postoperative hospital stay was 8 days (range, 3-66 days). The operative mortality rate was 1%, and the operative morbidity rate was 21%. Histologic examination of the resected specimen revealed malignant liver tumors in 62 (58%) patients, including hepatocellular carcinoma (HCC) (n = 48), cholangiocarcinoma (n = 8), lymphoma (n = 2), cystadenocarcinoma (n = 2), carcinoid tumor (n = 1), and malignant fibrous histiocytoma (n = 1). Benign pathologies were found in 45 (42%) patients, including focal nodular hyperplasia (n = 17), hemangioma (n = 12), angiomyolipoma (n = 5), cirrhotic regenerative nodule (n = 4), hepatic adenoma (n = 2), and others (n = 5). On multivariate analysis, male sex, age of greater than 50 years, and tumor size of greater than 4 cm were the independent predictive factors for malignant diseases. On retrospective analysis, 48 patients with HCC who presented with incidentalomas had significantly better survival outcomes after hepatic resection than did 646 patients with HCC who presented otherwise during the same study period. Hepatic resection for patients with incidentalomas is associated with a low operative mortality and acceptable morbidity. The diagnosis of malignant disease, especially HCC, should be considered in male patients older than 50 years who present with large hepatic lesions.

Carcinoma, Hepatocellular↗

Treatment of hepatic artery thrombosis after orthotopic liver transplantation.

OBJECTIVES: This study evaluated conservative treatment for delayed hepatic artery thrombosis after orthotopic liver transplantation (OLT). METHODS: Whole-graft OLTs (n=108) and live donor liver transplants (LDLTs; n=140) were performed in 237 patients between October 1991 and July 2002. Seven episodes of hepatic artery thrombosis were identified in six patients. Among the six patients, three had received whole-graft OLT and three had received right-lobe LDLT. Treatment included retransplantation, thrombectomy plus thrombolysis, and conservative treatment of hepatic and biliary complications. RESULTS: Five patients survived after treatment. Among the three LDLT recipients who received conservative treatment, two had subsequent collateral formation and one had spontaneous recanalization of arterial inflow. Of the three recipients of whole-graft OLT, the first died because of hepatic failure and technically difficult retransplantation, the second had thrombectomy plus thrombolysis but had recurrence of thrombosis that spontaneously recannulated during conservative treatment, and the third patient had successful retransplantation for graft failure. CONCLUSION: In the absence of hepatic failure, conservative treatment appears to be effective for patients with hepatic artery thrombosis. Collateralization is more likely to develop after LDLT than after whole-graft OLT.

Adult↗