The purpose of this study was to evaluate the role of angiogenesis, proliferative activity (assessed by Ki-67 expression), p53 and ras-oncogene (H-ras) expression, and conventional clinicopathologic factors in predicting overall survival rates in patients with pancreatic ductal adenocarcinoma. We followed-up 22 patients with ductal adenocarcinoma of the pancreas for a median of 19 months (range, 2 to 44 months). Angiogenesis was quantitated as vascular surface density (VSD) and the number of vessels per mm2 stroma (NVES) after microvessels were immunostained, using factor VIII-related antigen. p53, H-ras, and Ki-67 proteins were also determined immunohistochemically. VSD and NVES showed significant correlations with increased proliferative activity, poor tumor differentiation, and tumor size of 3 cm or more (P = 0.001, P = 0.013, and P = 0.047, respectively). The overall 2-year survival rate of 33.3% in patients with high VSD and NVES values was significantly worse than that of 66.6% estimated in patients with low microvessel count (log rank, 3.97; P = 0.046). In multivariate analysis using the Cox model, VSD was found to be an independent prognostic factor of survival (P = 0.039). H-ras and p53 expressions were not correlated with angiogenesis parameters. We conclude that, in pancreatic ductal adenocarcinoma, angiogenesis is closely related to tumor growth and patient survival.

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Background: The purpose of our study was to investigate the immunohistochemical expression of TGF-β1 and p27 in pancreatic adenocarcinomas and to compare the findings with the clinicopathological features and survival. We also aimed to evaluate the expression of TGF-β1 and p27 in the context of other cell cycle and proliferation markers such as cyclin D1 and Ki-67.

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Mirizzi's syndrome is a rare complication of long-standing cholelithiasis. Many surgical approaches of varying complexity have been advocated for treatment. However, the distorted extrahepatic biliary anatomy continues to be threatening, with a high risk of biliary complications. Presented here is a series of 25 patients with Mirizzi's syndrome who were treated at the Dokuz Eylul University Hospital since 1985. Type I lesion (without cholecystocholedochal fistula) was encountered in 11 patients, while the remaining 14 had type II lesions (with cholecystocholedochal fistula). Preoperative diagnoses were made in 14 of the 25 patients (56%). Follow-up in 17 patients ranged from 1 to 96 months (mean, 40 months). Unfortunately, the remaining 8 patients were lost to follow-up after discharge. The morbidity rate in our series was 32%, while no mortality was encountered. During long-term follow-up, no biliary stricture was diagnosed. Following an uneventful postoperative course, all of our patients are symptom-free and doing well, with normal liver function. We conclude that partial cholecystectomy alone is a safe and sound surgical approach for the treatment of type I lesions. For type II lesions, depending on the size of the fistula, either primary closure over a T-tube, or bilio-digestive anastomosis, preferably Roux-en-Y, can be an appropriate treatment modality, with a low morbidity rate.

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Primary hyperoxaluria type 1 (PH1) is a rare inherited metabolic disorder in which deficiency of the liver enzyme AGT leads to renal failure and systemic oxalosis. Timely, combined cadaveric liver-kidney transplantation (LKT) is recommended for end-stage renal failure (ESRF) caused by PH1; however, the shortage of cadaveric organs has generated enthusiasm for living-related transplantation in years. Recently, successful sequential LKT from the same living donor has been reported in a child with PH1. We present a sister-to-brother simultaneous LKT in a pediatric patient who suffered from PH1 with ESRF. Twelve months after transplantation, his daily urine oxalate excretion was decreased from 160 mg to 19.5 mg with normal liver and renal allograft functions. In addition to the well-known advantages of living organ transplantation, simultaneous LKT may facilitate early postoperative hemodynamic stability and may induce immunotolerance and allow for low-dose immunosuppression. (Liver Transpl 2003;9:433-436.) P rimary hyperoxaluria type 1 (PH1) is a rare, inherited metabolic disorder caused by a deficiency of the liver-specific peroxisomal alanine-glyoxylate aminotransferase (AGT). It is characterized by increased synthesis and urinary excretion of oxalate that leads to renal failure attributable to urolithiasis, nephrocalcinosis, and, subsequently, to oxalate accumulation in various extra-renal tissues such as the skeleton and the cardiovascular system. Because the liver is the site of the metabolic defect, isolated kidney transplantation (KT) is not a reasonable therapeutic alternative because of a rapid diffuse oxalate deposition in the allograft. 1 Preemptive liver transplantation (LT) has been successfully performed in some children before serious renal damage occurred. 2 If end-stage renal failure (ESRF) has been reached, early simultaneous or sequential liver-KT (LKT) may avoid the deleterious consequences of systemic oxalosis. 3 Shortage of donor organs remains the critical factor limiting the use of organ transplantation. This shortage has generated enthusiasm for living-related transplantation, offering hope not only for children but also for adolescents and even adults. Partial LT alone or sequential LKT from living donors have been successfully performed for PH1. 4,5 To date, there have been no reports describing combined simultaneous LKT from the same living donor in the treatment of PH1 complicated with ESRF.