In patients with advanced biliary malignancies a chance of curability is obtained by performing only major hepatectomy with concomitant pancreatoduodenectomy. This aggressive procedure carries two major risks: hepatic failure and pancreatic anastomotic leakage. Ten patients with advanced biliary malignancies were treated by major hepatectomy with pancreatoduodenectomy. Nine patients underwent right portal venous embolization before hepatectomy. Complete external drainage of pancreatic juice followed by second-stage pancreatojejunostomy was performed in five patients. Three of these five underwent concomitant resection of the hepatic artery, portal vein, or both. Pancreatogastrostomy was chosen for five patients who required no concomitant vascular resection. There were no hospital deaths or hepatic failures. Leaks from pancreatogastrostomy occurred in two patients. In five patients who underwent external drainage of pancreatic juice, there were no complications related to the pancreatic stump, although one had ischemic necrosis of the jejunal segment and laparotomy was repeated. Mean survival time was 31.8 months (range 13-59 months). Portal venous embolization and complete external drainage of pancreatic juice followed by late stage pancreatojejunostomy are recommended surgical procedures for patients undergoing major hepatectomy with pancreatoduodenectomy, especially when concomitant vascular resection is required for curative resection of the tumor in patients with a soft pancreatic parenchyma and thin pancreatic duct.
The favorable therapeutic effect of preoperative portal vein embolization (PVE) was analyzed by assessing various volumetric, cell kinetic and morphometric parameters and examining histologically the embolized and nonembolized lobes of 15 patients who underwent extended right lobectomy 2 to 3 weeks after PVE. Each lobar volume was calculated from computed tomography (CT) images, hepatocyte proliferation was evaluated by assessing proliferative cell nuclear antigen (PCNA) expression and mitosis, hepatocyte apoptosis was evaluated by the terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and the hepatocyte numerical density as well as the sinusoidal volumetric ratio (Vvs) and the mean hepatocyte volume (Cv) were calculated using morphometric methods. PVE induced hepatocyte apoptosis and atrophy of the embolized lobe (from 798 +/- 213 to 708 +/- 222 cm3; P < .05). The increased sinusoidal volume in this lobe (17.7% +/- 4.5% and 21.7% +/- 5.7%, periportal and pericentral area, respectively) may have been attributable to hepatocyte deletion. Cells in the nonembolized lobe entered a highly active phase of proliferation within 2 weeks after PVE. Further evidence of cellular proliferation was provided by the increased nonembolized lobar volume (from 379 +/- 132 to 545 +/- 130 cm3; P < .01) and numerical density of hepatocyte nuclei (Nv) (5.38 +/- 1.26 vs. 3.11 +/- 0.85 x 10(5)/mm3; P < .01, nonembolized vs. embolized lobe, respectively). In conclusion, these results indicate that the favorable effect of PVE is attributable to a net gain of functional hepatocyte mass and/or early induction of hepatocyte proliferation following hepatectomy.
The favorable therapeutic effect of preoperative portal vein embolization (PVE) was analyzed by assessing various volumetric, cell kinetic and morphometric parameters and examining histologically the embolized and nonembolized lobes of 15 patients who underwent extended right lobectomy 2 to 3 weeks after PVE. Each lobar volume was calculated from computed tomography (CT) images, hepatocyte proliferation was evaluated by assessing proliferative cell nuclear antigen (PCNA) expression and mitosis, hepatocyte apoptosis was evaluated by the terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and the hepatocyte numerical density as well as the sinusoidal volumetric ratio (Vvs) and the mean hepatocyte volume (Cv) were calculated using morphometric methods. PVE induced hepatocyte apoptosis and atrophy of the embolized lobe (from 798 +/- 213 to 708 +/- 222 cm3; P < .05). The increased sinusoidal volume in this lobe (17.7% +/- 4.5% and 21.7% +/- 5.7%, periportal and pericentral area, respectively) may have been attributable to hepatocyte deletion. Cells in the nonembolized lobe entered a highly active phase of proliferation within 2 weeks after PVE. Further evidence of cellular proliferation was provided by the increased nonembolized lobar volume (from 379 +/- 132 to 545 +/- 130 cm3; P < .01) and numerical density of hepatocyte nuclei (Nv) (5.38 +/- 1.26 vs. 3.11 +/- 0.85 x 10(5)/mm3; P < .01, nonembolized vs. embolized lobe, respectively). In conclusion, these results indicate that the favorable effect of PVE is attributable to a net gain of functional hepatocyte mass and/or early induction of hepatocyte proliferation following hepatectomy.
Background: The doubling times of liver metastases were calculated in order to clarify their usefulness in predicting the presence of residual cancer in the abdominal cavity in patients who had undergone curative resection of primary colorectal cancer. Patients and Methods: Tumor doubling times were calculated retrospectively in 22 patients by serial measurement of the size of their liver metastases. Results: Patients with a tumor doubling time of less than 92.4 days had a significantly poorer prognosis than those with a doubling time more than or equal to 92.4 days (p < 0.05). Local recurrence or peritoneal dissemination was significantly more likely to occur when the tumor doubling time was less than 92.4 days than when it was more than or equal to 92.4 days (p < 0.01). Conclusion: The doubling time of hepatic metastases in patients with colorectal carcinoma may be a useful prognostic indicator, with patients who have a shorter tumor doubling time carrying a greater risk of residual primary cancer in the abdominal cavity.
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