Chylous ascites after hepatopancreatobiliary surgery.

BACKGROUND: Postoperative chylous ascites following abdominal surgery is uncommon. It potentially induces malnutrition and immunodeficiency, contributing to increased mortality. In the field of hepatopancreatobiliary (HPB) surgery, no large studies have been conducted that focused on postoperative chylous ascites. The aim of this study was to determine the incidence, risk factors and management of chylous ascites following HPB surgery, with particular emphasis on pancreatic resection. METHODS: Consecutive patients who had HPB surgery between 2000 and 2011 at a single institution were reviewed retrospectively. Chyle leak was defined as 100 ml/day or more of milky, amylase-free peritoneal fluid with a triglyceride concentration of 110 mg/dl or above. Risk factors for chylous ascites associated with pancreatic resection and the clinical efficacy of octreotide in treating chylous ascites were evaluated. RESULTS: Of 2002 consecutive patients who underwent HPB surgery during the study period, 21 (1·0 per cent) developed chylous ascites. Chylous ascites occurred relatively frequently in patients who had a pancreatic resection, such as pancreaticoduodenectomy (3·3 per cent) or distal pancreatectomy (3·8 per cent). Multivariable analysis revealed that manipulation of the para-aortic area (P < 0·001), retroperitoneal invasion (P = 0·031) and early enteral feeding after operation (P < 0·001) were independent risk factors for chylous ascites following pancreatic resection. Octreotide treatment decreased drainage output of chylous ascites on day 1 after initiation of treatment (P = 0·002). CONCLUSION: Chylous ascites is a rare complication following HPB surgery. It is more common after pancreatic resection. Treatment with octreotide combined with total parenteral nutrition is recommended.

Increased circulating cell signalling phosphoproteins in sera are useful for the detection of pancreatic cancer.

BACKGROUND: Intracellular phosphoprotein activation significantly regulates cancer progression. However, the significance of circulating phosphoproteins in the blood remains unknown. We investigated the serum phosphoprotein profile involved in pancreatic cancer (PaCa) by a novel approach that comprehensively measured serum phosphoproteins levels, and clinically applied this method to the detection of PaCa. METHODS: We analysed the serum phosphoproteins that comprised cancer cellular signal pathways by comparing sera from PaCa patients and benign controls including healthy volunteers (HVs) and pancreatitis patients. RESULTS: Hierarchical clustering analysis between PaCa patients and HVs revealed differential pathway-specific profiles. In particular, the components of the extracellular signal-regulated kinase (ERK) signalling pathway were significantly increased in the sera of PaCa patients compared with HVs. The positive rate of p-ERK1/2 (82%) was found to be superior to that of CA19-9 (53%) for early stage PaCa. For the combination of these serum levels, the area under the receiver-operator characteristics curves was showing significant ability to distinguish between the two populations in independent validation set, and between cancer and non-cancer populations in another validation set. CONCLUSION: The comprehensive measurement of serum cell signal phosphoproteins is useful for the detection of PaCa. Further investigations will lead to the implementation of tailor-made molecular-targeted therapeutics.

Significance of repeated resection for recurrent intrahepatic cholangiocarcinoma.

BACKGROUND/AIMS: Management of patients with recurrent intrahepatic cholangiocarcinoma (ICC) following surgical resection is difficult, and surgical resection is rarely indicated. We retrospectively reviewed patients with recurrent intrahepatic cholangiocarcinoma. METHODOLOGY: Between April 1998 and March 2007, 57 consecutive patients with ICC underwent surgical resection. Mode of recurrence and treatment of recurrent tumors, especially surgical resection for these tumors, in patients with cancer recurrence were evaluated. RESULTS: 37 (65%) patients experienced tumor recurrence. Out of these patients, 24 underwent some type of cancer-directed therapy, including 9 patients (24%) for whom surgical resection was attempted: the latter included 4 hepatic resections, 2 pulmonary resections, 2 tumor resections, and 1 gastric resection. For 6 patients with recurrent tumor in the liver or the lung, microscopic complete resection was achieved, while incomplete resection was resulted in the remaining 3 patients. No postoperative mortality was encountered. Among patients with complete resection, 3 are alive without disease 32, 39 and 77 months after the second operation, one has lived with disease for 13 months, and 2 died of disease after 22 and 26 months. No significant difference in overall survival was observed between patients undergoing primary and second surgical resections, calculated from the primary and the second operations, respectively. CONCLUSIONS: Repeated surgical resection for recurrent ICC can be performed with acceptable morbidity, and affords selected patients a chance for long-term survival.

FGF10/FGFR2 signal induces cell migration and invasion in pancreatic cancer.

Pancreatic cancer has one of the highest mortalities among all malignancies and there is an urgent need for new therapy. This might be achieved by resolving the detailed biological mechanism, and in this study we examined how pancreatic cancer cells develop aggressive properties by focusing on signalling through the fibroblast growth factor (FGF)10 and FGF receptor (FGFR)2, which play important roles in pancreatic organogenesis. Immunostaining of pancreatic cancer tissues showed that FGFR2 was expressed in cancer cells, whereas FGF10 was expressed in stromal cells surrounding the cancer cells. Patients with high FGFR2 expression in cancer cells had a shorter survival time compared to those with low FGFR2 expression. Fibroblast growth factor 10 induced cell migration and invasion of CFPAC-1 and AsPC-1 pancreatic cancer cells through interaction with FGFR2-IIIb, a specific isoform of FGFR2. Fibroblast growth factor 10 also induced expression of mRNA for membrane type 1-matrix metalloproteinase (MT1-MMP) and transforming growth factor (TGF)-beta1, and increased secretion of TGF-beta1 protein from these cell lines. These data indicate that stromal FGF10 induces migration and invasion in pancreatic cancer cells through interaction with FGFR2, resulting in a poor prognosis. This suggests that FGF10/FGFR2 signalling is a promising target for new molecular therapy against pancreatic cancer.

Poor postoperative blood glucose control increases surgical site infections after surgery for hepato-biliary-pancreatic cancer: a prospective study in a high-volume institute in Japan.

Two hundred and sixty-five consecutive patients awaiting hepato-biliary-pancreatic surgery were prospectively observed for surgical site infections (SSIs). SSI rates differed according to type of hepato-biliary-pancreatic surgery. Multivariate analysis identified enteric anastomoses, poor postoperative blood glucose control and type of cancer as independent risk factors. SSI rates were directly correlated with the degree of hyperglycaemia encountered during the postoperative period. In particular, SSI rates were 5/25 (20%) among patients in whom a blood glucose level of <200mg/dL was maintained by insulin infusion therapy, which was significantly better than the rates of 49/94 (52%) among patients in whom a blood glucose level of <200mg/dL was not maintained despite insulin infusion therapy (P<0.01). It is necessary to maintain postoperative blood glucose levels of <200mg/dL in order to reduce SSI rates.

Results of surgical treatment for intrahepatic cholangiocarcinoma and clinicopathological factors influencing survival.

BACKGROUND: The results of surgical treatment for intrahepatic cholangiocarcinoma (ICC) and specific factors influencing survival are still unclear. METHODS: Between 1984 and 2001, 62 patients with ICC underwent laparotomy, with a 77 per cent (48 patients) resectability rate. The tumours in these 48 patients were reviewed retrospectively to examine the relationship between gross appearance (mass forming, periductal infiltrating, intraductal growth, and mass forming plus periductal infiltrating) and patient survival, as well as the manner of recurrence. In patients with mass-forming and mass-forming plus periductal infiltrating types, univariate and multivariate analyses of potential prognostic factors were performed. RESULTS: The 1-, 3- and 5-year survival rates were 62, 38 and 23 per cent respectively. All patients with the intraductal growth type remained alive after intervals ranging from 8 to 72 months. Univariate analysis showed multiple hepatic lesions, liver capsule invasion, presence of cancer cells in the resection margin, and high serum carbohydrate antigen (CA) 19-9 level to be significant negative prognostic factors. Lymph node involvement, however, was not identified as a significant prognostic factor. With multivariate analysis, multiple hepatic lesions and high serum CA19-9 concentration were found to be significantly related to prognosis. The most frequent recurrence site was the remnant liver. CONCLUSION: These results suggest that the intraductal growth type of tumour should be treated as a distinct entity compared with other types of ICC. Multiple tumours and high serum CA19-9 level were signs of dismal prognosis, whereas not all patients with lymph node involvement had a poor prognosis.

An approach to intrapericardial inferior vena cava through the abdominal cavity, without median sternotomy, for total hepatic vascular exclusion.

In surgical resection for hepatocellular carcinoma with tumor thrombus extending into the inferior vena cava and other malignancies involving the retrohepatic inferior vena cava, the usefulness of total hepatic vascular exclusion has been reported by several authors. Total hepatic vascular exclusion usually consists of clamping at three points; at the infrahepatic inferior vena cava, at the suprahepatic inferior vena cava, and in Pringles' maneuver. Tumor thrombus extending into the inferior vena cava at the intrapericardial level below the right atrium can be resected without the use of cardio-pulmonary bypass. The inferior vena cava at the intrapericardial level has been reported to be usually approached by median sternotomy such as Chevron incision. We herein demonstrate an approach to the intrapericardial inferior vena cava through the abdominal cavity without median sternotomy.

Vascular endothelial growth factor secreted by replicating hepatocytes induces sinusoidal endothelial cell proliferation during regeneration after partial hepatectomy in rats.

BACKGROUND: The aim of this study was to investigate regulatory mechanisms of sinusoidal endothelial cell (SEC) proliferation after hepatectomy in rats. METHODS: We investigated expressions of vascular endothelial cell growth factor (VEGF) and its receptors, flt-1 and KDR/flk-1, in regenerating liver after 70% hepatectomy. Proliferation of both hepatocytes and SECs was also monitored by evaluating the proliferating cell nuclear antigen (PCNA) labeling index. Furthermore, VEGF production by cultured hepatocytes isolated at different times after hepatectomy was measured in vitro. RESULTS: The expression of VEGF mRNA was increased markedly between 48 and 72 h after hepatectomy, and thereafter decreasing gradually. The immunohistochemical staining revealed that expression of VEGF started to increase 24 h after hepatectomy, with a peak at 72 h, and the majority of the VEGF-positive cells were hepatocytes located in periportal areas. Meanwhile, expression of flt-1 and KDR/flk-1 was observed along the sinusoids even before hepatectomy, but was increased between 72 and 120 h. Furthermore, VEGF production by cultured hepatocytes isolated 72 h after hepatectomy was significantly increased. The PCNA labeling index of the SECs exhibited a delayed and slower regenerative response in comparison to the hepatocytes, reaching a peak at 72 h. CONCLUSIONS: These data strongly suggest that VEGF secreted by proliferating hepatocytes may represent an important stimulator of SEC proliferation.

Benefits and limits of hepatic resection for gastric metastases.

BACKGROUND: The significance of hepatic resection for gastric metastases has been controversial. METHODS: Forty consecutive patients undergoing hepatic resection for gastric metastases were reviewed to examine the benefits and the limits of hepatic resection using univariate and multivariate analyses. RESULTS: The overall survival was 27% at 2 years, 18% at 5 years, and 11% at 10 years. Six patients survived more than 5 years. All of the 6 patients underwent anatomical hepatic resection more extensive than segmentectomy, with sufficient resection margin. There were recurrences in 31 patients, and 94% of the recurrences were in the remaining liver. Univariate analysis showed time of hepatic metastases (P = 0.0078) and resection margin (P = 0.024) as significant prognostic factors. Multivariate analysis indicated that only time of hepatic metastases was an independent prognostic factor that influenced survival. CONCLUSIONS: These results suggest that in patients with synchronous metastases we should consider patient selection more strictly, and that in patients with metachronous metastases we should perform anatomical hepatic resection with sufficient resection margin.

Nonsurgical management of ruptured pseudoaneurysm in patients with hepatobiliary pancreatic diseases.

OBJECTIVE: Rupture of a pseudoaneurysm is an unusual complication after surgical and interventional treatments in patients with hepatobiliary pancreatic diseases. However, it occurs abruptly and often results in a lethal outcome. The aim of this study was to retrospectively analyze our experiences of cases of rupture of pseudoaneurysms for providing appropriate therapeutic planning. METHODS: Between 1985 and 1998, we observed ruptures of pseudoaneurysms in 14 of 910 patients with hepatobiliary pancreatic diseases--six after pancreaticoduodenectomy, three after hepatic resection, two after hepatopancreaticoduodenectomy, two after percutaneous transhepatic biliary drainage, and one after gastrojejunostomy. Thirteen of the 14 patients underwent emergency angiography and transcatheter arterial embolization (TAE) or infusion therapies, and one of the 13 patients underwent surgical hemostasis because of incomplete hemostasis with TAE. The other patient, who did not undergo emergency angiography, had surgical hemostasis initially. RESULTS: TAE achieved hemostasis in 11 of 13 patients (85%), but only incomplete hemostasis in the remaining two patients. Of these two patients, one underwent laparotomy, but died of multiple organ failure (MOF) at 6 days after surgical hemostasis. The other died at 1 day after emergency angiography. Ten of 11 patients who obtained complete hemostasis by means of TAE could later be discharged, but one patient died of liver failure, and/or MOF. One patient who underwent laparotomy initially without angiography died of MOF at 43 days after the operation. The onset of rupture of a pseudoaneurysm was a mean of 35.4 days (range 12-76) after surgical or interventional procedures. The warning prodromal symptoms were upper abdominal oppression, nausea, and backache before the rupture of pseudoaneurysms. Fever, leukocytosis. hyperbilirubinemia, anastomotic leak, and intraabdominal abscess were frequent persistent signs in these patients. CONCLUSIONS: If the warning prodromal symptoms appear in patients along with these persistent signs, the impending rupture of pseudoaneurysms should be suspected. Thereafter, a diagnostic angiography should be performed immediately to enable early diagnosis and embolization therapy for rupture of pseudoaneurysms when hemorrhagic episodes appear in these patients. Early detection and immediate embolization might bring about a favorable outcome in patients with hepatobiliary pancreatic diseases who encounter rupture of pseudoaneurysms after surgical and interventional treatments.

Allelic loss in human intrahepatic cholangiocarcinoma: correlation between chromosome 8p22 and tumor progression.

Intrahepatic cholangiocarcinoma (ICC) is the second most common malignant primary tumor of the liver in Japan. Despite progress in operative techniques and adjuvant therapy, the prognosis of ICC remains very poor. Therefore, it is important to investigate the mechanism of carcinogenesis and progression of ICC. We screened allelic losses at 6 loci, including that of novel tumor-suppressor gene FEZ1 on chromosome 8p, and at 5 microsatellite loci to define the association with tumor-suppressor genes (HNPCC, APC, RB1, p53, DCC) in tumors from 18 unrelated ICC patients by PCR-loss of heterozygosity (LOH) assay and correlated the alterations with clinicopathological parameters. As a result, 61.1% (11 of 18) of patients showed LOH at 1 of the loci at least, and microsatellite instability was observed in 16.7% (3 of 18). At locus D8S258, relatively frequent LOH was detected (17.6%) compared with other loci on chromosome 8p. Among the other 5 chromosomal arms tested, the highest frequency of LOH (23.5%) was observed at D17S153. Fifty percent of cases with the mass-forming + periductal infiltrating type were frequently detected by LOH at D8S258 compared to cases of the mass-forming or intraductal growth type. In conclusion, we show that 1 putative tumor-suppressor gene on 8p22 may relate to progression of ICC and suggest that the p53 tumor-suppressor gene may be associated with carcinogenesis of ICC.

Reduced hepatic ischemia/reperfusion injury by IL-4: potential anti-inflammatory role of STAT6.

OBJECTIVE AND DESIGN: The ability of interleukin-4 (IL-4) to modulate activation of the transcription factors, NF-kappaB and STAT6, reduce proinflammatory cytokine expression and protect against liver injury induced by ischemia/reperfusion was assessed. MATERIALS AND SUBJECTS: C57BL/6 mice underwent 90 minutes of partial hepatic ischemia followed by 1 or 8 h of reperfusion with or without intravenous administration of 1 microg (0.5 microg just prior to ischemia, 0.5 microg at reperfusion) recombinant murine IL-4. Liver expression of TNFalpha mRNA was determined by RT-PCR. Activation of NF-kappaB and STAT6 in liver nuclear extracts was assessed by mobility shift assay. RESULTS: Hepatic ischemia/reperfusion increased hepatic expression of tumor necrosis factor-alpha (TNFalpha), induced significant neutrophil accumulation and liver injury. Treatment with IL-4 greatly suppressed liver TNFalpha mRNA expression, neutrophil accumulation and liver injury. IL-4 had no effect on liver NF-kappaB activation, but greatly increased the activation of STAT6. CONCLUSIONS: The data suggest that STAT6 activation by IL-4 may be responsible for the protective effects of this cytokine.

Obstructive jaundice impairs hepatic sinusoidal endothelial cell function and renders liver susceptible to hepatic ischemia/reperfusion.

BACKGROUND/AIMS: Obstructive jaundice is associated with increased surgical morbidity and mortality. While parenchymal injury has been defined in obstructive jaundice, the pathogenesis of hepatic sinusoidal endothelial cell injury in obstructive jaundice is unclear. The aims of this study were to investigate hepatic sinusoidal endothelial cell injury in obstructive jaundice by determining serum hyaluronic acid levels, purine nucleoside phosphorylase/alanine aminotransferase ratios, and hyaluronic acid elimination rate, and also to determine whether hepatic parenchymal cell injury in obstructive jaundice is induced more than in normal liver after hepatic ischemia/reperfusion. METHODS: Male Wistar rats underwent ligation and division of the common bile duct (obstructive jaundice group) or sham operation (Sham group). Serum hyaluronic acid levels and purine nucleoside phosphorylase/alanine aminotransferase ratios in both groups were examined at intervals up to 21 days after surgery. Hepatic blood flow, permeability, neutrophil accumulation, and hyaluronic acid elimination rates in both groups were measured 14 days after surgery. Changes in serum hyaluronic acid and alanine aminotransferase concentrations were determined after 15 min of hepatic ischemia followed by reperfusion. RESULTS: Serum hyaluronic acid levels remained elevated after bile duct ligation. Hepatic sinusoidal endothelial cell swelling was observed by electron microscopy, and hepatic permeability was increased 14 days after bile duct ligation in association with neutrophil accumulation. Hepatic blood flow in obstructive jaundice remained unchanged, but hyaluronic acid elimination capacity was less than that in the Sham group. After hepatic reperfusion, the disappearance rate of serum hyaluronic acid in obstructive jaundice was lower, and serum alanine aminotransferase levels were higher than those in the Sham group. CONCLUSIONS: Our findings suggest that obstructive jaundice impairs sinusoidal endothelial cells and that sinusoidal endothelial cell damage in association with sinusoidal deterioration during obstructive jaundice renders liver susceptible to ischemia/reperfusion relative to normal liver.

[Hepatectomy (parenchyma-preserving) for hilar cholangiocarcinoma].

The aim of this study was to evaluate the results of parenchyma-preserving hepatectomy as surgical treatment for hilar cholangiocarcinoma. Ninety-three resected patients with hilar cholangiocarcinoma were included in this study. The resected patients were stratified into three groups: the extended hepatectomy (EXH) group (n = 66); the parenchyma-preserving hepatectomy (PPH) group (n = 14); and the local resection (LR) group(n = 13). The EXH group underwent hepatectomy more extensive than hemihepatectomy, the PPH group underwent hepatectomy less extensive than hemihepatectomy; and the LR group underwent extrahepatic bile duct resection without hepatic resection. Surgical curability of the PPH and EXH groups was better than that of the LR group. Surgical morbidity was higher in the EXH group(48%) than in the LR group (8%) and the PPH group(14%) (p < 0.01 and p < 0.05, respectively). The survival rates after resection were significantly higher in patients who underwent hepatectomy, including PPH and EXH, than in patients who underwent LR (29% vs 8% at 5 years, respectively, p < 0.05). However, no significant difference in survival was found between the PPH and EXH groups. Univariate and multivariate analysis showed that significant prognostic factors for survival were resected margins, lymph node status, and vascular resection. In conclusion, PPH may be beneficial in highly selected patients based on cancer extent and high-risk patients with liver dysfunction and advanced age.

Regulation of liver inflammatory injury by signal transducer and activator of transcription-6.

Liver injury induced by hepatic ischemia/reperfusion is characterized by activation of the transcription factor NF-kappaB, increased production of tumor necrosis factor-alpha (TNFalpha), liver neutrophil accumulation, and hepatocellular damage. Exogenous administration of interleukin-4 (IL-4) or IL-13 was recently shown to regulate this inflammatory injury in association with activation of signal transducer and activator of transcription-6 (STAT6). The objective of the present study was to determine whether STAT6 was required for the regulation of liver inflammation by IL-4 and IL-13. Wild-type and STAT6 knockout mice underwent 90 minutes of hepatic ischemia followed by 8 hours of reperfusion. Hepatic ischemia/reperfusion in wild-type and STAT6 knockout mice significantly increased (P < 0.05) NF-kappaB activation, serum levels of TNFalpha, liver accumulation of neutrophils [measured by myeloperoxidase (MPO) content], and hepatocellular damage [measured by serum alanine aminotransferase (ALT)] compared to sham controls. In wild-type mice, activation of STAT6 was not observed after ischemia/reperfusion. Administration of 1 microg of IL-4 or IL-13 at reperfusion reduced serum TNFalpha, liver neutrophil accumulation, and hepatocellular injury in wild-type mice. Treatment with IL-4 or IL-13 had no effect on liver NF-kappaB activation but significantly increased activation of STAT6. In STAT6 knockout mice, neither IL-4 nor IL-13 had any effect on TNFalpha, MPO, or ALT values, the regulatory effects of these cytokines being completely abolished. The data suggest that activation of STAT6 may regulate liver inflammatory injury.

Beneficial effects of arterialization of the portal vein on extended hepatectomy.

BACKGROUND: Extended hepatectomy may result in postoperative liver failure. The aim of this study was to evaluate the effects of arterialization of the portal vein on oxygen supply, hepatic energy metabolism and liver regeneration after extended hepatectomy. METHODS: Portal haemodynamics were evaluated 0 or 10 days after arterialization of the portal vein in three experimental groups: 85 per cent partial hepatectomy, 85 per cent partial hepatectomy 10 days after arterialization of the portal vein and 85 per cent partial hepatectomy 10 days after ligation of the hepatic artery. Survival rates, weight of the regenerating liver, levels of adenine nucleotides and hepatic energy charge were assessed. RESULTS: Arterialization of the portal vein caused a significant increase in partial pressure of oxygen and oxygen saturation. Portal blood flow 10 days after arterialization was significantly increased. Survival rate and weight of the regenerating liver in the group with arterialization of the portal vein were significantly higher than those in the other two groups. The group with arterialization of the portal vein showed the highest levels of adenosine 5'-triphosphate. CONCLUSION: The increase in portal blood flow and oxygen supply produced by arterialization of the portal vein has beneficial effects on hepatic energy metabolism and liver regeneration, and leads to improved survival after experimental extended hepatectomy.

Unilateral hepatic artery reconstruction is unnecessary in biliary tract carcinomas involving lobar hepatic artery: implications of interlobar hepatic artery and its preservation.

BACKGROUND/AIMS: The interruption of hepatic arterial flow when performing a bilioenteric anastomosis has been reported to usually bring about serious postoperative complications, such as anastomotic leakage, hepatic abscess and infarction. We aimed to evaluate the surgical implications of the interlobar hepatic artery when patients with advanced biliary tract carcinomas undergo surgical resection with a bilioenteric anastomosis. METHODOLOGY: In 7 patients with advanced biliary tract carcinomas, the combined resection of the liver (greater than hemihepatectomy in 2 and less than hemihepatectomy in 5), extrahepatic bile duct, hepatic artery (right hepatic artery in 5, right and left hepatic artery in 1, left hepatic artery in 1), and the portal vein was performed in 4 patients. The portal vein was reconstructed in all 4 patients. The hepatic artery was reconstructed in only one patient, with combined resection of both right and left hepatic arteries, but was not reconstructed in 2 other patients, even though they underwent resection greater than hemihepatectomy. RESULTS: The interlobar hepatic artery running into the Glissonian sheath around the hepatic duct confluence could be preserved in 5 patients, as shown by angiography, but could not be preserved in 2 patients who underwent greater than hemihepatectomy. Moderate and transient ischemic liver damage occurred, but no serious postoperative complications were induced in any of the 5 patients in the unilateral hepatic artery preserved group. However, both cases without preservation of the hepatic artery encountered liver failure, liver abscess and leakage of bilioenteric anastomosis, and one patient died of multiple organ failure. CONCLUSIONS: One major lobar branch of the hepatic artery involved by cancer invasion could be safely resected without reconstruction in patients with advanced biliary tract carcinomas when the interlobar hepatic artery running into the Glissonian sheath around the hepatic duct confluence is preserved.

Changes in hepatic venous oxygen saturation related to the extent of regeneration after partial hepatectomy in rats.

BACKGROUND: Changes in hepatic oxygen metabolism in relation to the extent of liver regeneration are expected after partial hepatectomy. There are few reports, however, about hepatic oxygen metabolism during liver regeneration. In this study, we evaluated changes in hepatic oxygen metabolism related to the regeneration rate, and the relationship between hepatic venous oxygen saturation (Shvo2) and liver regeneration after partial hepatectomy. METHODS: The work was done using 50% hepatectomized rats with continuous infusion of octreotide for inhibition of liver regeneration or with saline as control. The hepatic hemodynamics, oxygen metabolism, and Shvo2 levels as well as the regenerating liver status were evaluated for 3 days after hepatectomy. RESULTS: Administration of octreotide resulted in a significant reduction of the regenerating liver weight on days 1 and 3 after hepatectomy compared with the control group. Significantly decreased DNA synthesis and proliferating cell nuclear antigen labeling index were also found on day 1. Meanwhile, hepatic oxygen consumption (HVO2) and oxygen extraction ratio were significantly decreased in the octreotide-treated group on day 1. In contrast, the Shvo2 levels in the octreotide-treated group were significantly higher than those in the control group, and were inversely correlated with the HVO2. CONCLUSION: The remnant liver demands an increased amount of oxygen in relation to the extent of regeneration, and changes in the Shvo2 are inversely correlated with the HVo2. Therefore, monitoring the Shvo2 could be useful for estimating liver regeneration after partial hepatectomy.

Management issues regarding hepatic adenomatosis.

Hepatic adenomatosis is a rare disease defined by multiple hepatic adenomas. There is controversy with regard to the optimal treatment for this disease because the potential for intraperitoneal hemorrhage or malignant transformation of the tumors is difficult to estimate. Furthermore, the technical difficulties of complete resection of all adenomas present unique operative challenges. We report experience with two patients and reviewed all reported cases from 1977. We define hepatic adenomatosis as five or more hepatic adenomas not associated with a medical history of glycogen storage disease, anabolic steroid use, or oral contraceptive use. The incidence of hepatic adenomatosis was preponderate among women [20 of 32 patients (63%)]. Thirteen of 32 patients (41%) had intratumoral bleeding, including four patients with intraperitoneal hemorrhage. Ten of 13 patients (77%) with intratumoral bleeding complained of abdominal pain; overall, 19 of 32 patients (59%) had abdominal pain. Twelve patients underwent hepatic resection, 6 patients underwent liver transplantation with no reported mortality, and 14 patients had no surgical treatment. Hepatocellular carcinoma was histologically confirmed in 2 of 32 patients (6%). Larger symptomatic adenomas exposed to liver surface have a bleeding propensity and should be surgically resected. Routine biopsy of other small nodules suspected as adenomas is recommended for definitive diagnosis.