A rare case of plexiform neurofibroma of the liver in a patient without neurofibromatosis type 1.

Plexiform neurofibroma is mainly associated with neurofibromatosis type 1 and is seldom observed in the liver. Its occurrence in the liver without neurofibromatosis type 1 is even rarer. We report an extremely rare case of plexiform neurofibroma of the liver diagnosed by laparoscopic biopsy in a patient without neurofibromatosis type 1. The patient was a 35-year-old man who had neither clinical signs nor any family history of neurofibromatosis type 1. Abdominal ultrasonography, as part of a health screening, had detected a hepatic tumor. Subsequent contrast ultrasonography, computed tomography, and magnetic resonance imaging showed the tumor extending from the retroperitoneal space around the aorta to the hepatic hilum and distal portal branches in the right hepatic lobe, gallbladder, and left hepatic lobe. 18F-fluorodeoxyglucose positron emission tomography showed no abnormal accumulation. Histopathological examination of the tumor obtained laparoscopically led to a diagnosis of plexiform neurofibroma. Because the patient was asymptomatic with no features of malignancy, he was only monitored and managed. At follow-up 10 years later, computed tomography showed a decrease in tumor size. It is important to recognize that, while rare, plexiform neurofibroma can occur without neurofibromatosis type 1. We recommend follow-up instead of unreasonable surgery in such cases.

Urinary trypsin inhibitor suppresses excessive superoxide anion radical generation in blood, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats.

OBJECTIVES: To investigate the effects of ulinastatin, a urinary trypsin inhibitor (UTI), on jugular venous superoxide radical (O2⁻·) generation, oxidative stress, early inflammation, and endothelial activation in forebrain ischemia/reperfusion (FBI/R) rats. METHODS: Fourteen Wistar rats were allocated to a control group (n = 7) and a UTI group (n = 7). Throughout the experiments, O2⁻· in the jugular vein was measured by the produced current using a novel electrochemical O2⁻· sensor. Forebrain ischemia was induced by occlusion of the bilateral common caroti darteries with hemorrhagic hypotension for 20 min, followed by reperfusion. In the UTI group, UTI (5 U/g) was administered intravenously immediately after reperfusion. At 60 min after reperfusion, plasma and brain were harvested, and malondialdehyde, high-mobility group box 1 (HMGB1) protein, and intercellular adhesion molecule-1 (ICAM-1) were measured. RESULTS: O2⁻· current increased gradually during forebrain ischemia in both groups. The current increased markedly in the control group immediately after reperfusion but was significantly attenuated in the UTI group after reperfusion. Brain and plasma malondialdehyde, HMGB1, and ICAM-1 were significantly attenuated in the UTI group compared with those in the control group, except for brain HMGB1, which was associated with the amount of O2⁻· generated during FBI/R. DISCUSSION: UTI suppressed jugular venous O2⁻· generation, oxidative stress, early inflammation, and endothelial activation in FBI/R rats. Therefore, UTI might be a useful agent for the therapy of the cerebral ischemia/reperfusion pathophysiology.

Moderate hypothermia suppresses jugular venous superoxide anion radical, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats.

The aim of this study was to assess the effect of moderate hypothermia (MH) on generation of jugular venous superoxide radical (O2-.), oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion (FBI/R) rats. Twenty-one Wistar rats were allocated to a control group (n=7, 37 degrees C), a pre-MH group (n=7, 32 degrees C before ischemia), and a post-MH group (n=7, 32 degrees C after reperfusion). MH was induced before induction of ischemia in the pre-MH group and just after reperfusion in the post-MH group. Forebrain ischemia was induced by occlusion of bilateral common carotid arteries with hemorrhagic hypotension for 10 min, followed by reperfusion. O(2)(-)(.) in the jugular vein was measured from the produced current using a novel O2-. sensor. The O2-. current showed a gradual increase during forebrain ischemia in the control and post-MH groups but was attenuated in the pre-MH group. Following reperfusion, the current showed a marked increase in the control group but was strongly attenuated in the pre- and post-MH groups. Concentrations of malondialdehyde, high-mobility group box 1 (HMGB1) protein, and intercellular adhesion molecule-1 (ICAM-1) in the brain and plasma 120 min after reperfusion in the pre- and post-MH groups were significantly lower than those in the control group, except for plasma HMGB1 in the post-MH group. In conclusion, MH suppressed O2-. measured in the jugular vein, oxidative stress, early inflammation, and endothelial injury in FBI/R rats.

Hyperglycemia enhances excessive superoxide anion radical generation, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats.

The aim of this study was to confirm the effect of acute hyperglycemia on the superoxide anion radical (O(2)(-)) generation, using a novel electrochemical O(2)(-) sensor in forebrain ischemia/reperfusion rats. Fourteen male Wistar rats were allocated to a normoglycemia group (n= 7) and a hyperglycemia group (n=7). Hyperglycemia was induced by intravenous infusion of glucose solution. Forebrain ischemia was induced by bilateral common carotid arteries occlusion with hemorrhagic hypotension for 10 min and then was reperfused. The generated O(2)(-) was measured as the current produced, which was integrated as a quantified partial value of electricity (Q), in the jugular vein using the O(2)(-) sensor. The reacted O(2)(-) current and the Q began to increase gradually during the forebrain ischemia in both groups. These values increased remarkably just after reperfusion in the normoglycemia group and were further increased significantly in the hyperglycemia group after the reperfusion. Concentrations of malondialdehyde (MDA) and high-mobility group box 1 (HMGB1) in the brain and plasma, and soluble intercellular adhesion molecule-1 (ICAM-1) in the plasma in the hyperglycemia group were significantly higher than those in the normoglycemia group. Brain and plasma MDA, HMGB1, and ICAM-1 were correlated with a sum of Q during ischemia and after reperfusion. In conclusion, acute transient hyperglycemia enhanced the O(2)(-) generation in blood and exacerbated oxidative stress, early inflammation, and endothelial injury after the forebrain ischemia/reperfusion in the rats.

Renal artery pseudoaneurysm after laparoscopic partial nephrectomy for renal cell carcinoma in a solitary kidney.

Renal artery pseudoaneurysms are a well-documented complication following trauma or percutaneous urological procedures, but are rare after partial nephrectomy. We present the case of a 34-year-old woman who, after undergoing a left nephrectomy in childhood due to Wilms' tumor, had a pseudoaneurysm in a solitary kidney after laparoscopic right partial nephrectomy with extraperitoneal approach for a renal cell carcinoma. The segmental renal artery feeding the pseudoaneurysm was embolized with coils without significant loss of residual renal function.

Traumatic renal artery thrombosis with renovascular hypertension.

A 15-year-old boy, who tumbled from a fourth-floor window, was transported to our hospital. Enhanced computed tomography (CT) 1.5 h after the injury showed a non-contrasted right kidney, and a repeat CT 6 h after the injury showed a growing retroperitoneal hematoma. The angiography showed complete obstruction of the right renal artery and bleeding from the subcapsular artery, which was successfully embolized. Renovascular hypertension developed on the second day after the injury; therefore, simple nephrectomy was performed.

Alterations to hepatic microcirculation in thioacetamide-induced cirrhotic livers of rats.

In liver cirrhosis, increased resistance of intrahepatic microvasculature contribute to the development of portal hypertension. This study aimed to reveal the alterations to hemodynamics in microvasculature of thioacetamide-induced fibrotic and cirrhotic rat livers, using in vivo microscopy. In fibrotic livers, although intrahepatic blood flow remained unaltered, area percentage of sinusoids was significantly decreased. In cirrhotic livers, intrahepatic blood flow was significantly increased concurrently with decrease in area percentage of sinusoids. The flow velocity and volume flow were significantly increased in terminal portal venules (TPVs) without changes in vascular diameters, whereas all these parameters were not altered in terminal hepatic venules (THVs). Intrahepatic shunts which emerged from TPVs and ran toward THVs, and anastomoses between neighboring THVs were formed in cirrhotic livers. These data indicate that the first occurring alteration of microcirculation in liver cirrhosis is decrease in sinusoidal beds.

Hemodynamics in the microvasculature of thioacetamide-induced cirrhotic rat livers.

BACKGROUND/AIMS: To evaluate the hepatic microcirculatory changes in liver cirrhosis, in vivo microscopic findings were assessed quantitatively in cirrhotic rats. METHODOLOGY: Using in vivo microscopy, the blood flow velocity through terminal portal venules and terminal hepatic venules, and their diameters were measured. The rats were classified into a normal group, fibrosis group, and cirrhosis group, histopathologically. To estimate intrahepatic blood flow of the liver surface, laser-Doppler flowmeter was used for the three groups, and portal venous pressures were measured. RESULTS: Blood flow velocity through terminal portal venules increased significantly in cirrhosis rats. However, among the three groups, there were no significant differences with blood flow velocity through terminal portal venules, diameters of terminal portal venules and terminal hepatic venules. Portal venous pressure and intrahepatic blood flow of the liver surface increased significantly. CONCLUSIONS: These data indicate that pre-sinusoidal alterations to hemodynamics become manifest in the liver cirrhosis, which might be related to intrahepatic shunt formation.