Small ileal neurofibroma causing intussusception in a non-neurofibromatosis patient

Neurofibromas in the small intestine are usually accompanied by von Recklinghausen's disease (neurofibromatosis), and usually originate in the intramuscular plexus of Auerbach. We present here a solitary neurofibroma, which caused an ileocolic intussusception, originating in the submucosal plexus of Meissner in a non-neurofibromatosis patient. To our knowledge, there is no previous report of a neurofibroma originating in the plexus of Meissner. This condition was clearly confirmed by macroscopic and microscopic evaluation.     

Role of Intrahepatic Portal-Systemic Shunts in the Reduction of Portal Blood Supply to Liver Cells in Cirrhosis

To assess the role of intrahepatic portal-systemic shunts in the reduction of portal blood supply to the liver cells in cirrhosis, we measured portal venous flow (blood flow in the portal trunk) by the pulsed Doppler flowmeter and intrahepatic portal-systemic shunt index from the counts over the lungs and liver in both the anterior and posterior projections after instillation of 99mTc-macroaggregated albumin in the portal vein, and calculated portal sinusoidal flow (blood flow into the sinusoids via the portal vein), using the equation, (sequence; see text) in 47 patients with posthepatitic cirrhosis, and measured portal venous flow in 63 healthy adults in whom portal sinusoidal flow should be comparable to portal venous flow. Portal sinusoidal flow was significantly reduced in cirrhotics with an intrahepatic portal-systemic shunt index averaging 24%, whereas portal venous flow was similar in the cirrhotics and control. There was a significant inverse correlation between intrahepatic portal-systemic shunt index and portal sinusoidal flow. When cirrhotics were divided into three stages, based on Child's grading, intrahepatic portal-systemic shunt index was significantly increased in the group order of Child's A (8 +/- 9%), Child's B (27 +/- 22%), and Child's C patients (46 +/- 19%), and portal sinusoidal flow was decreased in the same order. Portal sinusoidal flow was significantly reduced in Child's B and Child's C patients, but not in Child's A patients, compared with the control. In conclusion, intrahepatic portal-systemic shunts may play a role, at least in part, in the reduction of portal blood supply to the liver cells in patients with advanced stage of posthepatitic cirrhosis when large intrahepatic portal-systemic shunts develop.     

Flowcharts for the management of biliary tract and ampullary carcinomas

No strategies for the diagnosis and treatment of biliary tract carcinoma have been clearly described. We developed flowcharts for the diagnosis and treatment of biliary tract carcinoma on the basis of the best clinical evidence. Risk factors for bile duct carcinoma are a dilated type of pancreaticobiliary maljunction (PBM) and primary sclerosing cholangitis. A nondilated type of PBM is a risk factor for gallbladder carcinoma. Symptoms that may indicate biliary tract carcinoma are jaundice and pain in the upper right area of the abdomen. The first step of diagnosis is to carry out blood biochemistry tests and ultrasonography (US) of the abdomen. The second step of diagnosis is to find the local extension of the carcinoma by means of computed tomography (CT), magnetic resonance imaging (MRI), magnetic resonance cholangiopancreatography (MRCP), percutaneous transhepatic cholangiography (PTC), and endoscopic retrograde cholangiopancreatography (ERCP). Because resection is the only way to completely cure biliary tract carcinoma, the indications for resection are determined first. In patients with resectable disease, the indications for biliary drainage or portal vein embolization (PVE) are checked. In those with nonresectable disease, biliary stenting, chemotherapy, radiotherapy, and/or best supportive care is selected.     

Functional heterogeneity of colony-stimulating factor-induced human monocyte-derived macrophages

Objectives:   Macrophages (Mφs) have various functions and play a critical role in host defense and the maintenance of homeostasis. Mφs exist in every tissue in the body, but Mφs from different tissues exhibit a wide range of phenotypes with regard to their morphology, cell surface antigen expression and function, and are called by different names. However, the precise mechanism of the generation of macrophage heterogeneity is not known. In the present study, the authors examined the functional heterogeneity of Mφs generated from human monocytes under the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage-CSF (M-CSF).
Methodology:   CD14 positive human monocytes (Mos) were incubated with M-CSF and GM-CSF for 6–7 days to stimulate the generation of M-CSF-induced monocyte-derived Mφs (M-Mφs) and GM-CSF-induced monocyte-derived Mφs (GM-Mφs), respectively. The expression of cell surface antigens and several functions such as antigen presenting cell activity, susceptibility to oxidant stress, and the susceptibility to HIV-1 and mycobacterium tuberculosis infection were examined.
Results:   GM-Mφs and M-Mφs are distinct in their morphology, cell surface antigen expression, and functions examined. The phenotype of GM-Mφs closely resembles that of human Alveolar-Mφs (A-Mφs), indicating that CSF-induced human monocyte-derived Mφs are useful to clarify the molecular mechanism of heterogeneity of human Mφs, and GM-Mφs will become a model of human A-Mφs.     

Staging of Early Colorectal Cancers: Magnifying Colonoscopy versus Endoscopic Ultrasonography for Estimation of Depth of Invasion

BACKGROUND AND AIMS: Preoperative estimation of depth of invasion in early colorectal cancers (CRCs) is essential for patient management. This study was conducted to compare the diagnostic accuracies of magnifying colonoscopy and endoscopic ultrasonography (EUS) for estimating the depth of invasion of early CRCs. SUBJECTS AND METHODS: A total of 438 early CRCs were removed endoscopically or surgically from July 1993 through March 1999 at our hospital. Before removal, 102 lesions were evaluated with both magnifying colonoscopy and EUS and were included in this analysis. The diagnostic accuracy of each method, referring to the histology of the resected specimens, was evaluated. RESULTS: The overall diagnostic accuracies were 87% (89/102) for magnifying colonoscopy and 75% (76/102) for EUS (P = 0.0985). Subgroup analysis was also done for polypoid and non-polypoid lesions. For polypoid lesions, the overall diagnostic accuracies of magnifying colonoscopy and EUS were 88% (60/68) and 72% (49/68), (P = 0.0785), and for non-polypoid lesions, they were 85% (29/34) and 79% (27/34), (P = 0.7169). CONCLUSION: Although, there is a substantial difference in the overall diagnostic accuracies, it is not statistically significant. Therefore, we conclude that magnifying colonoscopy is at least as accurate as EUS for preoperative staging of early CRCs.     

Effect of the calcium antagonist,diltiazem, on beta-agonist-induced reduction of beta-adrenergic responsiveness in the guinea pig lung

This study was designed to clarify the mechanism of tolerance that occurs during prolonged administration of a beta-agonist in relation to membrane phospholipid degradation and to elucidate the effect of diltiazem, a calcium antagonist. Guinea pigs were divided into 3 groups: (1) control—physiological saline (0.5 ml) was injected once a day for 7 successive days; (2) metaproterenol (Mp)—Mp was injected intraperitoneally (10 mg/kg/day) for 7 successive days; (3) Mp + diltiazem—diltiazem was injected intraperitoneally (20 mg/kg/day) 30 min before Mp injection for 7 successive days. The number of beta-adrenoceptors and the 10⁻⁵ M (−)-isoproterenol-stimulated adenylate cyclase activity were significantly decreased in the metaproterenol group. Diltiazem reduced these decreases. Phospholipase activity was increased and phosphatidylcholine and phosphatidylethanolamine levels were decreased in the metaproterenol group. Diltiazem also reduced these changes. These results suggest that the degradation of membrane phospholipids by phospholipase may be involved in a decrease in beta-adrenergic response caused by successive administration of metaproterenol. Diltiazem protects membrane phospholipids from phospholipase attack, which in turn maintains beta-adrenergic responsiveness. Part of this study was presented at the Annual Meeting of the American Thoracic Society, May 12, 1987, New Orleans, Louisiana     

Aggressive surgical resection for hepatocellular carcinoma with tumor thrombus extending to inferior vena cava and synchronous pulmonary metastasis

We describe a 66-year-old man having hepatocellular carcinoma with tumor thrombus extending into the inferior vena cava and synchronous pulmonary metastasis. He was referred to Chiba University Hospital on May, 2000, complaining of emaciation. Radiological findings showed a huge hepatocellular carcinoma in the entire right lobe and tumor thrombus extended into the intrapericardial inferior vena cava. He also had a solitary pulmonary metastasis in the left pulmonary lobe (stage IVB). Right hemihepatomy was performed under total hepatic vascular exclusion without cardiopulmonary bypass, and tumor thrombus was completely removed. Thoracoscopic wedge resection of pulmonary metastasis was also performed. The patient had an uneventful postoperative course. Histopathological examination revealed that the tumor was moderately differentiated hepatocellular carcinoma The patient is still alive after 26 months with pulmonary recurrence, but without hepatic recurrence. To our knowledge, there has been no reported case of resection for both hepatocellular carcinoma invading the inferior vena cava and synchronous pulmonary metastasis. In conclusion, aggressive surgical resection for advanced hepatocellular carcinoma concomitant with pulmonary resection may bring about better prognosis in highly selected patients.     

Clinical and Portal Hemodynamic Features in Cirrhotic Patients Having a Large Spontaneous Splenorenal and/or Gastrorenal Shunt

Clinical and portal hemodynamic features in 28 cirrhotic subjects with a large spontaneous spleno- and/or gastrorenal shunt were studied in comparison with 30 control cirrhotic cases without such collaterals. Forty-six percent of the former had chronic hepatic encephalopathy, but none of the latter was encephalopathic. These patients with large renal shunts were divided into those with and those without encephalopathy. Large esophageal varices were significantly less common in patients with a large shunt and encephalopathy compared with those who had a large shunt but no encephalopathy, and the control. But there was no significant difference of past variceal bleeding among these three groups. In all those with encephalopathy, part of superior mesenteric venous blood was shunting through these collaterals into the left renal vein or inferior vena cava, but the same was not demonstrable in patients with a large shunt and no encephalopathy and control cirrhotics. In the chronic encephalopathic, portal venous flow was estimated to be less than one-half of that in control cirrhotics, and the portion of superior mesenteric venous blood that was flowing hepatofugally through a large shunt into the left renal vein seemed about the same or greater than the portal venous flow. Thus, a large spontaneous spleno- and/or gastrorenal shunt might prevent development of large esophageal varices but not variceal hemorrhage and it increased a risk of chronic hepatic encephalopathy.     

Morphology and biochemistry of the lung from guinea pig after repeated injections of freund’s complete adjuvant

Guinea pigs received 5 daily injections of Freund’s complete adjuvant and the changes in the lung were investigated by light microscope and electron microscope. In the 20th week of experiment, fibrotic changes were found around the granulomata close to the surface of the lung. In addition the fraction of glycosaminoglycans was isolated from the lung and analyzed quantitatively. As a result, a decrease in quantity of hyaluronic acid and an increase in quantity of dermatan sulfate were observed.     

Transient hypoglycorrhachia with paroxysmal abnormal eye movement in early infancy

Paroxysmal abnormal eye movement in early infancy is one of the initial symptoms of glucose transporter 1 deficiency syndrome (GLUT1DS). We describe four early infants with transient hypoglycorrhachia presenting with abnormal eye movements. Their symptoms disappeared after the introduction of a ketogenic diet (KD), and their development was normal. Since no variants in SLC2A1 were detected, the CSF-to-blood glucose ratios (C/B) were re-examined, and within normal range. None of the four patients displayed recurrent symptoms after withdrawal from the KD. Because long-term KD has potential adverse effects and could affect the quality of life of patients and their families, re-examination of CSF glucose during late infancy should be considered in the case of absence of the SLC2A1 pathogenic variant.