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Biomedical subjects

K Tanikawa

Publications and source records attributed to K Tanikawa.

At least 199 records · Page 11Linked to original sources

[Neoadjuvant chemotherapy of liver tumors metastasized by sigmoid colon cancer: a case report of CDDP/5-FU intraarterial infusion therapy followed by hepatectomy].

A case of liver tumors metastasized by Sigmoid colon cancer was treated with intrahepatic arterial infusion of CDDP (10 mg) and 5-FU (250 mg) via subcutaneously implanted reservoir. After 20 administrations of CDDP and 5-FU, the tumors in the right lobe of the liver disappeared, but those in the left lobe remained. Therefore left hepatectomy was carried out. Six months after the hepatectomy, a nodule recurrence was disclosed in the right lobe of the liver. With re-elevated serum CEA level, subsequent intrahepatic arterial infusion of CDDP and 5-FU the nodule size reduced with normalization of the serum CEA level.

Aged↗

Supplemental oxygen during endoscopic variceal ligation: effects on arterial oxygenation and cardiac arrhythmia.

OBJECTIVES: Endoscopic variceal ligation may affect cardiopulmonary function. The aim of this study was to determine the effect of either nasal oxygen (2 L/min) or no oxygen on arterial oxygenation and cardiac arrhythmia during variceal ligation. METHODS: A prospective, endoscopy team-blinded, randomized, cross-over study (first session vs second session) was conducted in 30 cirrhotic patients undergoing variceal ligation. Oxygen saturation (SaO2) and cardiac arrhythmia were assessed by a pulse oximeter. In this study, 15 patients received supplemental oxygen in the first sessions, and 15 received oxygen in the second sessions. RESULTS: Oxygen desaturation (nadir SaO2 < 90%) occurred in 23% of patients breathing room air but was prevented by oxygen (p < 0.01), and the nadir SaO2 was significantly lower in patients breathing room air than in those receiving oxygen (93.2 +/- 0.7% vs 98.3 +/- 0.3%, p < 0.01). During the procedure, premature ventricular contraction was more frequently observed in patients breathing room air than in those receiving oxygen (14.0 +/- 3.2/h vs 5.4 +/- 1.5/r, p < 0.05). CONCLUSIONS: These data suggest that oxygen desaturation and cardiac arrhythmia are common in patients undergoing variceal ligation and that low flow nasal oxygen can alleviate these events. Supplemental oxygen is therefore advisable to avoid potential serious cardiopulmonary accidents in patients undergoing variceal ligation.

Administration, Intranasal↗

Monitoring of lectin-reactive alpha-fetoproteins in patients with hepatocellular carcinoma treated using transcatheter arterial embolization.

OBJECTIVE: To evaluate the value of lectin-reactive alpha-fetoprotein (LR-AFP) levels for assessing therapeutic effects and for predicting prognosis in patients with hepatocellular carcinoma (HCC) treated using transcatheter arterial embolization (TAE). DESIGN: Twenty-nine patients with HCC were studied. METHODS: LR-AFP levels were measured using lectin-affinity electrophoresis coupled with antibody-affinity blotting. Patients who were initially LR-AFP-positive were divided into those who became negative after TAE and those who remained positive. Patients were also classified into groups showing a reduction in total AFP levels of 75% or more and those showing a reduction of less than 75% and into groups whose tumour size was reduced by 50% or more and those whose tumour size was reduced by less than 50%. RESULTS: Both the length of time between TAE and the recurrence of HCC and the cumulative survival rate differed significantly between the group of patients who became negative after TAE and that which remained positive. However, no significant differences in these parameters were found between the patients in the two classes for total AFP levels or tumour size. CONCLUSIONS: LR-AFP levels appeared to be more useful for predicting clinical results than the serum total AFP value or changes in tumour size.

Aged↗

[Precancerous stages of hepatocellular carcinoma].

Precancerous stages of hepatocellular carcinoma (HCC) may be broadly categorized into three groups: high risk group, chronic liver diseases and adenomatous hyperplasia nodule. The high risk group for HCC has been clearly defined as the HCC which in Japan develops exclusively in patients with chronic liver diseases due to persistent infection of HBV or HCV. The mechanisms of HCC development by these hepatitis viruses have been partly clarified, and our study has shown it takes 25 years on average from HCV infection to the diagnosis of small HCC. Secondly, almost all cases of HCC are accompanied with chronic liver diseases, especially cirrhosis. Thus, cirrhosis has been considered as a precancerous stage. Recent studies indicated that BrdU labeling index is significantly increased in the non-cancerous cirrhotic portion in the cirrhotics with HCC, suggesting HCC develops in cirrhotics with high DNA synthetic potency of hepatocytes. Lastly, adenomous hyperplasia has also been considered a precancerous stage of HCC because early HCC is often seen in the nodule of this lesion. In addition, the early HCC nodules are diagnosed by serial liver biopsy in following patients with adenomatous hyperplasia. Thus, this lesion is considered the precancerous stage of HCC in a narrow sense. However, the early HCC nodules developing in adenomatous hyperplasia lesions are not all early HCC.

Carcinoma, Hepatocellular↗

The present status of treatments for hepatocellular carcinoma.

In Japan, hepatocellular carcinoma (HCC) has developed almost exclusively in patients with chronic liver diseases associated with hepatitis B virus (HBV) or hepatitis C virus (HCV). Small HCCs have been found in considerable numbers when following up such patients. Percutaneous ethanol injection therapy (PEIT) has become an important therapy for small HCCs, with a 5-year survival rate of > 50%, similar to that of surgical resection. Such patients must be followed every 3 months even after the initial successful treatment in order to detect newly developed lesions. For nodular HCCs, transcatheter chemoembolization (TAE) is the treatment of choice for advanced disease, but it is not a curative treatment; it can be given with PEIT with better results. Very advanced HCCs are usually treated with intra-arterial chemotherapy and the prognosis has been improved by using an implantable injection port system. The search continues for a means to prevent the recurrence of HCC after successful treatment.

Carcinoma, Hepatocellular↗

Tubulovesicular transport of horseradish peroxidase in isolated rat hepatocyte couplets: effects of low temperature, cytochalasin B and bile acids.

The transcytotic vesicular pathway in isolated rat hepatocyte couplets was investigated using horseradish peroxidase. Ten to 20 min after horseradish peroxidase labeling, vesicles and tubules containing horseradish peroxidase were observed to be predominantly around the bile canaliculi. In hepatocytes incubated in a 4 degrees C medium for 10 min after horseradish peroxidase labeling, few horseradish peroxidase-containing structures were observed around the bile canaliculi, and the fine reticular immunofluorescence of microtubules was reduced. Cells treated with cytochalasin B (a microfilament inhibitor) showed a fair number of horseradish peroxidase-containing structures around the markedly dilated bile canaliculi and the distribution of microtubules was preserved. Cells labeled by horseradish peroxidase and then incubated for 10 min in a horseradish peroxidase-free medium containing 50 mumol/L of taurocholic acid, ursodeoxycholic acid or tauroursodeoxycholic acid had more tubular structures containing horseradish peroxidase around the bile canaliculi than control cells, whereas 50 mumol/L of taurochenodeoxycholic acid, taurodeoxycholic acid, dehydrocholic acid and taurodehydrocholic acid each failed to increase the number of tubular structures. These findings show that horseradish peroxidase was transported in hepatocyte couplets from the cell periphery to the bile canalicular front through the tubulovesicular pathway, depending on cytoplasmic microtubules. Cytoplasmic microfilaments appeared to play a minor role in this transport. Several specific bile acids such as taurocholic acid, ursodeoxycholic acid and tauroursodeoxycholic acid each promoted the tubular transformation.

Animals↗

Effects of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy.

Gastric mucosal hyperemia associated with elevated serum gastrin level has been suggested in cirrhotic patients with portal hypertensive gastropathy (PHG). Clinical evidence has shown that these patients may benefit from propranolol administration. The aim of this study was to investigate effect of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy. Gastric mucosal perfusion was assessed by laser Doppler flowmetry. Measurements were performed under basal conditions and after observer-blind administration of propranolol (30-60 mg/day, N = 9) or placebo (N = 9) for seven days. Placebo had no effect on either gastric mucosal perfusion or serum gastrin level. In contrast, propranolol administration significantly decreased both antrum gastric mucosal perfusion (from 0.88 +/- 0.28 to 0.73 +/- 0.26 V, P < 0.05) and corpus gastric mucosal perfusion (from 0.94 +/- 0.35 to 0.78 +/- 0.25 V, P < 0.05). However, this drug had no effect on serum gastrin level. We conclude that chronic propranolol administration in cirrhotic patients with portal hypertensive gastropathy may reduce gastric mucosal perfusion without changing serum gastrin level.

Double-Blind Method↗

Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis.

Hepatic venous catheterization is widely used to assess portal pressure. However, it remains unclear whether wedged hepatic venous pressure is a close indicator of portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis. To address this issue, we analyzed the data from our previous published studies. Forty patients with nonalcoholic cirrhosis (HBV infection in five, HCV infection in 28, and cryptogenic in seven) were available in this analysis. A vasoconstrictor (N = 14), vasodilator (N = 10), or combination (N = 16) was administered. The agreement of the changes between portal and wedged hepatic venous pressures during pharmacological manipulation was assessed by an intraclass correlation coefficient. The intraclass correlation coefficient in each subgroup was more than 0.60 (0.62 in vasoconstrictor group, 0.87 in vasodilator group, and 0.73 in combination group). When the analysis was performed according to the cause of liver disease, the values were 0.67 in HBV infection, 0.73 in HCV infection, and 0.74 in cryptogenic cirrhosis. These results suggest that wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in patients with nonalcoholic cirrhosis.

Female↗

Influence of nitroglycerin on portal pressure and gastric mucosal hemodynamics in patients with cirrhosis.

We studied 30 patients with cirrhosis to determine the effect of nitroglycerin on portal and gastric mucosal hemodynamics. Systemic hemodynamics, portal venous pressure (PVP), the hemoglobin index (IHB), and the oxygen saturation index (ISO2) of the gastric mucosa were measured before and after a continuous infusion of nitroglycerin. The patients were divided into two groups according to the presence or absence of major portal-systemic collateral routes on portograms. Nitroglycerin caused a reduction in PVP in all patients. Although there was no significant difference in systemic hemodynamic changes between the two groups, the reduction in PVP in patients with major portal-systemic collaterals was significantly higher than in those without major collaterals. A nitroglycerin infusion, at a dose of 1.0 micrograms/kg per min for 10 min, produced a reduction in both IHB (-16%, P < 0.001) and ISO2 (-13%, P < 0.001) in the gastric mucosa, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. These findings suggest that the continuous infusion of nitroglycerin reduces PVP in cirrhotic patients, particularly in those with major portal-systemic collaterals, and reduces the congestion of the gastric mucosa in patients with portal hypertension.

Adult↗

Cultured rat hepatic sinusoidal endothelial cells express intercellular adhesion molecule-1 (ICAM-1) by tumor necrosis factor-alpha or interleukin-1 alpha stimulation.

This study investigated the expression of intercellular adhesion molecule-1, a leukocyte adhesion molecule, on cultured rat hepatic sinusoidal endothelial cells during stimulation with tumor necrosis factor-alpha or interleukin-1 alpha. Using immunoelectron microscopy and the immunogold technique against intercellular adhesion molecule-1, gold particles were shown to increase significantly on the surface of sinusoidal epithelial cells treated with tumor necrosis factor-alpha (100 U/ml) or interleukin-1 alpha (10 U/ml) for 8 h compared with unstimulated cells. In addition, semi-quantitative analysis of intercellular adhesion molecule-1 on the sinusoidal endothelial cells was performed by cytofluorometer. Even without stimulation, intercellular adhesion molecule-1 was weakly expressed. However, 8 h after tumor necrosis factor-alpha or interleukin-1 alpha treatment, the expression of intercellular adhesion molecule-1 on cells was increased in a dose-dependent manner. Kinetic analysis showed that the expression of intercellular adhesion molecule-1 on sinusoidal endothelial cells treated with these cytokines increased gradually from the beginning of stimulation to 24 h. These findings suggest that hepatic sinusoidal endothelial cells may mediate the direct interaction between leukocytes and sinusoidal endothelial cells by expressing leukocyte adhesion molecules such as intercellular adhesion molecule-1.

Animals↗

Portal pressure after prophylactic sclerotherapy in patients with high-risk varices.

Portal hemodynamics and transhepatic portal venographic findings were studied before and after prophylactic sclerotherapy (mean duration = 40 +/- 14 days) in 16 patients with high-risk esophageal varices. Portal pressure, evaluated by the portal venous pressure gradient, increased by a mean of 21% in eight patients (50%) and decreased by a mean of 20% in eight patients (50%) with no statistically significant change overall. The two groups were further analyzed separately to identify the mechanism of the change in portal pressure. Intrahepatic vascular resistance did not change significantly in either group. However, the prevalence of extravariceal portosystemic shunts was greater in patients with decreased portal pressure than in those with increased portal pressure (88% vs. 25%, p < 0.05). Further, the enlargement of extravariceal portosystemic shunts was more marked in patients with decreased portal pressure than in those with increased portal pressure (88% vs. 0%, p < 0.01). In addition, liver function, assessed by intrinsic clearance, was not modified in the two groups. We conclude that prophylactic sclerotherapy increases or decreases portal pressure without modifying liver function. Although the mechanism of these portal pressure changes is not clear, intrahepatic vascular resistance does not play an important role and the presence of extravariceal portosystemic shunts may prevent further increases in portal pressure.

Esophageal and Gastric Varices↗

Ultrastructure of the intracellular membranous system of rat hepatocytes in intrahepatic cholestasis induced by phalloidin.

To investigate the effect of a thickened pericanalicular ectoplasm in tubulovesicular transport and biliary excretion, we examined the ultrastructure of the intracellular membranous system in rat hepatocytes with and without phalloidin treatment, by transmission electron microscopy and scanning electron microscopy combined with the Aldehyde prefix Osmium-Dimethyl Sulfoxide-Osmium method. Hepatocytes possessed elaborate networks of tubules around bile canaliculi, and some of them extended to the bile canaliculi in control rats. Vesicles were also present around the bile canaliculus. Treatment of rats with phalloidin produced a thick pericanalicular ectoplasm around the bile canaliculus visualized by transmission electron microscopy, and the density of vesicles (p < 0.001) and tubules (p < 0.001) within 0.5 microns around the bile canaliculus significantly decreased in phalloidin-treated rats. The number of lysosomes in hepatocytes apparently increased in phalloidin-treated rats; however, they were rarely observed around the bile canaliculus. The Aldehyde prefix Osmium-Dimethyl Sulfoxide-Osmium method produced an organelle-free space around the bile canaliculus by removing the thick pericanalicular ectoplasm in scanning electron microscopic examination, and the thickened pericanalicular ectoplasm inhibited the approach of intracellular membranes to the canalicular membrane in the transmission electron microscopic examination. In some pathological cholestatic conditions, the thickened pericanalicular ectoplasm may inhibit not only bile canalicular contraction but also biliary excretion of substances, which is mediated by the tubulovesicular transport system.

Animals↗

The extracellular matrix in hepatocellular carcinoma shows different localization patterns depending on the differentiation and the histological pattern of tumors: immunohistochemical analysis.

This study investigated cells producing type I, III, and IV collagens, laminin, and fibronectin, the major components of the extracellular matrix, and compared their localization patterns in relation to the grade of tumor differentiation and the histological pattern of hepatocellular carcinoma. Type I, III, and IV collagens, laminin, and fibronectin were produced by tumor, endothelial, and Ito cells. Regarding their localization pattern in relation to the histological pattern of tumors, although the extracellular matrix was present in the subendothelial spaces of sinusoids in every histological pattern, the localization of these components in the intercellular spaces of tumor cells was most marked in hepatocellular carcinoma with a compact pattern. These results suggest that the extracellular matrix produced by tumor, endothelial, and Ito cells is deposited in appropriate positions in hepatocellular carcinoma to sustain the tissue structure showing different histological patterns. In relation to the grade of tumor differentiation, in most cases, Type I, III, and IV collagens and fibronectin were present in the subendothelial spaces of sinusoids and the intercellular spaces of some tumor cells, while little laminin was observed in well-differentiated small hepatocellular carcinoma (less than 10 mm diameter). In undifferentiated hepatocellular carcinoma, little extracellular matrix was observed, except around vessels. These results suggest that sinusoidal capillarization may not yet have occurred in the early stage of hepatocarcinogenesis, although it develops as the tumors increase in size and the tumor cells dedifferentiate. In undifferentiated hepatocellular carcinoma, tumor cells are too atypical to produce each extracellular matrix component.

Adult↗

Fibrogenesis in acute liver injuries.

We describe changes in the hepatic extracellular matrix (ECM) and its producing cells in acute liver injuries, primarily referring to transforming growth factor-beta 1 (TGF-beta), which is the most important cytokine involved in fibrogenesis. In addition, we describe the relationship between vitronectin (VN) and plasminogen activator inhibitor 1(PAI-1) in the self regulating mechanism of TGF-beta action for fibrogenesis in acute viral hepatitis. In the very early stage of acute liver injury, following aggregation of platelets, immunolocalization of TGF-beta is observed in injured areas. And at the cell migration stage, the infiltration pattern of inflammatory cells was characterized by an ordered progression of inflammatory cells, beginning with platelets and followed by polymorphonuclear leukocytes and macrophages. Following recruitment of inflammatory cells to the necrotic area, it appears that TGF-beta could be produced and activated by these inflammatory cells, resulting in the intensification of active TGF-beta distributions in the injured area. At the fibrosis stage, TGF-beta could also be produced by Ito cells, endothelial cells and hepatocytes at the periphery of the necrotic area, and may play important roles in the promotion of production and accumulation of ECM components in injured regions. In addition, the consistent localization of PAI-1 with VN in ECM near the necroinflammatory areas suggests that PAI-1 and VN could be involved in the modulation of fibrogenesis in acute liver injuries. In many kinds of acute liver injuries, fibrogenesis is usually considered to be transient, and injured liver tissues able to nearly recover in order.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗