Kanzo

[title in Japanese]

[in Japanese], [in Japanese]

1999 Volume 40 Issue 4 Pages 201-204
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.201

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Hemodynamics of the Left Gastric Vein (LGV) before and after Endoscopic Injection Sclerotherapy (EIS) detected by Color Doppler Ultrasonography (CD-US)

Akira ASANO, Shigehiro KOKUBU

1999 Volume 40 Issue 4 Pages 205-216
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.205

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32 patients with portal hypertension and esophageal varices were submitted in this prospective study. We performed CD-US to them before and after EIS. Hepatofugal flow in LGV by CD-US was 88% before EIS. Mean flow velocity on LGV in post EIS state was significantly lower than that in pre EIS state (16.6±6.1 to 12.2±7.3cm/s; P<0.015). Diameter of LGV in post EIS state was significantly narrower than that in pre EIS state (5.0±1.6 to 4.4±1.3mm; P<0.0002). EIS effect defined as decreasing to undetectable flow velocity on LGV, narrowing to disappearance diameter of LGV. According to these criteria, EIS was effective for LGV in 84%. Subsequent arteriography was performed in these patients, and EIS was effective for LGV in 88%. These results suggested that CD-US had similar value arteriography for estimation of EIS effect to LGV.

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Evaluation of Effectiveness of Glucocorticoid Treatment using a Rat Acute Hepatic Failure Model

Akihiro SATO, Yasuhiro TAKIKAWA, Shinichiro SATO, Kazuyuki SUZUKI

1999 Volume 40 Issue 4 Pages 217-226
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.217

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We studied the effectiveness, mechanism of action and potential for clinical application of glucocorticoids using an acute hepatic failure model. Two hundred milligrams per kilogram of D-galactosamine and 10μg/kg of lipopolysaccharide were injected via the portal vein of 9-week-oldWistar rats to produce hepatic failure, and methylprednisolone (20 mg/kg) was injected via the portal veinfor treatment. In the untreated group, increases in the serum levels of tumor necrosis factor α (TNF-α) and interleukin-8 (IL-8), and hepatic cell apoptosis peaking at 3 hrs, 6 hrs and 12 hrs, respectively, from the injection of GalN/LPS were observed. Furthermore, a marked increase in the serum concentrations of transaminases and T. Bil., as well as massive hepatic cell death were observed 24 hrs after the injection of GalN/LPS. In the concomitantly treated group, the increase in serum levels of TNF-α was significantly inhibited (p<0.05), and apoptosis as well as hepatic failure, which developed 24 hrs after the injection was suppressed. However, in the delayed treatment group, suppression of neither hepatic damage nor massive hepatic cell death was evident. From the above results, it has been clarified that glucocorticoids inhibit both TNF-α production and the development of hepatic cell damage. However, the effect was not obvious when glucocorticoids were administered after the TNF-α peak . Therefore, the timing of glucocorticoid administration is an important factor that must be considered in the clinical application of glucocorticoids.

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Improvement of Flutamide-induced hepatotoxicity by Ursodeoxycholic acid in male rats

Eiji ICHIMURA, Kazuhisa HARA, Yasushi MATSUZAKI, Mikio DOI

1999 Volume 40 Issue 4 Pages 227-234
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.227

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Flutamide is an essential antiandrogen for the treatment of prostate cancer, but has potential toxicity to liver. The purpose of this work is to examine whether ursodeoxycholic acid (UDCA) could reduce the flutamide-induced hepatotoxicity in rat model.
First, we induced experimental hepatotoxicity of flutamide in male rats by the administration of phenobaribital (PB) with flutamide (0, 37.5, 75 and 150mg/kg) daily for 5 days under fasting condition. GOT, GPT and GLDH levels rose in dose -dependent manner, and map-like necrosis of hepatocytes with hemorrhage was histopathologically observed. These changes were not observed in flutamide alone group.
Secondly, we examined the effect of UDCA (10, 0, 40mg/kg) on the hepatotoxicity of rats treated with PB and flutamide (150mg/kg). Simultaneous administration of UDCA significantly improved hepatotoxic parameters, such as GOT, GPT and GLDH, without affecting serum concentrations of flutamide and its metabolites. Hepatic necrosis was also smaller than those observed in PB+flutamide group.
These results suggest that UDCA might improve flutamide-induced liver.

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Clinical Relevance of Magnetic Resonance Imaging and Magnetic Resonance Spectroscopy for the Cirrhotic without Overt Hepatic Encephalopathy

Yukou FUJISHIMA, Akinobu KATO, Kazuyuki SUZUKI

1999 Volume 40 Issue 4 Pages 235-242
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.235

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To clarify the changes of pallidal high intensity on T1-weighted magnetic resonance imaging (MRI) and brain metabolites on magnetic resonance spectroscopy (MRS) as related to the severity of hepatic functions, the concentrations of blood ammonia (B-NH₃) and the levels of trace elements (Mn, Cu and Zn), 30 patients with liver cirrhosis without hepatic encephalopathy (HE) and 5 age-matched healthy control subjects underwent MRI and proton MRS. Pallidal high intensity (Pl index) and glutamine are higher in cirrhosis, and myo-inositol is lower than that of control statistically. In cirrhosis, there were statistically negative correlation between B-NH₃ and myo-inositol and positive correlation between B-NH₃ and glutamine. There was a statistically lower myo-inositol and higher Pl index, glutamine as the severity of hepatic functions increased. Furthermore there was a statistically positive correlation between Pl index and Mn. These data suggest that the changes of MRI and MRS findings already detected in cirrhosis without HE and these abnormalities may be reflect the B-NH₃ and Mn metabolism and the severity of the hepatic functions.

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The Draining Vessel of Advanced Hepatocellular Carcinoma Assessment of Color Doppler Findings in Comparison with Histopathological Findings

Hitoshi TOCHIO, Syusuke TOMITA, Masatoshi KUDO, Yoshihiro OKABE, Kazut ...

1999 Volume 40 Issue 4 Pages 243-252
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.243

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Efferent flow signal, which shows continuous waveform, adjacent to afferent pulsatile wave signal is often detected within hepatocellular carcinoma (HCC) by color Doppler imaging. It is hypothesized that this signal may reflect the draining efferent blood flow within the preexisting portal vein, which remained in the advanced stage HCC nodule. In order to clarify whether this hypothesis is correct, 11 resected advanced HCC with such signals were analyzed histopathologically. The size of tumor ranged 1.2-5.1cm (Mean±SD=2.5±1.3cm). In 8 out of 11 (73%), Glisson sheath including patent portal vessel were observed within the tumor. These portal veins were located within entire tumor in small, well-differentiated HCC, where as those were located in the periphery of the tumor in large, relatively poorly differentiated HCC. These results suggested that the portal vein, which remained within the advanced HCC, may act as a draining vessel in some advanced HCCs. Furthermore, portal vein is an efferent draining vessel already in small, well-differentiated HCC.

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Case of congenital hepatic fibrosis performed by redevasucularization of the abdominal esophagus and cardia for recurrence ruptured gasiric varices

Koji NAMEKATA, Shigeru TAKAMORI, Kuniaki KOJIMA, Masaki FUKASAWA, Tomo ...

1999 Volume 40 Issue 4 Pages 253-259
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.253

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A Case Of Hyalin Degenerative Mass Lesion Of The Liver

Atsushi MIYAMOTO, Hiroaki NAGANO, Masato SAKON, Koji UMESHITA, Terumas ...

1999 Volume 40 Issue 4 Pages 260-263
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.260

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese]

1999 Volume 40 Issue 4 Pages 264-265
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.264

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...

1999 Volume 40 Issue 4 Pages 266-267
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.266

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...

1999 Volume 40 Issue 4 Pages 268
Published: April 25, 1999
Released on J-STAGE: February 22, 2010

DOIhttps://doi.org/10.2957/kanzo.40.268

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