Kanzo

[title in Japanese]

[in Japanese]

1995 Volume 36 Issue 10 Pages 559-560
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.559

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Significance of serum HCV RNA titer, determined by branched DNA probe assay, in patients with chronic hepatitis C treated with interferon (IFN)

Tatsuro OSADA, Shogo IWABUCHI, Masao TAKATORI, Kiyomi YASUDA, Shiro II ...

1995 Volume 36 Issue 10 Pages 561-567
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.561

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Serum HCV RNA titer was determined by branched DNA probe assay (Quantiplex HCV, Chiron Diagnosis) in serial samples from 97 patients with chronic hepatitis C who received recombinant IFN-α 2b therapy. In 30 (31%) of the patients, the pretreatment titer was below the cut-off value (0.5Meq/ml). Complete response (CR) to IFN therapy was seen in 70%, 29% and 6% of patients in whom pretreatment titers were lower than 1.0Meq/ml, 1.0-10Meq/ml and more than 10Meq/ml, respectively. After 2 weeks of daily IFN administration, HCV RNA titers were below the cut-off value in all patients with CR, 88% of transient responders and 43% of non responders. The CR rate was significantly higher in HCV subtype III/2a and IV/2b than in subtype II/1b, given a similar titer of HCV RNA. When the patients were divided into 2 groups according to total dose of IFN (mean: 440MU), there was no significant difference in CR rate between the higher-dose group (more than 440MU) and the low-dose group in patients with III/ 2a or IV/2b. However, high-dose IFN was required in patients with subtype II/1b in order to obtain a CR rate similar to that for subtype III/2a and IV/2b, even in those with HCV RNA titer below 1.0Meq/ml.

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Histopathological study of chronic type C hepatitis with interferon therapy

Takeshi TSUCHIHASHI, Masaki SATO, Akitaka SHIBUYA

1995 Volume 36 Issue 10 Pages 568-576
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.568

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To assess the effect of interferon therapy on the histopathological findings in chronic hepatitis type C, we compared the liver biopsy findings of 58 cases before and after therapy. A histopathological improvement rate (HIR) was calculated by comparing histology activity index (HAI) scores of specimens. All cases were classified into 5 groups on the basis of their HCV genotype and histopathological grade of chronic hepatitis. All groups showed histopathological improvement with interferon therapy. To date, interferon appeared to be ineffective clinically in the group with genotype 1b and CAH-2B histopathological grade; however these showed a 30.9% HIR with therapy. Even cases with a high virus burden and advanced fibrosis in the liver specimen showed a 30.8% HIR. These results suggest that much greater improvement (in histopathological and laboratory findings) may be expected with a larger dosage and longer period of interferon administration.

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A role of urokinase type plasminogen activator (u-PA) in invasion and growth of hepatocellular cancer cells, in vitro

Toshiya KAMIYAMA

1995 Volume 36 Issue 10 Pages 577-583
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.577

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Urokinase type plasminogen activator (u-PA) plays a crucial role in the invasion and metastasis of cancer cells. We investigated the role of u-PA in invasion and proliferation of human hepatocellular cancer cell in vitro using human hepatocellular cancer cell lines; HLE, HLF, and HC-4. u-PA antigen concentration in the culture media of these cells were 603.0±7.9, 356.7±10.1, and 0ng/ml/10⁶ cells/48 hrs respectively. The invasive activity of these cell lines was evaluated in vitro using Transwells, filters of which were coated with extracellular matrix (Matrigel). Invasion Index (%)=I.I was determined with MTT assay. I.Is of HLE, HLF, and HC-4 cells were 30.1±9.5, 18.8±0.9, and 11.0±2.5% respectively, which linked to the secreted amount of u-PA. I.Is of HC-4 and HLF increased when two chain u-PA (0.5μg/ml) was added. The proliferation of these cell lines was inhibited by addition of two chain u-PA (5.0μg/ml). These data suggest that u-PA plays an important role in invasion of hepatocellular cancer cell lines, and inhibits proliferation of cell lines which have low production of u-PA.

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A case of acute hepatitis C after needlestick injury in the pregnancy

Eiji KAJIWARA, Yuriko MAKINO, Koichi AZUMA, Kaoru ONOYAMA

1995 Volume 36 Issue 10 Pages 584-588
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.584

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A 31-year-old nurse with 31 weeks of pregnancy was admitted because of nausea, vomiting, and elevation of aminotransferases and bilirubin. She had the needlestick injury 42 days before, when manipulating anti-HCV-2 positive cirrhotic patient's blood. At the time of accident her liver function test was normal and anti-HCV-2 was negative. She showed positive HCV-RNA at the admission, and anti-HCV-2 became positive 8 weeks after the admission. She had the same HCV genotype, type 2b (IV), as the patient. After the conservative therapy she had a normal delivery at 40 weeks of pregnancy. Liver biopsy performed 23 weeks after the onset, being 14 weeks after the delivery, showed a residual state of acute hepatitis. Her diagnosis was confirmed as acute hepatitis C due to the needlestick injury. Then, she was treated with recombinant interferon α-2b 10 M units during 11 weeks. Thereafter, aminotransferases improved to the normal level and HCV-RNA disappeared and remained unchanged for more than 1 year. Mother to infant transmission of hepatitis C virus was not detected in this case.

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A case of Wilson's disease with fulminan hepatic form survived with plasma exchange, glucagon-insulin (GI) therapy, prostaglandin E₁ (PGE₁) and haptoglobin

Toru ISHIKAWA, Naoki ISHIKAWA, Hironobu OOTA, Toshiaki YOSHIDA, Akira ...

1995 Volume 36 Issue 10 Pages 589-593
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.589

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A 15-year-old girl was admitted to our hospital, because of general malaise and icterus. Based on the data of urinar copper and seum ceruloplasmin as well as Kayser-Fleisher ring in the cornea, this case was diagnosed as Wilson's disease. Although D-pennicillamine was administered, hepatic encephalopathy, ascites and icterus progressed. The maximum level of total bilirubin showed 80.26mg/dl. We treated this case with repeated plasma exchange, GI therapy, PGE₁ and haptoglobin, because she presented progressive hepatic failure and hemolytic anemia. By using the combination therapies descrived above, the clinical course of this case showed remarkable improvement after five months from onset.
This report presented a survived case of Wilson's disease with fulminant hepatic form, and pointed out the importance of various kinds of active therapies.

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Hepatic encephalopathy due to porto-systemic shunt as an initial sign of primary biliary cirrhosis

Case report of a 82-year-old female

Makiko IMAMURA, Kouichi FUKAMI, Masanobu TSURU, Toshio FUKAZAWA, Motoj ...

1995 Volume 36 Issue 10 Pages 594-600
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.594

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A case of primary biliary cirrhosis (PBC) in an elderly with an unique first presentation was reported.
A 82-year-old female was admitted to our hospital with a complaint of disturbance of consciousness. Neither past history of itching nor of jaundice was noted. Serum chemistry on admission revealed moderate rise of ALP and LAP. Immunoglobrin M was elevated and anti-mitochondria antibody was positive. Plasma NH₃-level was high. Histology of liver biopsy was compatible with PBC, stage III. Abnormal blood vessels were suggested on CT and Color Doppler ultrasonography in left lower abdomen. Angiography detected a porto-systemic shunt between inferior mesenteric vein and inferior vena cava. Level of consciousness returned normal after treatments of hyperammonemia.
This was the eldest case of PBC with rare initial sign of hepatic encephalopathy due to porto-systemic shunt.

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A resected case of fibrolamellar carcinoma in the liver

A distinctive features in diagnostic imagings

Toru BEPPU, Tatsuo KUBOTA, Shigeru KATAFUCHI, Kenichi HONMA, Fuzio MAT ...

1995 Volume 36 Issue 10 Pages 601-607
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.601

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We reported a case of 15-year-old boy with fibrolamellar carcinoma of the liver. The patient showed normal liver function and tumor marker. The tumor was revealed as a hypervascular lesion with central scar, micking like focal nodular hyperplasia. Cintigram was useful in the differential diagnosis of the tumor; the tumor was presented as a cold area in ^99mTc-Sn colloid and ^99mTc-GS asialo cintigrm and a hot area in ⁶⁷Ga cintigram. The extended left lobectomy was successfully performed. The patient is tumor free and doing well seven months after the operation.

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Two cases of hepatic biloma after transcatheter arterial embolization (TAE)

Isao MATSUO, Nobuhiro IKUNO, Katsuhisa OMAGARI, Kohei KOMATSU, Kunihik ...

1995 Volume 36 Issue 10 Pages 608-614
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.608

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We reported two cases of hepatic biloma which is characterized by the dilatation of intrahepatic bile ducts (IHBD) with elevation of hepatobiliary enzymes approximately two months after TAE. The first case was a 70-year-old male and TAE was performed to the hepatocellular carcinoma (HCC) with a mixture of epirubicin, mitomycin and Lipiodol before embolization with Gelfoam. Left lobectomy of the liver with partial resection of the caudate lobe was performed for HCC and marked dilatation of IHBD. The bile lake, containing bile juice extended from the destructed bile duct, was observed in the resected specimen pathologically. The second case was a 75-year-old male and TAE was performed to the HCC with a mixture of epirubicin, mitomycin and Lipiodol before embolization with Gelfoam. It can be suggested that the hepatic biloma was caused by the obstruction of peribiliary plexus and hepatic artery, and chemical toxity of anticancer drug to the artery.

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An autopsy case of acute lymphocytic leukemia with localized massive necrosis of the liver

Shosaku ASAKA, Ryotaro KAYO, Teisuke MATSUMIYA, Keiichi FUKUNISHI, Kos ...

1995 Volume 36 Issue 10 Pages 615-620
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.615

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We reported an autopsy case, a 50-years-old man, of acute lymphocytic leukemia with localized massive necrosis of the liver. He had been suffering from acute lymphocytic leukemia for two years, and a huge low density area in the right lobe of the liver probably due to invasion of leukemic cells was detected by CT scan and ultrasonography two weeks before his death. At autopsy, a wedge-shaped necrotic lesion, which looks like infarct, was seen in the right anterior segment, but there were no obstructive lesions of the branches of portal vein or hepatic artery. Microscopically, the necrotic lesion was formed by massive necrosis. In the wedge-shaped necrotic lesion, subendothelial proliferation of loose connective tissue was noted in a large number of the sublobular hepatic veins (localized veno-occlusive disease) and leukemic cells were found to be severely invaded into the sinusoids. In the liver, in addition to the wedge-shaped necrotic lesion, focal and random coagulative hepatocellular necrosis due to DIC (disseminated intravascular coagulation) was seen sporadically. Then, we suppose that the wedge-shaped necrotic lesion was localized massive necrosis resulted from augmentation of DIC-induced hepatocellular necrosis by sinusoidal microcirculatory disturbances due to the localized venoocclusion and invasion of leukemic cells into the sinusoids.

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[title in Japanese]

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

1995 Volume 36 Issue 10 Pages 621-622
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.621

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[title in Japanese]

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

1995 Volume 36 Issue 10 Pages 623-624
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.623

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[title in Japanese]

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

1995 Volume 36 Issue 10 Pages 625-627
Published: October 25, 1995
Released on J-STAGE: July 09, 2009

DOIhttps://doi.org/10.2957/kanzo.36.625

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