Takashi Kato

Publications (10)21.9 Total impact

• Source

  Available from: Tatsuo Kanda

  Article: Urgent surgery for intraperitoneal bleeding from GIST during imatinib therapy

  Takehiko Enomoto, Tatsuo Kanda, Kazuhito Yajima, Seiichi Hirota, Atsushi Matsuki, Shin-ichi Kosugi, Takashi Kato, Yoichi Ajioka, Katsuyoshi Hatakeyama
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  ABSTRACT: The rupture or bleeding of a gastrointestinal stromal tumor (GIST) is a life-threatening adverse event that can happen during imatinib therapy, but few such cases have been reported in the medical literature. Here, we report a case of intraperitoneal bleeding from GIST during imatinib therapy. A 75-year-old man was diagnosed with a large GIST with liver metastasis and admitted to our hospital for abdominal pain on the 13th day of imatinib therapy. The pain disappeared after 7 days of hospitalization; however, the patient complained of diffuse abdominal pain 5days after discharge. He presented with muscular guarding, and abdominal-pelvic CT demonstrated dense ascites. The tentative diagnosis was peritoneal hemorrhage from GIST, and urgent laparotomy was performed. During the laparotomy, we noted hemoperitoneum of approximately 500ml; we resected a bulky metastatic tumor on the greater omentum and a primary tumor on the jejunum. The patient took imatinib (400mg daily) from the ninth postoperative day and underwent monthly checkups for 9months after the surgery. When GIST patients complain of sudden and severe abdominal pain during imatinib therapy, bleeding from GIST should be considered as a possible adverse effect of imatinib. KeywordsGastrointestinal stromal tumor-Imatinib mesylate-Rupture-Surgery
  Clinical Journal of Gastroenterology 04/2012; 3(2):73-77.
• Article: Loss of liver-intestine cadherin in human intrahepatic cholangiocarcinoma promotes angiogenesis by up-regulating metal-responsive transcription factor-1 and placental growth factor.

  Masaaki Takamura, Satoshi Yamagiwa, Toshifumi Wakai, Yasushi Tamura, Hiroteru Kamimura, Takashi Kato, Atsunori Tsuchiya, Yasunobu Matsuda, Yoshio Shirai, Takafumi Ichida, Yoichi Ajioka, Yutaka Aoyagi
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  ABSTRACT: Liver-intestine cadherin (LI-cadherin) represents a novel type of cadherin within the cadherin superfamily that comprises seven cadherin repeats and a short cytoplasmic domain. In this study, we first examined LI-cadherin expression immunohistochemically in 34 specimens of human intrahepatic cholangiocarcinoma (ICC). LI-cadherin expression was positive (defined as positivity in > or = 10% of cells) in 18 of the ICCs (52.9%). LI-cadherin negativity was significantly correlated with tumor dedifferentiation (P=0.026) and vascular invasion (P=0.015). The cumulative survival rate of patients with LI-cadherin-negative ICC was significantly shorter than that of patients with LI-cadherin-positive ICC (P=0.021). Multivariate analysis identified the extent of LI-cadherin staining as an independent prognostic factor for ICC survival (P=0.027). Next, to elucidate the mechanism of loss of LI-cadherin-mediated aggressiveness in ICC, we knocked down LI-cadherin expression in an ICC cell line using small interfering RNA (siRNA) technology, and screened for genes that were expressed differentially between these cells and ICC cells transfected with scrambled siRNA using microarray analysis with real-time polymerase chain reaction confirmation. Among 21 identified genes, we focused on metal-responsive transcription factor-1 (MTF-1), whose target genes might contribute to tumor aggressiveness. Expression of placental growth factor (PlGF), one of the MTF-1 target genes, was up-regulated in the ICC cells transfected with LI-cadherin siRNA. Likewise, PlGF expression was up-regulated in LI-cadherin-negative ICC specimens. There was a significant inverse relationship between these expressions (P=0.033). Furthermore, the microvessel density of LI-cadherin-negative ICC specimens was higher than that of LI-cadherin-positive specimens. These findings suggest that loss of LI-cadherin in ICC is associated with tumor dedifferentiation and vascular invasion, and thus poor prognosis. Loss of LI-cadherin results in up-regulation of MTF-1 and PlGF, thereby regulating angiogenesis in ICC.
  International Journal of Oncology 01/2010; 36(1):245-54. · 2.40 Impact Factor
• Article: Reduced expression of thrombopoietin is involved in thrombocytopenia in human and rat liver cirrhosis

  TORU ISHIKAWA, TAKAFUMI ICHIDA, YASUNOBU MATSUDA, SOICHI SUGITANI, MOTOYA SUGIYAMA, TAKASHI KATO, HIROSHI MIYAZAKI, HITOSHI ASAKURA
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  ABSTRACT: It is widely accepted that thrombocytopenia associated with liver cirrhosis is caused by increased platelet destruction in the enlarged spleen, but this issue has not yet been analysed sufficiently in terms of platelet production. Thrombopoietin is produced mainly in the liver and strongly promotes platelet production. We studied serum thrombopoietin and the levels of its mRNA in liver tissue of cirrhotic patients and also in a rat model of liver cirrhosis. Furthermore, to clarify the influence of the spleen, we investigated thrombopoietin mRNA in splenectomized rats. The serum thrombopoietin level in humans with liver cirrhosis was not significantly reduced instead of thrombocytopenia. The expression of thrombopoietin mRNA in liver tissue decreased with the progression of liver cirrhosis in both patients and the rat model and no compensatory expression was observed in other organs or nonparenchymal cells. The level of thrombopoietin mRNA did not differ significantly in splenectomized cirrhotic rats before or after administration of dimethylnitrosamine, but was lower than that in splenectomized rats without cirrhosis. We conclude that thrombocytopenia in liver cirrhosis is caused not only by platelet destruction but also by decreased platelet production, perhaps due to reduction of thrombopoietin mRNA in the liver.
  Journal of Gastroenterology and Hepatology 06/2008; 13(9):907 - 913. · 2.87 Impact Factor
• Article: Management of major portosystemic shunting in small-for-size adult living-related donor liver transplantation with a left-sided graft liver.

  Yoshinobu Sato, Satoshi Yamamoto, Toshiyuki Takeishi, Kenichiro Hirano, Takashi Kobayashi, Takashi Kato, Yoshiaki Hara, Takaoki Watanabe, Hidenaka Kokai, Katsuyoshi Hatakeyama
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  ABSTRACT: We investigated the mechanisms of small-for-size graft syndrome by time-lag ligation, a novel approach to treating major portosystemic shunts in small-for-size adult living-related donor liver transplantation (LRDLT) using left-sided graft liver. Five patients with end-stage liver failure and major splenorenal shunting underwent LRDLT using left lobe grafts. The average graft volume to recipient body weight (GV/RBW) ratio was 0.68 +/- 0.14. Two patients underwent time-lag ligation of their splenorenal (SR) shunts on postoperative days (PODs) 8 and 14, respectively. The shunts of the other three patients were untreated. The portal pressures in the first patient who underwent time-lag ligation rose above 300 mmH(2)O and remained there for 2 weeks. Thus, we ligated the SR shunt in the second patient on POD 14, resulting in an increase from 177 mmH(2)O to 258 mmH(2)O, but it decreased again thereafter. In the other three patients, the SR shunt was not ligated because portal blood flow volumes remained sufficient. Total bilirubin levels in the first time-lag ligation patient rose to 16 mg/dl, paralleling the rise in portal pressures. Although they increased after ligation in the second patient, they did not exceed 10 mg/dl. We recommend time-lag ligation if portal venous blood flow decreases in the early post-transplant period, but not until at least 2 weeks after transplantation. If the portal venous blood flow does not decrease, early postoperative ligation is unnecessary. If there are no major portosystemic shunts, making a portosystemic shunt might decompress excessive portal hypertension. With donor safety priority in LRDLT, novel approaches must be developed to enable the use of smaller donor grafts. We describe a potential means of using left lobe grafts in adult LRDLT.
  Surgery Today 02/2006; 36(4):354-60. · 1.22 Impact Factor
• Article: Association of NKT cells and granulocytes with liver injury after reperfusion of the portal vein.

  Kazuhiko Shimamura, Hiroki Kawamura, Toru Nagura, Takashi Kato, Tetsuya Naito, Hitoshi Kameyama, Katsuyoshi Hatakeyama, Toru Abo
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  ABSTRACT: Reperfusion of the liver was conducted by clamping the portal vein for 30 min in mice, followed by unclamping. Unique variation in the number of lymphocytes was induced and liver injury occurred thereafter. The major expander cells in the liver were estimated to be natural killer T cells (i.e., NKT cells), whereas conventional T cells and NK cells increased only slightly or somewhat decreased in number and proportion at that time. Reflecting the expansion of NKT cells in the liver, a Th0-type of cytokine profile was detected in sera, and cytotoxic activity was enhanced in liver lymphocytes. In NKT cell-deficient mice including CD1d (-/-) mice and athymic nude mice, the magnitude of liver injury decreased up to 50% of that of control mice. It was also suspected that accumulating granulocytes which produce superoxides might be associated with liver injury after reperfusion. This might be due to stress-associated production of catecholamines. It is known that granulocytes bear surface adrenergic receptors and that they are activated by sympathetic nerve stimulation after stress. The present results therefore suggest that liver injury after reperfusion may be mainly caused by the activation of NKT cells and granulocytes, possibly by their cytotoxicity and superoxide production, respectively.
  Cellular Immunology 04/2005; 234(1):31-8. · 1.97 Impact Factor
• Article: Involvement of natural killer T cells and granulocytes in the inflammation induced by partial hepatectomy.

  Takashi Kato, Yoshinobu Sato, Satoshi Takahashi, Hiroki Kawamura, Katsuyoshi Hatakeyama, Toru Abo
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  ABSTRACT: Natural killer T (NKT) cells are present in the liver of mice. We examined whether NKT cells and other leukocytes were associated with hepatic inflammation after partial hepatectomy. Approximately 70% of the liver was removed from mice using the method described by Higgins and Anderson. Partial hepatectomy induced the expansion of NKT cells in the liver and the elevation of transaminase. These responses were completely suppressed by the administration of tacrolimus. NKT cell-deficient mice showed a decreased level of transaminase after partial hepatectomy. Perforin (-/-) mice showed an elevation of transaminase while B6-gld/gld mice (Fas ligand-) showed a decreased elevation of transaminase. In TAP-1(-/-) mice which lacked CD8+ cytotoxic T cells, inflammation remained at a normal level after partial hepatectomy. Since NKT cell-deficient mice showed up to 50% decrease in the level of inflammation, we examined the association of other leukocytes with the remaining inflammation. The number and proportion of granulocytes were increased by partial hepatectomy. Both NKT cells and granulocytes participated in the hepatic inflammation after partial hepatectomy. The function of NKT cells, but not of granulocytes, was found to be sensitive to the immunosuppressive effect of tacrolimus.
  Journal of Hepatology 03/2004; 40(2):285-90. · 9.26 Impact Factor
• Article: Thrombopoietin receptor (c-Mpl) is constitutively expressed on platelets of patients with liver cirrhosis, and correlates with its disease progression.

  Toru Ishikawa, Takafumi Ichida, Satoshi Sugahara, Satoshi Yamagiwa, Yasunobu Matsuda, Kazuhiro Uehara, Takashi Kato, Hiroshi Miyazaki, Hitoshi Asakura
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  ABSTRACT: Thrombocytopenia is one of the major complications of liver cirrhosis. Except for hypersplenism associated with portal hypertension, it is not known which abnormalities of thrombopoiesis cause thrombocytopenia. To evaluate thrombopoiesis in liver cirrhosis, we analyzed thrombopoietin (TPO) and its receptor c-Mpl levels in cirrhotic patients. Expression of c-Mpl on platelets and the serum level of TPO were investigated from 38 patients with various stages of liver cirrhosis by flow-cytometric analysis and enzyme-immuno assay. Samples obtained from 22 individuals without evidence of liver disease were used as controls. Neither platelet counts nor TPO levels correlated with disease progression defined by the Child-Pugh classification. c-Mpl was constitutively expressed on the platelets of cirrhotic patients, and its expression level was reduced with disease progression defined by the Child-Pugh classification. In this study, serum TPO did not fluctuate according to the grade of cirrhosis. However, its receptor c-Mpl, which is expressed on platelets, was decreased significantly in severely cirrhotic patients with thrombocytopenia. Thus, a correlation between reduced c-Mpl expression and the progression of liver cirrhosis was demonstrated. We conclude that, in addition to hypersplenism, the reduced expression of c-Mpl may play a significant role in the thrombocytopenia observed in severe liver cirrhosis.
  Hepatology Research 07/2002; 23(2):115-121. · 2.20 Impact Factor
• Article: FK506 may reduce early liver injury following living related liver transplantation.

  Takashi Kato, Yoshinobu Sato, Isao Kurosaki, Satoshi Yamamoto, Kenichiro Hirano, Hideki Nakatsuka, Takashi Kobayashi, Hitoshi Kameyama, Takaoki Watanabe, Yoshio Shirai, Katsuyoshi Hatakeyama
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  ABSTRACT: We investigated the influence of FK506 which has been used frequently after transplant surgery as an immunosuppressant, on liver injury after partial hepatectomy by comparing laboratory data from donors and recipients after liver transplantation. Seventeen donors and respective recipients who underwent living related donor liver transplantation were included in the present study. Serum levels of transaminases and cytokines were measured and compared preoperatively and in the early period after the operation. Serum level of asparaginic acid aminotransferase in the postoperative day 1 was significantly higher in the donor group. Serum levels of alanine aminotransferase in the early period after the operation were significantly higher in the donor group. Serum levels of interferon y and soluble Fas ligand in the early period after the operation were significantly higher in the donor group. Steroid doses administered were significantly higher in the recipient group. FK506 administration and steroid administration in larger doses were thought to reduce serum transaminase levels of the recipient group. These findings might suggest that cell-mediated immunity weigh heavier than the operation time of ischemia-reperfusion injury as a cause of liver injury after partial hepatectomy.
  Hepato-gastroenterology 53(70):580-3. · 0.66 Impact Factor
• Article: Carbon monoxide hemoglobin and bilirubin metabolism in adult living-related liver transplantation.

  Kenichiro Hirano, Yoshinobu Sato, Takashi Kobayashi, Satoshi Yamamoto, Hideki Nakatsuka, Hiroshi Oya, Takashi Kato, Takaoki Watanabe, Hitoshi Kameyama, Katsuyoshi Hatakeyama
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  ABSTRACT: Hemeoxygenase-1 produces carbon monoxide as a byproduct of hemoglobin metabolism. The present study examines the relationship between carbon monoxide production and hyperbilirubinemia following adult living-related liver transplantation with special attention to the contribution of shear stress in retarding regeneration. Case records from 16 patients who underwent adult living-related liver transplantation from March 1999 to May 2001 were reviewed. Patients were divided into group A (graft weight: recipient body weight ratio > or = 1) and group B (graft weight: recipient body weight ratio < 1). Clinical characteristics and outcome in the two groups were compared. Total serum bilirubin concentration and the direct: total serum bilirubin concentration were higher in group B than group A (p < 0.01). Further, the carbon monoxide-hemoglobin concentration correlated with the total serum bilirubin concentration (r = 0.81, p < 0.0001) and also was higher in group B than group A (p < 0.05). The arterial: ketone body ratio rose similarly during the first week in both groups. Persistent hyperbilirubinemia in small-for-size grafts and concomitant carbon monoxide-hemoglobinemia reflect both parenchymal and Kupffer cell dysfunction. The role of shear stress in the portal system and its relationship to portal hypertension are discussed.
  Hepato-gastroenterology 50(54):1745-8. · 0.66 Impact Factor
• Article: Living related heterotopic auxiliary partial liver transplantation for extremely small-for-size graft in fulminant liver failure.

  Yoshinobu Sato, Satoshi Yamamoto, Toshiyuki Takeishi, Takashi Kobayashi, Takashi Kato, Takayuki Watanabe, Toshihiko Shimamura, Takafumi Ichida, Katsuyoshi Hatakeyama
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  ABSTRACT: Adult living related liver transplantation seeks a balance between donor safety and the need to save the recipient's life. A small-for-size graft is a major obstacle for high-risk patients. We experienced a case of heterotopic auxiliary partial liver transplantation with extremely small-for-size graft for fulminant liver failure. The other reasons why we chose to perform heterotopic auxiliary partial liver transplantation were acute renal failure, subshock state, and a left lobe volume of 24% in the standard liver volume of the donor. Hepatic vein reconstruction was made using an inferior meserteric vein patch graft. Portal vein reconstruction was made using end-to-side anastomosis employing an interposed left external iliac vein. The left hepatic artery of the graft was connected to the distal gastroduodenal artery. The patient was discharged 3 months after transplantation. We would recommend heterotopic auxiliary partial liver transplantation as an optional procedure for patients with severe preoperative conditions or extremely small-for-size graft donors.
  Hepato-gastroenterology 50(53):1220-2. · 0.66 Impact Factor