Hidetoshi Yoda
Shinshu University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Hidetoshi Yoda.
Gastroenterologia Japonica | 1991
Manabu Takei; Hidetoshi Yoda; Noboru Kamijo; Hirotaka Kawakami; Kazuko Hirabayashi; Takao Aizawa; Katsuhide Simakura; Kendo Kiyosawa; Seiichi Furuta
SummaryA 48-year-old woman with Caroli’s disease accompanied by hepatolithiasis, choledocholithiasis, and cholangiocarcinoma is reported. Magnetic resonance imaging was useful for the diagnosis of the cholangiocarcinoma. The relationship between cholangiocarcinoma and hepatolithiasis, choledocholithiasis, and chronic cholangitis in Caroli’s disease is discussed.
Gastroenterologia Japonica | 1986
Kendo Kiyosawa; Shuichi Wada; Yasuharu Imai; Takeshi Sodeyama; Eiji Tanaka; Hidetoshi Yoda; Seiichi Furuta; Mitsuaki Kameko; Masamitsu Kanai
SummaryIgM antibody to hepatitis B core antigen (anti-HBc) was assayed using a commercial kit in acute and chronic hepatitis B virus (HBV) infection and evaluated for its diagnostic and clinical significance. IgM anti-HBc was positive in all of 21 cases with type B acute hepatitis in the acute phase, and was also detected in 5 of 20 cases with type B chronic persistent hepatitis, in 4 of 20 patients with type B chronic active hepatitis and in one of 10 with type B liver cirrhosis. The absence of this marker was noted in all of 20 asymptomatic hepatitis B surface antigen (HBsAg) carriers and in 50 with HBsAg-negative patients with liver disease and in 200 healthy blood donors. The cut-off index of IgM anti-HBc was greater than 2.0 in all serum samples obtained in the acute phase of type B acute hepatitis, but was below 2.0 in type B chronic liver disease. A close relationship was found between the presence of IgM anti-HBc and the degree of inflammatory activity in patients with HBsAg-positive chronic liver disease.These data show that examination of IgM anti-HBc is useful in distingushing type B acute hepatitis from type B chronic liver disease, and also in evaluating the severity of disease in type B chronic liver disease.
Journal of Gastroenterology and Hepatology | 1988
Kendo Kiyosawa; Nobuyoshi Yamamura; Takeshi Sodeyama; Hidetoshi Yoda; Yasuharu Imai; Haruhiko Imai; Suenia M.T. Franca; Seiichi Furuta
Intrahepatic expression of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) was investigated in 46 asymptomatic HBsAg carriers by a direct immuno‐fluorescent method. In 21 HBeAg positive carriers, HBsAg was expressed diffusely on the membrane of hepatocytes, with associated cytoplasmic localization in a few scattered hepato‐cytes. HBcAg was expressed in the nucleus of many hepatocytes and in the cytoplasm of a few scattered hepatocytes, but not on the cell membrane. In 25 anti‐HBe positive carriers, HBsAg was expressed on the surface and in the cytoplasm of hepatocytes diffusely and/or focally, but neither intrahepatic HBcAg nor serum HBV‐DNA was detected. Repeat liver biopsies were performed in 17 patients. In eight of 13 HBeAg‐positive HBsAg carriers, who developed histologically proven chronic hepatitis and liver cirrhosis, the localization of HBsAg in liver had changed from a membranous to a mixed (membrane and cytoplasm) pattern, and localization of HBcAg in liver had changed from a predominantly nuclear to a predominantly membranous and cytoplasmic pattern. However, in two HBeAg and two anti‐HBe positive cases who showed no biochemical and histologic change at follow‐up, the intrahepatic expressions of HBsAg and HBcAg in the second biopsies remained unchanged. Thus, decrease in membranous expression of HBsAg and increase in membranous and cytoplasmic expression of HBcAg were associated with progression to chronic liver disease. This suggests that membranous HBcAg may represent the major target in the process of injury to hepatocytes.
Kanzo | 1988
Hidetoshi Yoda; Kendoo Kiyosawa; Takeshi Sodeyama; Eiji Tanaka; Yukio Gibo; Yoshimoto Ooike; Yasuharu Imai; Takuroo Hayata; Yoshiyuki Nakano; Seiichi Furuta
急性肝不全を発症し重篤な病態を呈したHepatitis B virus (HBV) carrier 7例を経験した.Hepatitis delta virus, Hepatitis A virus, Epstein Barr virus, cytomegalo virusの重感染例はなく,多量飲酒および薬剤による急性肝不全発症例もみられなかった.輸血歴のない4例では3例で発症時HBV-DNA-polymerase (HBV-DNA-p)あるいはHBV-DNAが陽性であり,HBVのactive replicationが急性肝不全の発症に関与していると考えられた.輸血歴を有する3例ではHBV-DNA-p, HBV-DNA, IgM HBc抗体陽性例はなく,非A非B型肝炎ウイルスの重感染の可能性が推察された.全例にグルカゴン-インスリン療法および血漿交換療法を施行したが救命例は1例のみであった.acute hepatic failure on chronic liver disease (acute on chronic)と考えられた4例では生存例はなく,acute on chronicの予後は不良であると考えられた.
Kanzo | 1985
Takeshi Sodeyama; Kendo Kiyosawa; Shuichi Wada; Makoto Nakamura; Hidetoshi Yoda; Atsuo Nagata; Seiichi Furuta; Yoshihiro Akahane; Eiji Tanaka
HBs抗原carrier 89例につき血清HBV-DNAを測定し,その意義について,HBV関連抗原抗体系およびHBV DNA-polymeraseと比較検討した.血清HBV-DNAはHBe抗原陽性69例中55例(79.7%)に,HBe抗原陰性20例中1例(5.0%)に検出された.HBe抗原陽性例のうち無症候性HBs抗原carrier (AsC)16例では全例に血清HBV-DNAが検出されたが,慢性肝疾患例(CLD) 53例では39例(73.6%)に検出された.HBV-DNA量はCLDではAsCに比し低値であった.10例につき経時的検索を行なったところ,血清HBV-DNAはTransaminaseの上昇にやや先行して増加がみられ,HBe抗原のseroconversionに伴い検出不能となった.HBe抗体が高力価持続陽性にもかかわらずTransaminaseが著明に変動していた2例中1例に血清HBV-DNAが検出された.また,血清HBV-DNAは,Interferon投与によるHBVの減少を反映し,定量域も広く,抗ウイルス療法の効果判定に有効な指標となりうると考えられた.
Liver | 2008
Kendo Kiyosawa; Yukio Gibo; Takeshi Sodeyama; Kiyoshi Furuta; Haruhiko Imai; Hidetoshi Yoda; Yuriko Koike; Kaname Yoshizawa; Seiichi Furuta
Journal of Medical Virology | 1988
Kendo Kiyosawa; Takeshi Sodeyama; Suenia T.M. Franca; Hidetoshi Yoda; Yoshimoto Ohike; Haruhiko Imai; Yasuharu Imai; Seiichi Furuta
Kanzo | 1986
Takeshi Sodeyama; Kendo Kiyosawa; Shuichi Wada; Eiji Tanaka; Yoshimoto Ooike; Makoto Nakamura; Hidetoshi Yoda; Yukio Gibo; Atsuo Nagata; Seiichi Furuta; Yoshihiro Akahane
Kanzo | 1991
Eiji Tanaka; Takeshi Sodeyama; Yoshiyuki Nakano; Makoto Nakamura; Hidetoshi Yoda; Kazuyuki Uemura; Takuro Hayata; Yasuharu Imai; Yukio Gibo; Kendo Kiyosawa; Seiichi Furuta; Tetsuo Takayama
Acta Gastro-Enterologica Belgica | 1987
Kiyoshi Furuta; Yukio Gibo; Takeshi Sodeyama; Haruhiko Imai; Makoto Nakamura; Hidetoshi Yoda; Yoshimoto Ooike; Kendo Kiyosawa; Seiichi Furuta; Osamu Hasebe; Sumio Ichikawa