Toshinori Harada

Morphologic studies of the liver cell dysplasia.

Light and electron microscopic changes in human liver cells which were considered to be precancerous lesions, were studied. In our micrometrical examination, dysplastic liver cells were classified into two types: large and small dysplastic cell. Each type had nuclear pleomorphism and multinucleation; however, the nucleocytoplasmic ratio of the large dysplastic cell remained normal. Electron microscopically, the large dysplastic cell had some features of regenerative cells. The nucleocytoplasmic ratio of the small dysplastic cell was between that of normal hepatocytes and liver cancer cells. The difference in the incidence of the small and large dysplastic cells in normal livers and cirrhotic livers having hepatocellular carcinoma was statistically significant. In addition, the small dysplastic cell had more of a tendency to produce a small round focus. It was morphologically suggested that the more important candidate for the precancerous cell in the liver was the small dysplastic cell.

Early lesions and development of primary hepatocellular carcinoma in man--association with hepatitis B viral infection.

SummaryIt is well known that primary hepatocellular carcinoma could be derived from chronic hepatitis and liver cirrhosis in epidemiologic studies. However, it is still not clear what kinds of hepatocyte are premalignant cells. Recently we have focused on liver cell dysplasia as a possible premalignant cell, and showed localization of α-fetoprotein in the cytoplasma of these cells. Although the dysplastic cells were often seen in the liver of chronic active hepatitis, hepatitis B virus associated DNA polymerase activity was also significantly high in the sera from the patients with chronic active hepatitis. In this paper, we discuss the possible role of hepatitis B virus through hepatocarcinogenesis in human.

Complication of laparoscopy in Japan.

SummaryTrends of examinees and complications of laparoscopy were examined by a questionaire sent to all representative institutions in Japan. As a conclusion, the rate of complication by this examination was 10 times higher, while its mortality was 25 times higher, as compared with gastroenterological endoscopie examination.This article may indicate the present status of laparoscopy in Japan.

Complete necrotization of hepatocellular carcinoma by chemotherapy and subsequent intravascular coagulation: a case report.

A 45‐year‐old man with hepatocellular carcinoma who developed intravascular coagulation following complete tumor regression by chemotherapy is described. After 2 doses of 10 mg of Mitomycin C given into the hepatic artery at the time of selective angiography, and 16 intravenous doses of 5‐fluorouracil and Mitomycin C, 2 doses per week, subjective symptoms and hepatomegaly disappeared. Alpha‐fetoprotein became negative and a remarkable change in tumor size and vasculature was noted in the arteriogram. Three months after chemotherapy, the patient developed thrombocytopenia, intravascular hemolysis, and acute renal failure. Autopsy disclosed a 8 × 7 × 5 cm solitary, encapsulated hepatocellular carcinoma in the right lobe. The tumor was surrounded by a thick capsule and completely necrotized. Neither intrahepatic invasion nor extrahepatic metastasis was observed. In the kidney, generalized fibrin thrombi were seen in the afferent arterioles of glomeruli as accounted for by intravascular coagulation.

Representation of T cell functions in liver bearing hepatocellular carcinoma

SummaryThymus-derived cells (T cells) were stained by the immunofluorescent technique, and found to predominate around the cancer cell nests, in the interstitium, and in the lumen of the sinusoid of the liver bearing hepatocellular carcinoma (hepatoma). The marked T cell predominance in the liver obtained at autopsy in 9 of 13 patients with hepatoma indicates that specific T cell-mediated immunity may be maintained even in the terminal stage of cancer in these patients.

Clinical course on patients with primary hepatocellular carcinoma surviving longer than one year.

当内科において,1969年から1975年まで化学療法をうけた原発性肝癌患者70例中12例は少なくとも1年以上の長期生存例であった.ここ2～3年,このような長期生存患者数は増加傾向にあった.これは早期診断と治療法の進歩による. 長期生存12症例について,既往歴,臨床経過,臨床生化学的所見ならびに病理解剖所見を検討した.8例は慢性肝疾患の経過観察中に発見されたもので,これら患者の5例は糖尿病を合併していた.長期生存例12症例中7例にHB抗原が認められた.したがって,HB抗原陽性,また糖尿病合併慢性肝疾患を厳重に追跡すべきである. 患者の血清アルブミン値や末梢血リンパ球数は末期では初期に比し有意に低下し,AFPや血清ビリルビンは増加した.これらは患者の予後判定因子として有用であろう.

A case of primary hepatocellular carcinoma cured by anticancer chemotherapy

制癌剤投与により腫瘍組織が完全に壊死に陥ったと考えられる切除不可能な原発性肝細胞癌の1症例を報告した.患者は45歳の男性で右季肋部痛にて入院.著明な肝腫を認め,α-Fetoproteinが陽性で,肝シンチでは右葉下外側に広範囲の陰影欠損像が,また,肝動脈造影では右葉分枝に著明なTumor Stainが認められた.肝生検による組織診断はEdmondson II型の肝細胞癌であった.Mitomycin C (10mg)の固有肝動脈内注入を2回, 5-Fu(250～500mg)・MitomycinC(4mg)の全身性投与を週2回の割合で16回施行した結果,自覚症状及び肝腫の消失,α-Fetoproteinの陰性化,肝動脈造影所見の著明な改善を認めた.患者は治療中止約3カ月後に急性腎不全で死亡したが,剖検上,肝右葉に見られた8×5×7cmの厚い被膜で覆われた腫瘍組織は完全に壊死に陥っており,肝内肝外に転移巣なく,肝実質障害も殆ど認められなかった.本症例は,若し合併症がなかったならば,長期に生存が可能であったものと考えられた.

Thoracic duct lymph of a patient with dubin-Johnson’s syndrome

ConclusionIn the case of thoracic duct lymph of a patient with Dubin-Johnson’s syndrome, the slightly elevated pressure, increased protein concentration, normal flow rate and disturbed BSP excretion were observed. The phenomenon of re-elevation of serum BSP on BSP-test was given whereas the thoracic duct lymph was drained from the body. It was suggested that the second elevated curve of serum BSP on BSP-test was resulted from the direct regurgitation of BSP from hepatic parenchymal cells to blood stream.

Transfer into the blood stream following retrograde infusion of bsp in the common bile duct

Thin layer chromatography was applied to analyse direct react ing bi l i rubin in the human bile. Azo pigment in the h u m a n bile, which was prepared by adding ani l ine diazo-reagent, was separated into three f ract ions Rf 0.79, 0.33 and 0.19 with th in layer chromatography under solvent system of n-BuOH-C~H~COOH-H20 (10 : 1 : 1, V/V). Unconjugated bi l i rubin Azo pigment was found in f ract ion I (Rf 0.79) and Azo pigment of bi l i rubin glucuronide was in fract ion II (Rf 0.33). Identification of f rac t ion III (Rf 0.19) was still uncer ta in . Gallbladder bile obtained from cases with the disease not involving bi l iary t ract contained Azo pigment of b i l i rubin glucuronide as much as 51.8N88.8% (82.5%) on the contrary from cases with the biliary t r ac t disease 27.0~96.5% (72.3%) and hepatic bile of the cases with the bil iary t rac t disease consisted of 43.2~94.0% (66.9%) azopigment of bi l i rubin glucuronide. In conclusion, over 70% bil irubin glucuronide was found in the normal human bile and only minimal difference was encountered in pathological bile except for a few samples.