ACUTE DIFFUSE INTERSTITIAL FIBROSING PNEUMONITIS AND BILATERAL RENAL CORTICAL NECROSIS

An autopsy case of a 69-year-old male with acute diffuse interstitial fibrosing pneumonitis complicated by bilateral renal cortical necrosis was presented. Autopsy revealed acute diffuse interstitial fibrosing pneumonitis, bilateral renal cortical necrosis, non-bacterial thrombotic endocarditis, involving the aortic and mitral valves, and some interesting vascular lesions, dissemination of fibrinoid change of arterioles and fibrin thrombus of small vessels in various organs; accumulation of polymorphonuclear leukocytes in the lumen of the smaller interlobular arteries and arterioles of the kidney with cellular infiltration and disintegration of the wall; severe disorganization of the wall with intraluminar and intramural fibrinous exudation in smaller branches of the hepatic artery; diminution and disarrangment of muscle fibers and patchy hyalinization in the media of the renal and interlobar arteries. The inter-relationship between acute diffuse interstitial fibrosing pneumonitis, bilateral renal cortical necrosis which may be regarded as a 'hallmark' of the generalized Shwartzman reaction, and disseminated intravascular coagulation was discussed.     

PROTRACTED HISTOPATHOLOGICAL CHANGE OF THE LIVER NECROSIS INDUCED BY SHWARTZMAN REACTION

Severe pathological fibrotic change of rabbits treated with endotoxin was produced. The liver of the rabbits that died within 14 days showed severe architectural distortion through wide fibrotic band which could be called morphologically post necrotic liver cirrhosis. On the other hand, in the liver of the rabbits that remained alive more than 14 days thin septal nodular structures were observed. This experimental model is proposed as a tool for the further study of the pathogenesis of human liver cirrhosis.     

A STUDY ON THE MECHANISM OF ACUTE HEPATIC NECROSIS FOLLOWING PARTIAL RESECTION OF THE LIVER

Endotoxin was injected intravenously into rats 48 hours after 70% he-patectomy. The remaining hepatic tissue demonstrated marked hemorrhagic necrosis in high frequency. However, hepatic lesions were slight in other groups such as the group in which heparin was administered simultaneously with injection of endotoxin 48 hours after 70% hepatectomy and the group in which endotoxin was injected 10 days after 70% hepatectomy. Difining of this marked necrosis to be a univisceral Shwartzman reaction in the liver may be justified from (i) conformity of experimental manipulations to those employed in the Shwartzman reaction, (ii) macroscoplcal as well as histological evidence, (iii) formation of microthrombl in hepatic lesions, (iv) inhibition of occurrence of the reaction by heparin, and (v) absence of any remarkable change in other organs. We concluded that the hepatic regenerative state might correspond theoretically to a state of preparedness for the Shwartzman reaction.     

THE TERMINAL DISTRIBUTION OF THE HEPATIC ARTERY AND ITS RELATIONSHIP TO THE DEVELOPMENT OF FOCAL LIVER NECROSIS FOLLOWING INTERRUPTION OF THE PORTAL BLOOD SUPPLY

The terminal distribution of the hepatic artery of the human liver was examined by arterial injection of india ink and serial sectioning. The branches of the hepatic artery form capillary networks around the bile duct in the portal tract, from which the capillaries (terminal venous branch) arise and connect with sinusoids at the most peripheral zone of the liver lobules. Evidence of direct anastomosis between the hepatic artery and portal vein inside the portal tract or presence of "innere Pfortaderwurzeln" as well as the intralobular arteriole was not demonstrated.
The authors also studied the hepatic changes caused by interruption of the portal blood supply to the liver lobule. It was demonstrated that the portal tract and its components as well as several layers of liver parenchymal tissue around the portal tract are nourished from blood via the peribiliary capillary plexus and thus remains unaffected by portal obstruction, while other parts of the liver lobule will undergo coagulation necrosis.
Based on the present investigation, the authors believe that the hepatic artery plays the main role in the nourishment of the bile duct while it has little to do with that of the liver lobule, except for the most peripheral layers of the liver lobules adjacent to the portal areas.     

INCREASED MITOTIC ACTIVITY IN THE LIVER AND OTHER ORGANS IN A CASE OF ACUTE RENAL TUBULAR NECROSIS

A case is presented in which numerous mitotic figures were found in the liver, pancreas, and adrenal glands of a patient who died in uraemia due to acute tubular necrosis.     

FLORID DUCT LESIONS AND EXTENSIVE BILE DUCT LOSS OF THE INTRAHEPATIC BILIARY TREE IN CHRONIC LIVER DISEASES OTHER THAN PRIMARY BILIARY CIRRHOSIS

Intrahepatic biliary tree with either florid duct lesions or a moderate to severe degree of the duct loss in four livers with chronic hepatic diseases other than primary biliary cirrhosis were studied with histometric and serial section observations. Florid duct lesions, distributed segmentally in the liver, were found in one case with incomplete septal cirrhosis and one case with idiopathic portal hypertension. The florid duct lesions including marked plasma cell infiltration and occasional periductal granulomas, were not associated with any bile duct loss in the two cases. The duct lesions were reversible in one case during a long clinical course. On the other hand, a moderate to severe bile duct loss with biliary epithelial degeneration and necrosis was associated with no or little periductal inflammatory cell infiltration in one other case with chronic intrahepatic cholestasis, probably drug-induced, and in one case with idiopathic portal hypertension. Although florid duct lesions and bile duct loss were important diagnostic features of primary biliary cirrhosis, one of them was observed to develop independently in severely diseased livers, not consistent with a diagnosis of primary biliary cirrhosis, sclerosing cholangitis or intrahepatic bile duct paucity syndrome.     

ULTRASTRUCTURAL STUDIES ON LIVER CELL NECROSIS AND LYMPHOCYTES IN EXPERIMENTAL HEPATITIS B

Ultrastructural studies on liver cell necrosis and the interaction of lymphocyte and liver cell were carried out in experimental hepatitis B in chimpanzees. Two types of liver cell necrosis were identified. One was a lytic necrosis, and the other was a coagulation necrosis. Both types of liver cell necrosis were closely associated with the apposition of lymphocytes. The interaction (or close contact) of lymphocyte and non-necrotic liver cell infected with HBV was also detected. There were two distinct patterns of the contact. One was the direct contact, and the other was the contact with the intervention of electron-dense fuzzy material containing 20 to 22 mu spherical particles and 51 to 55 mu double-layered spherical particles. The ultrastructural characteristics of lymphocytes in each pattern of the contact were different. The results suggested that the pathogenesis of liver cell necrosis in hepatitis B was closely associated with the action of lymphocytes, and two modes of lymphocytic reaction were conceivable. ACTA PATHOL. JPN. 35 : 1359 -1374, 1985.     

肝癌患者肝动脉的变异

对己确诊为肝癌的327位患者做的486人次肝动脉插管介入治疗过程中,发现肝癌患者肝动脉的变异很大。327位肝癌患者首次肝动脉造影,肝动脉有变异的35例,变异率为10.7％。经过1～3次肝动脉化疗栓塞后肝动脉造影159人次,共115例,肝动脉有变异的37例,肝动脉变异率为32.1％,变异的肝动脉主要是由肠系膜上动脉、右膈下动脉或直接由腹主动脉和脾动脉发出。本文详细叙述了肝癌患者变异肝动脉的起始方位,以便对我们在今后肝癌导管治疗中有所帮助。     

核糖体相关基因在大鼠再生肝及肝肿瘤中表达异同的比较

目的在基因转录水平了解核糖体相关基因在大鼠再生肝(RL)和肝脏肿瘤(LT)中的表达异同。方法用搜索网站资料和查阅相关论文等方法获得核糖体发生、组装和功能相关基因及它们在肝脏肿瘤中的表达变化,用大鼠基因组230 2.0芯片检测它们在大鼠再生肝中的表达情况,用统计学方法比较上述基因在再生肝和肝脏肿瘤中的表达异同。结果初步证实上述基因中75个基因与肝再生相关。其中,18个基因在再生肝和肝脏肿瘤中表达上调,6个基因在两者中表达下调,51个基因在肝脏肿瘤中未发生有意义的表达变化。结论再生肝的核糖体相关基因表达谱与肝脏肿瘤有相同之处,也有不同之处,前者的基因表达更具阶段性和复杂性。     

兔,鼠肝起始淋巴管的分布及形态学测量

用酶、免疫组织化学染色法，半薄、超薄切片光、电镜观察和淋巴管间接注射法等多种技术研究了兔和Ｗｉｓｔａｒ大鼠肝的起始淋巴管（毛细淋巴管），以明确肝起始淋巴管的分布和形态特征，并测量了有关数据，为研究肝淋巴生成机理提供必要的依据。结果发现，肝起如淋巴管仅存在于较大的门管区结缔组织内，而肝小叶内无起始淋巴管。起始淋巴管在门管区的出现率约为２５％；其最大平均直径兔为２２．６μｍ，鼠为２７．６μｍ；平均横截     

AFP,CA19—9联检在原发性肝癌和肝硬化鉴别诊断中的临床意义

为提高原发性肝癌的诊断率和与肝硬化，其他慢性肝病的鉴别诊断，本文采用放射免疫分析法和免疫放射分析法。对５０例健康体检者、４８例原发性肝癌、３９例肝硬化，３６例其他一肝病患者，分别检验其血清中甲胎蛋白，糖类抗原１９－９肿瘤标志物的含量，结果进行比较。     

DIFFUSE PAPILLOMATOSIS OF THE GALLBLADDER COMPLICATED WITH TUBERCULOSIS

A rare case of diffuse papillomatosis of the gallbladder complicated with tuberculosis is reported. The mucosa of the gallbladder displayed a diffuse papillary pattern composed of excrescences that varied in size and height. The proliferative glands contained many Paneth cells, and the diffuse papillomatosis appeared to be derived from metaplastic-type epithelium. Tuberculous granulomas were observed in the serous layer of the gallbladder. The relationship between diffuse papillomatosis and tuberculosis of the gallbladder is discussed. ACTA PATHOL JPN 38: 1473–1480, 1988.     

肝脏干细胞和胰脏干细胞与其他细胞的联系和转分化

肝脏和胰脏均属消化腺，都具有内分泌和外分泌功能，都来源于内胚层，在发生上有密切联系，肝脏干细胞、胰脏干细胞与其他细胞在发生、功能、再生中的联系和转分化研究得越来越深入，我们就有关这方面的进展作简要综述。     

LYMPHANGIOSIS CARCINOMATOSA OF THE LIVER

A study of lymphangiosis carclnomatosa of the liver was performed. Lymphangiosis carclnomatosa Is a disease showing diffuse lymphangitic spread of cancer cells in the interstitium of the organ. Among a total of 762 cases of malignant disease, lymphangiosis carclnomatosa of the liver was found in 10 cases out of 250 with liver metastases. Among a total of 10 cases of primary cancer showing this condition, 8 were gastric cancer, the other 2 being pancreas cancer and gallbladder cancer. With regard to the histological type of primary cancer In this disease, all cases were poorly differentiated adenocarcinoma. On the basis of the histological findings, the spread of this disease seems to occur in a retrograde manner from the large lymphatics of the hllum to the periphery.     

MUCOEPIDERMOID CARCINOMA OF THE LIVER

An autopsy case of mucoepidermoid carcinoma of the liver associated with congenital cysts in a 78-year old man was reported. The liver weighed 1,900 g, and there was a massive tumor of 11 × 10 × 6.5 cm in the left lobe with multiple sero-mucinous cysts. Histologically, the tumor cells consisted of four types of cells: mucus-secreting cells, squamous cells, intermediate cells, and oxyphilic cells. The variety of tumor cells quite resembled that of mucoepidermoid carcinoma of the salivary gland. The sero-mucinous cysts were lined with a single layer of cuboidal or columnar cells and were not communicated with the biliary ducts. Part of the cysts with benign lining cells was in continuity with tumor cells of the intermediate type. Discussion was made on the histogenesis of hepatic mucoepidermoid carcinoma in particular emphasis on the association of the congenital cysts.     

ELECTRON MICROSCOPIC STUDIES OF THE SPLEEN AND LIVER IN HEREDITARY SPHEROCYTOSIS

Electron microscopic findings of the red pulp of the spleen and liver from three patients with hereditary spherocytosis have been reported.
The sinus lumen of the spleen contained various amounts of red cell with reduced deformability. Pronounced engorgement of erythrocytes in the cordal space and various stages of erythrophagocytosis by the cordal macrophages were characteristic findings. The sinus lining cells also showed erythrophagocytosis and contained numerous dense bodies. Cordal macrophages and fibrous elements seemed to be more increased in the older patient.
Acid phosphatase activity of varied intensity was demonstrated in the erythrophagocytic vacuoles of cordal macrophages. As the intracellular degradation progressed, more intense activity of this enzyme was noted, indicating their lysosomal origin.
Splenic conditioning and enhanced destruction of defective red cells in the spleen were the main cause of hemolysis in hereditary spherocytosis.
In the liver, erythrophagocytosis by the Kupffer cells was also not infrequently noted, but the liver was estimated to play a minor role in HS.
The mechanism of hemolysis and the role of the spleen and liver in elimination of hereditary spherocytes have been discussed.