No abstract available.
Cytoskeleton/*ultrastructure ; Hepatocytes/*ultrastructure ; Humans ; Liver Diseases/*pathology

Clinical, light and electron microscopic studies of 6 cases of acute and 8 cases of chronic active hepatitis were made and results were compared. Light microscopically acute viral hepatitis was dominated by intralobular changes characterized by ballooning degeneration, random individual and small group cell necrosis of hepatocytes with mononuclear cell reaction, cholestasis and Kupffer cell proliferation, while chronic. active hepatitis was dominated by periportal and portal changes characterized by piecemeal necrosis, heavy mononuclear cell infiltration, moderate fibrosis and mild biliary proliferation. Kupffer cell proliferation with large amount of diastase-resistant PAS positive pigments and patchy reticulin condensation were noted in both acute and chronic active hepatitis, but reticulin condensation was more advanced in chronic active hepatitis. Electron microscopically, acute hepatitis showed marked changes of nucleus, RER, bile canaliculus, and decrease of glycogen content, while chronic active hepatitis showed marked changes of mitochondria with giant fomrs and intramitochondrial inclusion, increase of polyribosomes and glycogen content, and appearance of collagen bundles in the sinusoidal wall. Kupffer cell changes were very marked in both acute and chronic active hepatitis showing large numbers of dense bodies. These dense bodies in acute cases were in the form of secondary lysosomes while they were residual bodies in chronic cases. A case which showed ground glass appearing cytoplasm by light microscopy showed massive fibrillar and tubular structures by electron microscopy. In all cases, no definite virus-like particles were observed within either the nucleus or cytoplasm. From the data, it was evident that distinction between acute and chronic active hepatitis is more clearly made with light microscopy, and the ultrastructural changes of intralobular lesions showed more similarities than differences. The meaning of minor ultrastructural differences is not clear and further evaluation is desirable. Clinically, acute cases showed higher serum bilirubin, transaminase level and hypoalbuminemia while in chronic active hepatitis serum globulin level was higher and hepatomegaly was more regularly observed.
Hepatitis, Viral, Human/pathology* ; Human ; Liver/ultrastructure*

Leigh's disease is a rare progressive neurological disorder that is characterized light microscopically by focal spongy necrosis in the brain and electron microscopically by mitochondriopathy. We report an autopsy case of Leigh's disease that showed abnormalities in the liver, kidney and skeletal muscle as well as the central nervous system. The patient was an 18-month-old girl who has carried a diagnosis of cerebral palsy ever since her birth to a 20-year-old mother. The baby was generally hypertonic and mentally retarded. She died of severe metabolic acidosis. Postmortem examination showed growth retardation, fatty liver, fatty kidney and soft brain. Brain section showed multifocal softenings in the brainstem, basal ganglia and periventricular areas. Microscopically increased capillaries with endothelial proliferation, vacuolar degeneration and mild gliosis were seen in the brain. The axons were relatively preserved. Liver and kidneys showed microvesicular fatty change. Myofiber degeneration of the skeletal muscle was also noted. Electron microscopic examination showed markedly increased mitochondria in the parenchymal cells of the brain, liver and kidney. The mitochondria showed round to ovoid ballooned appearance including electron-dense core-like structures and pseudoinclusions of glycogen granules.
Brain/pathology/ultrastructure ; Female ; Humans ; Infant ; Kidney/pathology/ultrastructure ; Leigh Disease/*pathology ; Liver/pathology/ultrastructure ; Mitochondrial Encephalomyopathies/pathology ; Muscles/pathology

OBJECTIVETo explore the ultrastructural changes of hepatocyte fibrogenesis in cholelithiasis in biliary tract.

METHODSl0 liver biopsies were taken from the patients suffered from gallstone and choledocholithiasis during surgical treatment and the ultrastructural changes were observed under electromicroscope.

RESULTSThere were plentiful collagenous microfibrils (CMFs) grown within some hepatocytes. These CMFs distributed locally or diffusely in cytoplasm even extended into nucleus. In 7 cases numerous megamitochondrias appeared in several hepatocytes, the inclusions mimicking fibrils could be frequently seen and grew beyond the envelope. Furthermore, typical CMFs could be seen in the large microbodies, and several vesicular or cystic structures similar as fibroblast were presented in marginal areas of the hepatocytes.

CONCLUSIONSWe deduce that the fibrosed hepatocytes may be remained and take part in the hyperplasia of hepatic fibrous tissue.

Adult ; Cholelithiasis ; pathology ; ultrastructure ; Female ; Hepatocytes ; pathology ; ultrastructure ; Humans ; Liver Cirrhosis ; pathology ; Male ; Middle Aged

OBJECTIVETo investigate the ultrastructure of small artery wall in patients with spontaneous rupture of hepatocellular carcinoma (HCC).

METHODSTransmission electron microscopy was used to study 11 specimens from ruptured HCC and 11 cases with non-ruptured HCC.

RESULTSThe phenomenon of activated phagocytosis in macrophage could be found in 3 cases with ruptured HCC and 10 cases with non-ruptured HCC, respectively (P < 0.05). In 9 specimens with ruptured HCC, the evidence of vascular injury characterized as less cell junctions and larger fenestrae in endothelial cells, broken elastic lamina, proliferated and fragmented elastin and damaged structure of collagen was found in small arteries. The phenomenon of electron-dense deposit in the elastic lamina, and signs of more protein synthesis in endothelial cells were also present in these specimens. In the patients with non-ruptured HCC, the evidence of vascular injury can be found only in 2 cases (P < 0.01). Less cell junctions and larger fenestrae could increase the permeability of vascular wall. The electron-dense deposition in elastic lamina may represent the deposition of antigen-antibody complex in elastic membrane which had been found in our previous study. The vascular injury was postulated to be caused by the deposition of antigen-antibody complex in vascular wall which was identified by our previous study. The vascular wall in the patient with ruptured HCC could become stiff and weak due to the proliferated fragment elastin and damaged collagen which would make the blood vessels more prone to splitting and result in hemorrhage and the rupture of HCC.

CONCLUSIONSThe vascular injury caused by antigen-antibody complex deposition might related to the spontaneous rupture of HCC.

Carcinoma, Hepatocellular ; pathology ; ultrastructure ; Humans ; Liver Neoplasms ; pathology ; ultrastructure ; Macrophages ; immunology ; Microscopy, Electron ; Rupture, Spontaneous ; pathology

No abstract available.
Chronic Disease ; Hepatocytes/*ultrastructure ; Humans ; Inclusion Bodies/*ultrastructure ; Liver Diseases/*pathology

OBJECTIVETo investigate the effects of postburn fluid resuscitation on the pathohistological and ultrastructural changes of multiple organs with dysfunction in severely burned dogs.

METHODSForty - four mongrel dogs were randomly divided into four groups: (1) immediate infusion (II, n = 8), (2) delayed infusion (DI, n = 15), (3) no infusion (NI, n = 14), (4) normal control (NC, n = 7). The dogs were inflicted with 50% TBSA III degree flame burn produced by napalm in concentration of 30g/L burning for 30 seconds on the back. Small pieces of tissue samples of heart, lungs, liver, kidneys and gastrointestinal tract were taken from injured dogs at 72 postburn hours (PBHs) or moribund stage for the examination with light microscope (LM) and transmission electron microscope (TEM).

RESULTSDifferent degrees of blood circulation disturbance and degenerative changes were found in all above internal organs. These changes were more evident in DI than in II and NI groups.

CONCLUSIONDelayed postburn fluid resuscitation could induce multiple organ dysfunction in early postburn stage.

Animals ; Burns ; complications ; therapy ; Digestive System ; pathology ; ultrastructure ; Dogs ; Fluid Therapy ; Kidney ; pathology ; ultrastructure ; Liver ; pathology ; ultrastructure ; Lung ; pathology ; ultrastructure ; Multiple Organ Failure ; etiology ; pathology ; prevention & control ; Myocardium ; pathology ; ultrastructure ; Time Factors

OBJECTIVETo investigate the clinicopathological features of infantile cytomegalovirus hepatitis.

METHODLiver biopsies from 30 cases of infantile cytomegalovirus hepatitis were observed under optical microscope and electronic microscope.

RESULTThe main clinical manifestations were jaundice, splenohepatomegaly and hypohepatia. Laboratory test showed dysfunction of liver, high level of CMV DNA, and high titer of anti-CMV antibody. Imaging examination demonstrated hepatomegaly. The histological changes were hepatocellular degeneration, necrosis, apoptosis, and fibrosis. The histological characteristics of cytomegalovirus hepatitis, including intranuclear inclusions in multinucleated giant cells and pseudo-lumens, were also observed under optical microscope. In addition, virion was observed in the nuclei and cytoplasm of hepatocytes under electronic microscope.

CONCLUSIONThe viral DNA and serological tests have limited utility for the diagnosis of infantile cytomegalovirus hepatitis, and the final diagnosis depends on histopathology.

Biopsy, Needle ; Cytomegalovirus Infections ; pathology ; Female ; Hepatitis, Viral, Human ; pathology ; Hepatocytes ; pathology ; ultrastructure ; Humans ; Inclusion Bodies, Viral ; pathology ; Infant ; Infant, Newborn ; Liver ; pathology ; Male ; Mitochondria, Liver ; pathology ; ultrastructure

OBJECTIVETo investigate the ultrastructural changes of the extraintestinal organs of newborn mice with human retrovirus (RV) infection to probe into the mechanism and clinical diagnose and therapy of extraintestinal RV infection.

METHODSHuman RV was inoculated into the abdominal cavity of the newborn mice, and the ultrastructural changes of the heart, lung, livers, and kidneys of the infected and control mice were observed by transmission electron microscope.

RESULTSThe mice with intraabdominal RV injection showed pathological changes of the cells in the small intestinal villus, liver, and kidneys. Shortened small intestinal villus, nuclear membrane disorganization, massive vacuolization, mitochondrial swelling and rough endoplasmic reticulum dilation were observed in the cells of the small intestinal. In the liver of the mice, marked mitochondrial swelling and agglutination, cell nucleus pyknosis or collapse, presence of numerous lipid droplets and vacuoles were seen in the liver cells, with lymphocyte and plasmacyte infiltration. Obvious dilatation and shedding of the microvillus were seen in cholangioles. The mitochondria of the proximal convoluted renal tubule showed mild swelling, but the cells in the heart and lung did not display obvious changes.

CONCLUSIONThe small intestinal villi were highly susceptible to RV infection, and systemic spread of human RV may cause damage of various extraintestinal organs especially the liver, which can also be susceptible to RV.

Animals ; Animals, Newborn ; Female ; Intestine, Small ; ultrastructure ; virology ; Kidney ; ultrastructure ; virology ; Liver ; ultrastructure ; virology ; Lung ; ultrastructure ; virology ; Male ; Mice ; Microscopy, Electron, Transmission ; Rotavirus Infections ; pathology ; virology

OBJECTIVETo explore the role of sinusoidal endothelial cell in the development of liver fibrosis, and to dissect the relationship among hepatic microcirculation disorders, hepatic sinusoidal capilarization and liver fibrosis.

METHODSLiver biopsy was performed in fifty-six patients with chronic hepatitis B. The liver tissues were observed under light microscope and transmitted electronic microscope.

RESULTSOf 56 cases, 39 cases were mild hepatitis, 10 were moderate hepatitis, and 7 were severe hepatitis. The morphology of hepatic stellate cells (HSCs) was similar to that of fibroblasts in the tissues of the patients with chronic hepatitis B. Collagenous fibers were deposited around the hepatic stellate cells. Electron-dense materials were deposited between sinusoidal endothelial cell and hepatic stellate cell. The size and amount of fenestraes of sinusoidal endothelial cells were reduced in 53 of 56 cases. The consecutive or inconsecutive membrane-like materials were observed along sinusoidal endothelial cells in 20 cases. Collagen fibers were observed in the space of Disse in 15 cases. Even in the patients with normal hepatic functions, red blood cells aggregation and microthrombi could be observed in the liver tissues.

CONCLUSIONSinusoidal endothelial cells are involved in development of liver fibrosis by interacting with hepatic stellate cells. Hepatic microcirculation disorders and sinusoidal capillarization are important changes in the early stage of liver fibrosis.

Adult ; Aged ; Biopsy, Needle ; Endothelial Cells ; pathology ; ultrastructure ; Female ; Hepatic Stellate Cells ; pathology ; ultrastructure ; Hepatitis B, Chronic ; complications ; pathology ; Humans ; Liver ; blood supply ; pathology ; ultrastructure ; Liver Circulation ; Liver Cirrhosis ; etiology ; pathology ; Male ; Microcirculation ; Microscopy, Electron ; Middle Aged ; Young Adult