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Biomedical subjects

C Balabaud

Publications and source records attributed to C Balabaud.

At least 91 records · Page 5Linked to original sources
PubMed1988

Hepatic fibrosis in patients with idiopathic thrombocytopenic purpura.

Three patients showing all the symptoms of idiopathic thrombocytopenic purpura underwent a splenectomy. A wedge liver biopsy revealed hepatic fibrosis around central veins and an increased perisinusoidal network on Sirius red staining. Fibrosis was moderate or mild. Liver histology was otherwise normal, as were liver function tests. Hepatic fibrosis could not be attributed to any known causes. Electron microscopy showed numerous Kupffer cells with intense phagocytic activity, and perisinusoidal cells with some of the characteristics of fibro/myofibroblasts. The mechanisms of fibrosis remain unknown but could be attributed, by analogy to agnogenic myeloid metaplasia, to the massive destruction of platelets liberating PDGF and to increased activation of macrophages.

Adolescent↗
PubMed1988

[Pit cell].

Explore the source record for details and available documents.

Animals↗
PubMed1988

Chance discovery of hepatic fibrosis in patient with asymptomatic hypervitaminosis A.

A liver biopsy specimen was obtained from a 50-year-old patient whose clinical and functional liver tests showed no abnormalities but who had for some time a high vitamin A intake (109 X 10(6) IU over four years). Liver architecture was normal. Sinusoids were slightly dilated in zone 2. Perisinusoidal cells were numerous and enlarged. On Sirius red staining, there was mild fibrosis of the central veins, portal tracts, and terminal portal venules and perisinusoidal fibrosis in zone 1 of the acinus. Liver vitamin A level was increased. By electron microscopy, perisinusoidal cells filled with numerous lipid droplets had slightly dilated rough endoplasmic reticulum, numerous minute filament condensations below the plasma membrane, and stellate-shaped processes giving them the appearance of fibroblast-myofibroblast-like cells. Numerous collagen bundles, fibrils, amorphous material, and fragments of basement membrane-like material were identified in Disse's space. Immunocytochemistry showed increased amounts of collagen types I, III, IV, laminin, and fibronectin. This observation suggests that vitamin A per se, and not the cellular damage often seen in hypervitaminosis A, is responsible for fibrosis.

Biopsy↗
PubMed1988

The increase in the number of liver sinusoidal pit cells in four patients with primary or metastatic cancer of the liver.

Four patients with liver carcinoma (case 1: hepatocellular carcinoma; cases 2 and 3: metastases; case 4: adenocarcinoma possibly of hepatic origin) underwent a wedge liver biopsy taken at some distance from the tumor. Liver histology was normal in cases 2 and 3. Sinusoids were dilated in case 4. Fibrosis formed bridges between portal tracts in case 1. In all 4 cases, sinusoids contained lymphocytic cells. By electron microscopy (perfusion-fixation with glutaraldehyde) numerous lymphocytes could be identified as pit cells with characteristic dense granules and occasional rod-cored vesicles. The majority of the pit cells were luminal cells in contact with endothelial or Kupffer cells; some were in the Disse space. It is now accepted that pit cells are resident large granular lymphocytes with natural killer activity. The increase in the number of pit cells in liver carcinoma compared to the number observed in the control group (uncomplicated gallbladder lithiasis) could be hypothetically interpreted as a defense mechanism against tumor extension.

Aged↗
PubMed1987

Perisinusoidal fibrosis of the liver in patients with thrombocytopenic purpura.

10 patients with thrombocytopenic purpura (TP) underwent splenectomy. Eight of these patients had idiopathic TP (certain or probable). All had normal liver function tests. Liver histology of the surgical biopsy was normal with the exception of a non specific mild portal infiltration in 6 cases. On Sirius red staining the perisinusoidal network was normal in 3 cases, mildly or moderately increased in 5 cases and often associated with perivenular fibrosis. Collagen types I, III, IV, laminin and fibronectin were increased in the 8 biopsies tested. On semi-thin sections, numerous Kupffer cells were observed. Under the electron microscope, sinusoidal abnormalities were very similar in all 7 patients studied: numerous Kupffer cells containing abundant lysosomes, numerous collagen bundles in the Disse space, active endothelial cells, transformation of some perisinusoidal cells into cells with some of the characteristics of fibroblasts (increased RER) and myofibroblasts (peripheral condensations of the filamentous network), increased fragments of basement membrane-like material. In two cases there was an increase in the number of perisinusoidal cells loaded with lipids. The similarity of the lesions and the absence of other fibrogenic causes (except in 2 cases) suggest that TP may represent another group of diseases with perisinusoidal fibrosis. The aetiology of fibrosis remains unknown but platelet derived growth factor and activated macrophages may play a major role.

Adolescent↗
PubMed1987

Removal of cellular debris formed in the Disse space in patients with cholestasis.

Using electron microscopy, we investigated how cellular debris, formed in the Disse space during cholestasis, was cleared. Ten patients with cholestasis of varied origin and severity were studied and compared with 10 controls without liver disease. In cholestatic patients, sinusoidal cells contained variable amounts of amylase PAS-positive material. In clean perfusion-fixed sinusoids the endothelial cells often appeared swollen and active, with few fenestrations. Hepatocyte blebs and cellular debris were sometimes seen in the Disse space. Two mechanisms were apparently involved in the clearing process: phagocytosis by macrophages either infiltrated into the Disse space, or forming the barrier; and the passage of debris from the Disse space into the sinusoidal lumen through the endothelial wall. Debris was either forced through enlarged pores or through the wall, with a progressive invagination followed by an outpouching in the lumen. The force, possibly provided by endothelial massage, may not be sufficient to push out cellular debris from the Disse space; morphological data seemed to indicate that endothelial damage may be a necessary factor. Debris present in the lumen was phagocytized by numerous active macrophages. Cellular debris was not observed in the Disse space of control patients.

Adult↗
PubMed1987

Agnogenic myeloid metaplasia, portal hypertension, and sinusoidal abnormalities.

A patient with agnogenic myeloid metaplasia suffered from gastrointestinal bleeding due to ruptured esophageal varices. The portal vein and its intrahepatic branches were patent. Except for the presence of myeloid cells, mainly megakaryocytes, in the sinusoids, liver histology was more or less normal. However, on Sirius red staining there was marked perisinusoidal fibrosis. In addition to numerous collagen bundles in the Disse space, electron microscopy also revealed the presence of hemopoietic cells, the transformation of perisinusoidal cells into fibroblasticlike or myofibroblasticlike cells, or both, and fragmentary deposits of basement membrane-like material. In the pathogenesis of sinusoidal hypertension as it occurs in agnogenic myeloid metaplasia, all the factors mentioned above should probably be taken into consideration.

Biopsy, Needle↗
PubMed1987

Perisinusoidal fibrosis and basement membrane-like material in the livers of diabetic patients.

A direct correlation exists between collagenization of Disse's space and the presence of diabetic microangiopathy in type I diabetes. To confirm and extend this finding, we studied four liver biopsy samples from two patients with type I diabetes (one with retinopathy) and two patients with type II diabetes (no retinopathy). All had normal or subnormal results on liver function tests and normal liver architecture. Levels of collagen types I, III, and IV, laminin, and fibronectin, as determined by immunocytochemical techniques, appeared increased in all patients. Liver biopsy samples were perfusion fixed for electron microscopy of sinusoids and sinusoidal cells. Numerous and thick collagen bundles could be seen in Disse's space, as could the increase of basement membrane-like material underlying the endothelial cells, perisinusoidal cells, and sinusoidal membrane of hepatocytes. Perisinusoidal cells were active and had abundant rough endoplasmic reticula and thick processes. This preliminary study indicates that collagenization of Disse's space is not specific to a certain type of diabetes. The increase of basement membrane-like material raises the question of whether liver sinusoids are truly different from other capillaries as far as diabetic microangiopathy is concerned.

Adult↗
PubMed1987

Liver sinusoids and sinusoidal cells in patients with agnogenic myeloid metaplasia.

The origin of sinusoidal portal hypertension often remains unknown in patients with agnogenic myeloid metaplasia. Four consecutive patients with agnogenic myeloid metaplasia had liver biopsies examined under light and electron microscopy. Two of the four had obvious clinical portal hypertension; of these two, only one had portal vein thrombosis. All four cases showed sinusoidal infiltration by myeloid cells (from very mild to obvious) and an increased perisinusoidal collagen network. Under electron microscopy we observed (a) the collagenization of the Disse space, (b) myeloid cells in the lumen and the Disse space, (c) the transformation of perisinusoidal cells into transitional cells, and (d) fragments of basement membrane-like material. It is possible that all these abnormalities, and not only sinusoidal infiltration, contribute to increase vascular resistance, even when there is no clinical evidence of portal hypertension unrelated to vascular thrombosis.

Aged↗
PubMed1987

Benign recurrent cholestasis: a light and electron microscopic study with emphasis on sinusoidal cells.

A liver biopsy was performed on a patient with benign recurrent cholestasis. Cholestasis was mainly centrolobular with infiltration by sinusoidal macrophages. There was no necrosis. All the classic and specific ultrastructural criteria of cholestasis were observed in hepatocytes under electron microscopy. Perfusion-fixation of the biopsy allowed in addition a good visualization of sinusoids and sinusoidal cells. Numerous macrophages (Kupffer cells) with intense phagocytic activity were present in the lumen; some formed the sinusoidal barrier or were infiltrated in the Disse space. Endothelial cells contained numerous dense bodies and had few fenestrae. Cellular debris of hepatocytic origin which were not phagocytized in the Disse space were extruded in the lumen either through enlarged endothelial pores or by progressive invagination in the endothelial wall followed by outpouching in the sinusoid. In an enlarged Disse space containing amorphous material and collagen fibrils some perisinusoidal cells were transitional cells. These results indicate that pure cholestasis leads not only to hepatocyte injury with intense phagocytic activity but also to some degree of sinusoidal cell damage and extracellular matrix changes.

Adult↗
PubMed1987

Hepatocellular carcinoma developed on noncirrhotic livers. Sinusoids in hepatocellular carcinoma.

In hepatocellular carcinoma, there is modification of cell-to-cell and cell-to-extracellular matrix interactions. Two cases of well-differentiated hepatocellular carcinoma that developed in noncirrhotic livers were explored by light and electron microscopy on perfusion-fixed liver biopsy specimens. In addition, immunocytolocalization of collagen types I, III, and IV, laminin, and fibronectin was assessed. The main features included the following: absence of collagen staining inside the tumor with Sirius red; decrease of collagen types I and III and the increase of collagen type IV, laminin, and fibronectin; widening of Disse's spaces containing numerous, discontinuous, and thick fragments of basement membrane-like material piled up beneath endothelial cells and around perisinusoidal cells; transformation of perisinusoidal cells into cells with the characteristics of fibroblasts and myofibroblasts; decreased numbers of fenestrae for endothelial cells with processes often overlapping and attached with tight junctions; and rarefaction of Kupffer's cells. Expression of cellular and extracellular material abnormalities are related to the tumor differentiation. The study of these abnormalities may have implications in prognosis.

Capillaries↗
PubMed1986

The sinusoidal barrier in alcoholic patients without liver fibrosis. A morphometric study.

Alcohol induces morphological changes in the endothelial and perisinusoidal cells at the fibrotic stage of alcoholic liver diseases. Directly or indirectly, through hemodynamic disturbances linked to the enlargement of steatotic hepatocytes, alcohol may modify this barrier before the onset of fibrosis. Liver biopsies were obtained from control and from alcoholic patients and perfusion-fixed. Volume and surface densities of endothelial cells, perisinusoidal cells and their processes were measured. Liver histology was normal in the 2 groups except for steatosis in the alcoholics. Volume densities represented 8.2%, 4.7% and 3.2% of the sinusoid in controls for endothelial cells, perisinusoidal cells and their processes whereas surface densities represented respectively 0.5, 0.23, 0.21 m2/cm3 of sinusoid. Morphometric values were not significantly different in the alcoholic patients. In none of the alcoholic patients did fine morphological studies of sinusoidal cells give any indication of the possible evolution of the alcoholic disease towards fibrosis. These results indicate that in the group of patients studied, alcohol, before the fibrotic stage, did not significantly alter the sinusoidal barrier.

Adult↗
PubMed1986

Perisinusoidal cells in patients with normal liver histology. A morphometric study.

We measured the number and the morphometric characteristics of perisinusoidal cells in perfusion-fixed biopsy samples from 7 control patients with normal liver histology. On 1-micron section, the number of cells was 18 +/- 1.5/0.1 mm2; 25% of cells did not apparently contain lipids. There were no significant zonal differences. The volume density of the cells represented 1 +/- 0.2% of the hepatic parenchyma. On ultrathin sections, the volume and surface densities of processes were 3.2 +/- 0.7% of sinusoid and 0.21 +/- 0.04 m2/cm3 of sinusoid respectively which represented 70% and 90% of total PSC volume and surface densities. Lipid volume density was 20.5 +/- 7.3% of the nucleated cell. More than 30% of cells contained less than 10% of lipids. There was no correlation between lipid volume density and RER surface density.

Adult↗
PubMed1986

Ultrastructure of sinusoidal cells in a benign liver cell adenoma.

A typical benign liver cell adenoma was removed from a 25-year-old female taking an oral contraceptive. The biopsy was perfusion-fixed, allowing good visualization of sinusoids and sinusoidal cells. Kupffer cells were seldom seen. Endothelial cells were of irregular thickness; most of them had few fenestrae and were attached to each other by well visible junctions. Normal perisinusoidal cells (PSC) were not seen but were replaced by myofibroblast-like cells with thick subendothelial processes. A basement membrane often underlaid endothelial cells and the processes of PSC. The enlarged Disse space with a flattened sinusoidal hepatocyte membrane contained occasional red blood cells and an abundant extracellular matrix but few collagen fibers. These sinusoidal abnormalities leading to the capillarization of sinusoids, either the cause or the consequence of the disease, indicated a loss of normal hepatocyte homeostasis.

Adenoma↗
PubMed1986

Sinusoids ultrastructure of human hepatocellular carcinoma.

Sinusoids ultrastructure was studied in a case of hepatocellular carcinoma developed in the non cirrhotic liver of a 40-year-old man. The surgical biopsy was perfusion-fixed with 1.5% glutaraldehyde. The number of Kupffer cells was very low. Endothelial cells with signs of hyperactivity were very irregular; digitations were often attached by numerous well identified junctional complexes to their own cell processes or to adjacent cell processes. Perisinusoidal cells without lipids resembled fibro-myofibroblasts. Discontinuous basement membranes underlaid endothelial cells and perisinusoidal cells. In addition numerous strands of short basement membranes segments were seen in the Disse space. Well organized bundles of collagen were not seen. The sinusoidal membranes of hepatocytes were flattened. The perfusion-fixation revealed to be a very useful technique in the identification of all these changes which have also been reported to some degree in benign liver cell adenoma and in cirrhosis; these two conditions are known to be associated with hepatocellular carcinoma.

Adult↗
PubMed1986

Ultrastructure of sinusoids in patients with agnogenic myeloid metaplasia.

Four patients with agnogenic myeloid metaplasia underwent liver biopsies. Under light microscopy, sinusoidal infiltration was very mild or moderate, liver architecture was normal with sinusoids slightly dilated and the perisinusoidal collagen network was increased. Under electron microscopy, in perfusion-fixed sinusoids, the following abnormalities were noticed. a) Presence of hemopoietic cells (erythroid, megakaryocytic, lymphoid, myeloid) at different stages of maturation. More frequently observed in the lumen than in the Disse space, they were usually isolated and never exceeded 2 or 3 cells. In the Disse space, hepatocytes in contact with hemopoietic cells were devoid of microvilli. In the lumen they were close to endothelial cells and Kupffer cells. Kupffer cells were numerous with intense phagocytic activity. b) Numerous collagen bundles encircling sinusoids. c) Transformation of perisinusoidal cells into transitional cells with few lipids, prominent RER, long and thick processes containing filaments sometimes condensed below the plasma membrane. Although only one patient showed clinical evidence of portal hypertension of sinusoidal origin, these results suggest that hepatic vascular resistance might be raised in agnogenic myeloid metaplasia.

Cell Adhesion↗
PubMed1985

The sinusoidal barrier in rats with portacaval anastomosis: a morphometric study.

Shunting of portal blood in the rat leads to liver atrophy and to an increase in arterial blood flow with microcirculatory disturbances. The aim of this study was to investigate the effects of these disturbances on the liver sinusoidal barrier (endothelial and perisinusoidal cells) using morphometric techniques. Rats with portacaval anastomosis (PCA) and sham operated pair-fed controls were studied 3 months after the shunt. Sinusoidal volume density in PCA increased but not significantly and the volume density (Vv) of total endothelial (EC) and perisinusoidal cells (PSC) increased by 104.54% compared to sham operated pair-fed rats. The increase of EC Vv was not associated with an increase in surface density (Sv) suggesting a fall in the number of small fenestrations and an increase in cell thickness. This interpretation supports the morphological observations. The increase of PSC Vv was mainly related to the increase in their subendothelial processes Vv and not to that of the cell body Vv. Lipids Vv and RER Sv expressed per sinusoidal cells remained unchanged suggesting that the balance between the 2 hypothetical functions of the PSC, namely fibrogenesis and storage of vitamin A, was maintained. In conclusion, changes of EC and PSC after PCA result mainly in thickening of the sinusoidal barrier. This increase may impair exchanges between the sinusoidal lumen and Disse space and contribute to functional abnormalities.

Animals↗