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J P Merlio

Publications and source records attributed to J P Merlio.

87 records · Page 5Linked to original sources
PubMed1988

Plasmacytoma and gastric amyloidosis associated with nodular pulmonary amyloidosis.

The authors report an association of gastric and pulmonary amyloidosis in a 74 year old woman. The patient had had a gastric plasmacytoma for the last 11 years. On autopsy, the stomach was found to contain intramural deposits of amyloid, and was infiltrated by plasma cells secreting monoclonal IgG lambda light chain. In the lungs, the plasma cells in the vicinity of the amyloid deposits proved to be polytypic, suggesting that these deposits originated from circulating precursor proteins.

Amyloidosis↗
PubMed1988

Radiohistology as a new diagnostic method for barium granuloma.

Barium granulomas are rare complications of the barium enema. They pose diagnostic problems to the gastroenterologist, who may suspect a carcinoma, and to the pathologist, who may have difficulty in determining the precise nature of the foreign body. From four cases we suggest a simple and quick diagnostic method: paraffin-block roentgenography.

Adult↗
PubMed1988

[Pit cell].

Explore the source record for details and available documents.

Animals↗
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

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

Detection of CD1 positive cells in the peripheral blood of patients suffering from cancer-associated malnutrition.

The immunological phenotyping of peripheral blood mononuclear cells (PBMC) was assayed in a series of 22 patients suffering from severe cancer-associated malnutrition. A marked decrease of the T-lymphocyte subsets (CD3+, CD4+, CD8+) and of the CD20+ B lymphocytes occurred; there was however an increased percentage of monocytes but their absolute number was normal. Interestingly, 5% of the PBMC expressed "activated T-cell antigens". The specificity of two different monoclonal antibodies (MoAbs) towards CD1 epitopes (OKT6 and D47) was assessed by indirect immunofluorescence (IIF): about 5% of CD1+ thymocytes were detected with no antigen (Ag) cross reactivity with the small subset of activated T cells. It is hypothesized that some relationship may exist between such cells and malnutrition and/or cancer.

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↗
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↗
PubMedDate not supplied

[Lymphoproliferative syndrome with granular lymphocytes of CD8+ phenotype: a clonal pathology with a chronic course].

The syndrome of CD8 hyperlymphocytosis with neutropenia is a heterogeneous disorder ranging from reactive benign state to neoplastic pathology. The prognosis for LGL (Large Granular Lymphocyte) leukemia depends likely on its phenotype:-NK phenotype, extremely poor prognosis and rapidly fatal-T phenotype (CD8+), chronic disease with slow progression. Here, we report four cases of CD8+ hyperlymphocytosis with neutropenia, which are CD2+/-, CD3+, CD4-, CD8+, CD16-, CD56+/-, CD57+ phenotype. These lymphocytic proliferations were associated with clonal rearrangement of T-cell receptor b gene. In two cases, characteristic blood hyperlymphocytosis appeared only after splenectomy, but retrospective bone marrow analysis showed that the CD8+, CD57+ lymphocyte proliferation previously existed. These lymphocytes had a low natural killer activity against K562 cell line. HTLV1 proviral sequence was not integrated in leukemic cell DNA. This monoclonal pathology has a chronic clinical course, with a thirteen year evolution in one case. Splenectomy did not correct neutropenia but allowed the control of hemolytic anemia and auto-immune thrombocytopenia in one case.

Adult↗