Biomedical subjects

B Guigui

Publications and source records attributed to B Guigui.

11 recordsLinked to original sources

PubMed1996

Localized epidermolysis bullosa acquisita of the esophagus in a patient with Crohn's disease.

Epidermolysis bullosa acquisita is a rare autoimmune subepidermal bullous disease that affects both the skin and mucosae and is frequently associated with Crohn's disease. We report the case of a 27-yr-old man with Crohn's disease who presented with localized epidermolysis bullosa acquisita of the esophagus, without any other mucosal or cutaneous lesions. The patient was successfully treated with sulfasalazine.

Adult↗

PubMed1989

Pancreatic cystic neoplasms.

Cystic neoplasms are an uncommon group among pancreatic tumors. Because of advances in noninvasive diagnostic procedures, these lesions are more frequently detected and surgically treated. New pathological entities have been recently described with their own prognosis. 1. In a large number of cases, the imaging procedures can differentiate microcystic adenoma from mucinous cystadenoma, the more frequently encountered lesions. A well-defined mass with innumerable small cysts producing a honeycomb appearance with central stellate septae is suggestive of microcystic adenoma. A well-defined multilocular mass containing thin, straight or curvilinear septae with papillary projections and local thickening is suggestive of mucinous cystadenoma. 2. No sonographic or CT finding allows the differentiation between mucinous cystadenoma and cystadenocarcinoma, however; the imaging features depend on the grade of malignancy. 3. Thus, in the majority of cases of cystic lesions, fine needle aspiration with appropriate stains is recommended.

Biopsy, Needle↗

PubMed1988

Copper and copper-binding protein in liver tumors.

The presence of copper and copper-binding protein was histochemically investigated in 39 hepatocellular carcinomas, 24 metastatic tumors of the liver, and eight benign hepatic tumors. None of the hepatocellular carcinomas was fibrolamellar. The presence of copper (demonstrated by rhodanine) and of copper-binding protein (demonstrated by modified orcein) was simultaneously observed in 11 of the 39 hepatocellular carcinomas (28%). Deposition was mild in three cases, moderate in two cases, and marked in six cases, and it was significantly related to the presence of bile within the tumor. Copper and copper-binding protein granules were not found in metastatic tumors of the liver, and were observed in two of the eight cases of benign hepatic tumors. These results suggest that the presence of copper and copper-binding protein in tumor cells may be found in all variants of hepatocellular carcinomas and not only in fibrolamellar carcinomas as previously suggested, and might be helpful in differentiating primary from secondary liver tumors.

Adult↗

PubMed1988

Toxicity of phorbol myristate acetate-stimulated polymorphonuclear neutrophils against rat hepatocytes. Demonstration and mechanism.

Human polymorphonuclear neutrophils (PMN), when exposed to soluble or particulate stimuli, can destroy various types of cells. The purpose of the present work was to investigate the toxicity of phorbol myristate acetate (PMA)-stimulated PMN against hepatocytes. Neutrophils were incubated in basal conditions or after stimulation by 100 ng/ml PMA in the presence of rat hepatocytes isolated by collagenase digestion. Cytotoxicity was quantified by the percentage of alanine aminotransferase (ALAT) activity released by hepatocytes in the culture medium. Whereas unstimulated PMN had only minor effects, PMA-stimulated PMN induced, after a 16-hour incubation, a 29.5% ALAT activity release at a PMN/hepatocyte ratio of 20/1. At the same ratio, stimulated PMN induced a 1.5% and a 16.6% ALAT activity release at 1 and 4 hours, respectively. At 1 hour, electron microscopy showed intimate contacts between PMN and hepatocytes; hepatocytes appeared morphologically normal. Hepatocytic lesions were moderate at 4 hours and marked at 16 hours. Neutrophil-induced hepatocyte toxicity could not be explained by the production of reactive oxygen intermediates since: (a) hepatocyte toxicity was not prevented by either superoxide dismutase or by catalase; (b) PMN obtained from a subject with chronic granulomatous disease were as toxic as PMN obtained from a normal subject. By contrast, a proteinase-mediated mechanism could be implicated since: (a) the supernatant of stimulated PMN induced a 45.9% ALAT activity release, after 16 hours of incubation; (b) three neutral proteinase inhibitors (i.e., alpha 1-proteinase inhibitor, phenylmethylsulfonylfluoride, soybean trypsin inhibitor) as well as fetal calf serum decreased this toxic effect by 82, 86, 81 and 70%, respectively. These inhibitors had no or minor protective effect on the toxicity of stimulated PMN coincubated with hepatocytes. This could be explained by the existence of intimate contacts between PMN and hepatocytes impeding the action of antiproteinases. Our results suggest that PMA-stimulated PMN can damage hepatocytes through the release of proteinases and that the existence of close contacts between PMN and hepatocytes might play a major role in this toxic effect.

Animals↗

PubMed1988

Lymph node biopsy in chronic lymphocytic leukemia: prognostic significance of histopathological, morphometry and immunohistological findings.

The morphological patterns of 20 lymph node biopsies from well differentiated lymphocytic proliferation (CLL and DWDL) were studied using conventional morphology and morphometric technics; immunohistochemistry analysis were performed in 12 cases. Four subtypes of histological patterns were described according to the number and the distribution of large lymphoïd cells. These aspects were compared to the nuclear area distribution curve and clinical staging. Patients with numerous large lymphoïd cells had a right deviation of the curve and were clinically stage C. In stage B patients, the analysis of nuclear area distribution curve individualized patients with a worse prognosis. In 12 cases immunohistochemical technics were applied to determine SmIg, B cell differentiation antigens (CD19, CD20, CD21, BL14, FmC7) and T cells subsets (CD2, CD3, CD4, CD8) the quantification of the various T cell subsets showed that CD3, CD4, positive T cell were lower in advanced stages of CLL.

Antigens, Differentiation, B-Lymphocyte↗

PubMed1987

The hepatic sinusoid in hairy cell leukemia: an ultrastructural study of 12 cases.

Ultrastructural lesions of the liver were studied in 12 cases of hairy cell leukemia, with the alterations of the sinusoidal barrier receiving special emphasis. Portal and sinusoidal tumoral infiltration was observed in all cases. It was associated with angiomatous lesions of the sinusoids in eight cases; these lesions consisted of randomly distributed cavities lined by hairy cells and containing hairy cells and erythrocytes. In addition to the attachment of hairy cells to the sinusoidal wall, other striking electron microscopic abnormalities of the sinusoids included 1) wide areas of communication between the sinusoidal lumen and Disse's space, allowing extravasation of blood cells; 2) focal disruption of the sinusoidal wall; and 3) replacement of the sinusoidal cell lining by tumor cells in close contact with hepatocytes. Most of these changes closely resembled those observed in peliosis hepatis. As in peliosis, sinusoidal alterations in hairy cell leukemia might be due to the destruction of the sinusoidal wall, and tumor cells could play a role in the pathogenesis of the lesions. The pattern of liver involvement in hairy cell leukemia, which is peculiar among hepatic localizations of blood malignancies, might reflect the unique phenotype of the tumor cells.

Humans↗

PubMed1986

Prognostic significance of a morphometric study of lymph node biopsies in chronic lymphocytic leukaemia.

In 18 chronic lymphocytic leukaemia (CLL) and 2 diffuse, well-differentiated lymphoma (DWDL) lymph node biopsies, morphometric results analysing nuclear area distribution curves by the skewness coefficient were compared to histological findings, clinical stage and survival. Lymphocytic proliferation was subclassified according to the number and the distribution of large lymphoid cells. All cases with a component of large lymphoid cells had a right deviation of the nuclear area distribution curve and a positive value of the skewness coefficient in contrast to those where lymphocytic proliferation was monomorphous. Good correlation was observed between histological findings, morphometric analysis and survival: most patients with a right deviation of nuclear area distribution curve and positive skewness coefficient are clinically stage C, or died within 2-44 months, in contrast to patients with a symmetric distribution of nuclear area curve who are clinically stage A or B and still alive. The results indicate that in CCL and DWDL the lymph node biopsy with quantitative analysis has prognostic significance.

Biopsy↗

PubMed1986

Periportal tuberculous adenitis: CT features.

The computed tomographic (CT) findings in six patients with periportal tuberculous adenitis were reviewed retrospectively to analyze the main morphologic features of the disease. In all patients, hypodense lymph nodes were observed close to the porta hepatis, with peripheral enhancement seen after administration of contrast material. In one patient, this hypodense adenopathy was associated with homogeneous, normally enhancing lymph nodes. These different features on the CT scans could signify the evolving pathologic stages of the disease, with early noncaseating granulomas and subsequent caseation necrosis. Recognition of these hypodense lymph nodes, especially in patients at risk, should help optimize the correct diagnosis of periportal tuberculous adenitis.

Adult↗

PubMedDate not supplied

In vitro toxicity of polymorphonuclear neutrophils to rat hepatocytes: evidence for a proteinase-mediated mechanism.

Human polymorphonuclear neutrophils, when exposed to soluble or particulate stimuli, can destroy various types of cells. The aim of this study was to investigate their toxicity against hepatocytes. Human polymorphonuclear neutrophils were incubated in basal conditions and after stimulation with 5 mg per ml opsonized zymosan in the presence of rat hepatocytes isolated by collagenase digestion. Cytotoxicity was quantified by the percentage of ALT activity released by hepatocytes in culture medium. Whereas unstimulated neutrophils exhibited only minor effects, opsonized zymosan-stimulated neutrophils induced, after 16 hr incubation, a 24.0 +/- 4.1% (mean +/- 1 S.E.) ALT activity release at a neutrophil/hepatocyte ratio of 5, and a 51.7 +/- 6.8% ALT activity release at a ratio of 20. At this ratio of 20, the ALT activity release was 9.0% at 1 hr and 24.0% at 4 hr. Three proteinase inhibitors (i.e., soybean trypsin inhibitor, alpha 1-proteinase inhibitor and fetal calf serum) decrease cytotoxicity by 78, 76 and 78%, respectively. The protective effect of proteinase inhibitors was not due to a nonspecific effect of proteins, since bovine serum albumin did not decrease the toxicity of stimulated polymorphonuclear cells. The supernatant of stimulated neutrophils was also found to be toxic against hepatocytes, and again, this effect was inhibited by soybean trypsin inhibitor, alpha 1-proteinase inhibitor and fetal calf serum. Finally, the role of proteinases was supported by the demonstration of a cytotoxic effect of two purified proteinases: porcine pancreatic elastase and human neutrophil cathepsin G. The toxicity of these proteinases was also markedly reduced by the specific inhibitors used in the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Amiodarone-induced hepatic phospholipidosis: a morphological alteration independent of pseudoalcoholic liver disease.

In order to study the relationship between amiodarone-induced hepatic phospholipidosis and liver disease, liver biopsies obtained from 13 patients treated with amiodarone for 4 months to 15 years were investigated by light and electron microscopy. Light microscopy showed pseudoalcoholic liver lesions that were probably related to amiodarone in four cases, various alterations (i.e. cirrhosis, three cases; steatosis and fibrosis, two cases; chronic venous congestion, one case; acute hepatitis, one case) that could be explained by another cause than amiodarone in seven cases and normal liver in two cases. In all cases, electron microscopy showed intralysosomal myelin figures suggestive of phospholipidosis. These myelin figures were associated with intralysosomal electron-dense deposits. In the four cases in which analysis by electron microprobe was performed, it demonstrated large amounts of iodine in the electron-dense deposit-containing lysosomes, indicating the accumulation of amiodarone. These results show that hepatic phospholipidosis is constantly observed in amiodarone-treated patients, whether or not pseudoalcoholic liver lesions are present. This phospholipidosis, which could be only a morphological marker of intrahepatic accumulation of the drug, should not therefore be considered grounds for attributing liver disease to the drug.

Aged↗

PubMedDate not supplied

In vitro toxicity of hydrogen peroxide against normal vs. tumor rat hepatocytes: role of catalase and of the glutathione redox cycle.

Hydrogen peroxide produced by stimulated phagocytic cells or during the metabolism of drugs, is toxic to various cell types. The aim of this study was to investigate its toxicity against normal vs. tumor rat hepatocytes. Isolated normal hepatocytes and tumor hepatocytes from three hepatocarcinoma cell lines, Fao, C2 (Faof1C2) and HTC, were incubated in the presence of a H2O2-generating system consisting of glucose and varied concentrations of glucose oxidase. The toxicity of H2O2 was quantified by measuring the percentage of lactate dehydrogenase activity released in the culture medium after various times of incubation. By comparison to normal hepatocytes, tumor hepatocytes exhibited an increased susceptibility to lysis by H2O2. At a concentration of 100 mU per ml, glucose oxidase induced a lactate dehydrogenase activity release of only 6.1 +/- 2.2% (mean +/- S.E.) from normal hepatocytes and of 71.0 +/- 2.9, 45.5 +/- 2.5 and 34.7 +/- 3.4% from Fao, C2 and HTC cells, respectively, after an 18-hr incubation. At a concentration of 10 mU per ml, glucose oxidase had no toxic effect to normal hepatocytes or HTC cells, whereas it induced a lactate dehydrogenase activity release of 58.7 +/- 7.6 and 51.2 +/- 5.6% from Fao and C2 cells, respectively. In addition, the time courses of lactate dehydrogenase activity release, studied with 500 mU per ml glucose oxidase, demonstrated that Fao cells, C2 cells and, to a lesser degree, HTC cells were lysed more rapidly than normal hepatocytes. The toxicity of glucose oxidase was suppressed by the addition of catalase, indicating that it was actually mediated by H2O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗