1/11. Reactive lymphoid hyperplasia of liver coexisting with chronic thyroiditis: radiographical characteristics of the disorder.BACKGROUND: Reactive lymphoid hyperplasia of the liver is an extremely rare entity, with six cases reported so far. methods: We encountered a 47-year-old Japanese female with reactive lymphoid hyperplasia of the liver, which coexisted with chronic thyroiditis. The lesion was discovered incidentally as a hypo-echoic mass with a hyper-echoic rim at a routine ultrasonography examination. It increased from 12 to 17 mm diameter in 6 months. Radiological studies, such as contrast-enhanced computerized tomography (CT) and angiography demonstrated a hypervascular lesion. RESULTS: It was consequently diagnosed as a neoplasm with malignant potentiality and she underwent partial hepatectomy. The lesion was composed of small mature lymphocytes which formed prominent lymphoid follicles with germinal centres, scattered plasma cells and stromal fibrosis. Immunohistochemical study revealed polyclonal origins of the involved lymphocytes. dna analysis for the immunoglobulin heavy gene and the T cell receptor beta gene using Southern blot hybridization showed no monoclonality. The following features have characterized the images in past cases, as well as ours: hypo-echoic mass, occasionally with a rim, in ultrasonography and hypervascularity, shown by angiography and enhanced CT.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
2/11. A pathological and immunohistological case report of fatal infectious mononucleosis, Epstein-Barr virus infection, demonstrated by in situ and Southern blot hybridization.We present an autopsy case of 20-month-old boy who had a fulminant course of infectious mononucleosis, with severe hepatic failure. autopsy revealed marked infiltration of immunoblasts in the lymph nodes, liver, spleen, thymus and kidneys. We identified a large number of Epstein-Barr virus (EBV) genomes in the immunoblasts of the lymph nodes, liver and spleen by in situ hybridization. EBV genomes were also detected in the liver and spleen by Southern blot hybridization. histology of the liver revealed diffuse feathery degeneration of the hepatocytes. However, EBV genomes were not detected in the hepatocytes by in situ hybridization and monoclonal antibody studies. Immunostaining of the autopsy liver specimen revealed a large number of suppressor/cytotoxic T cells (Leu2a positive) in the portal areas and of natural killer (NK) cells (Leu7 positive) in the portal areas and sinusoids of the liver. We therefore suggest that the hepatocellular damage was not caused by the viral replication in the hepatocytes but was mainly caused by the abnormal killer cell activity of the suppressor/cytotoxic T cells and NK cells.- - - - - - - - - - ranking = 7keywords = hybridization (Clic here for more details about this article) |
3/11. cytomegalovirus infection, fetal liver disease, and neonatal hemochromatosis.Neonatal hemochromatosis is an uncommon disorder, clinicopathologically defined by severe and generally fatal liver disease of intrauterine onset associated with extrahepatic siderosis that spares reticuloendothelial elements (hemochromatotic siderosis). The agent or agents of liver disease in neonatal hemochromatosis are not known. It also is not known if intrauterine liver disease of defined infective etiology can lead to hemochromatotic siderosis. We present two patients with fetal liver disease and hemochromatotic siderosis whose cases help address these points. In the first patient rare hepatobiliary and numerous renal tubular cytomegalovirus (CMV) inclusions were found; CMV infection was confirmed by the polymerase chain reaction. Studies of the mother of the second patient 1, 5, and 9 weeks post-partum showed recent seroconversion against CMV; seroconversion against other infectious agents (toxoplasma, rubella, herpes, parvovirus B19, hepatitis A/B/C) was not present. Histologic, immunohistochemical, in situ hybridization, or polymerase chain reaction evidence of CMV infection was not present in infant tissues, even though peripartum maternal seroconversion against CMV was observed. We conclude that hemochromatotic siderosis may accompany chronic fetal liver disease of defined infective etiology (patient no. 1) and that recent maternal seroconversion against CMV in the presence of severe fetal liver disease does not necessarily mean that transplacentally acquired CMV infection caused the fetal liver disease (patient no. 2). polymerase chain reaction documentation of infective-agent genomic sequences in fetal or infant tissues permits more accurate interpretation of maternal serologic data.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
4/11. Primary squamous cell carcinoma of the liver arising from a complex liver cyst: report of a case.A 65-year-old man who had received radiation therapy for nasopharyngeal cancer (NPC) 3 years earlier presented with a 3-week history of right upper quadrant abdominal pain and a feeling of fullness. There had been no evidence of metastasis on his follow-up examinations. Computed tomography scan showed a huge complex cyst with septa in the right hepatic lobe, and we performed an extended right hepatectomy to relieve his symptoms. Pathological examination revealed a large hepatic cyst with malignant cells along the cyst wall. The cytokeratin stain and CK-14 stains were positive, indicating an undifferentiated squamous cell carcinoma (SCC). The final diagnosis of primary SCC of the liver was confirmed by the clinical pathological features and negative in situ hybridization of Epstein-Barr ribonucleic acids (EBERs). We used EBERs to determine whether the cystic tumor was a primary lesion or a metastatic lesion from the previous NPC.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
5/11. Epstein-Barr virus and persistent graft dysfunction after liver transplantation.Epstein-Barr virus infection has been associated with a broad spectrum of clinical manifestations, depending on the immune status of the host. In this report, we describe two liver transplant patients who received hepatic allografts from donors serologically positive for Epstein-Barr virus and who experienced primary infection with Epstein-Barr virus associated with prolonged liver graft dysfunction. In both patients, Epstein-Barr serologies converted within 3 mo of liver transplantation, and hepatic histological study revealed mononuclear infiltration of the sinusoids evolving to pronounced immunoblastic features suggestive of evolving lymphoma. In both cases, in situ hybridization studies confirmed the presence of Epstein-Barr virus genome in the liver. Furthermore, polymerase chain reaction analysis suggested that high levels of Epstein-Barr virus dna were present in biopsy specimens obtained during the episode of acute hepatitis that followed Epstein-Barr virus seroconversion. The degree of Epstein-Barr virus dna estimated by polymerase chain reaction appeared to increase in parallel with the progression of parenchymal lymphocytic infiltrates. In one patient, a biopsy sample from a cervical node also revealed high levels of Epstein-Barr virus dna estimated using the polymerase chain reaction technique. Furthermore, in these patients, Epstein-Barr virus dna levels appeared to decrease dramatically after discontinuing azathioprine administration and beginning treatment with acyclovir. These two cases illustrate the dynamics of Epstein-Barr virus immune regulation and confirm chronic hepatic allograft dysfunction related to Epstein-Barr viral infection.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
6/11. Persistence of hepatitis a virus in fulminant hepatitis and after liver transplantation.A peroxidase-labelled, specific mouse monoclonal antibody to hepatitis a virus (HAV) and an in situ hybridization technique (streptavidin-biotin-horseradish peroxidase reaction) with an HAV-specific cDNA probe (recombinant plasmid pAWHA comprising 1.8 kb of the HAV-specific cDNA, located toward the 3' end of the genome) were used to detect HAV in liver tissues in two patients with fulminant viral hepatitis type A treated by liver transplantation after a protracted (day 40: case 1) and relapsing (day 60: case 2) clinical course. HAV antigens and HAV-specific genomic sequences were detected in the hepatectomy tissues and in serial biopsies of the liver grafts through to final follow-up at 2 months (case 2) or death at 7 months after re-grafting for chronic rejection (case 1). In the fulminant liver parenchyma, numerous degenerating and some surviving hepatocytes were positive and randomly scattered. The immunoperoxidase staining was predominantly cytoplasmic and often granular. The localization of the cDNA probe was predominantly nuclear/perinuclear but was occasionally cytoplasmic. High-titre IgM-anti-HAV antibodies persisted until death (case 1) or resolution (5 months) of an acute hepatitis (case 2), which occurred at 2 months, accompanied by HAV antigen (ELISA), in stool. Intact replicating virus particles must have been present in one or more sites in each case, including extrahepatic locations, with a viraemia as the most likely explanation for subsequent reinfection of the grafts.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
7/11. Demonstration of Epstein-Barr virus dna in a previously healthy boy with fulminant hepatic failure.A previously healthy 9-year-old boy died from acute liver failure during an acute Epstein-Barr virus infection. Epstein-Barr virus dna could be demonstrated in the liver by Southern blot--and by in situ hybridization techniques. The identification of the virus in the liver suggests a causal relation between the Epstein-Barr virus and the acute massive liver cell necrosis.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
8/11. Discordance of hepatitis B e antigen/antibody and hepatitis b virus deoxyribonucleic acid in serum. Analysis of 1063 specimens.hepatitis b virus dna was determined in 1063 serum samples from 252 patients with hepatitis B surface antigen by the spot hybridization technique. The results were correlated with hepatitis B e antigen and antibody. hepatitis b virus dna was detected in 87% of hepatitis B e antigen-positive patients, in 18% of hepatitis B e antibody-positive patients, and in 18% of those negative for both. Discordance of antigen/antibody and hepatitis b virus dna, i.e., the presence of the dna in antibody-positive sera or the absence of the dna in antigen-positive sera, was observed in 209 of 997 (21%) samples. Of 121 patients with histologic diagnosis, this discordance was observed in none of 20 patients with nonspecific changes, in 13% of 39 with chronic persistent hepatitis, in 21% of 38 with chronic active hepatitis, and in 38% of 24 with cirrhosis. Thus, hepatitis B e antigen/antibody testing alone failed to predict the presence or absence of circulating hepatitis B virion in a significant proportion of patients with advanced chronic liver disease.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
9/11. Epstein-Barr virus-related localized hepatic lymphoproliferative disorders after liver transplantation.BACKGROUND. Localized hepatic post-transplant lymphoproliferative disease is uncommon. In such cases, lymphocyte Epstein-Barr virus (EBV) infection may promote an intrahepatic B-lymphocyte monoclonal expansion. methods. From 1990 to 1991, 149 patients underwent liver transplantation for various liver failures. Immunosuppressive therapy was azathioprine, cyclosporine-A, and methylprednisolone. Rejection episodes were treated by methylprednisolone bolus injection with or without OKT3 therapy. Three patients (2%), aged 38, 50, and 47 years, developed lymphoproliferative disease localized in the transplanted livers within 5 months of liver transplantation (a patient had been immunosuppressed for 3 years before the lymphoproliferative disease occurred within the third allografted liver). Diagnoses were obtained by fine needle aspiration. In situ hybridizations were performed with the kappa/lambda mRNA-kit FITC DAKO (DAKO Corporation, Carpenteria, CA) and the early mRNA-EBER oligonucleotide FITC DAKO. RESULTS. Lymphoproliferative diseases were all classified as diffuse polymorphic large cell lymphomas in the working formulation and considered as lymphoproliferative disorders with polymorphic large cells in the Frizzera classification. All large cells were CD20-positive, CD45-positive and CD45RO-negative. In situ mRNA light chain hybridization demonstrated monoclonality in two cases. In all three cases, EBV mRNA was detected in large cells by early mRNA-EBV (EBER) in situ hybridization. patients were treated with doxorubicin, cyclophosphamide, vincristine, and VM26. Two patients maintained a complete remission 3 years after six cycles of chemotherapy, whereas one died of an early opportunistic infection. CONCLUSION. Epstein-Barr virus may play a special role in the pathogenesis of lymphoproliferative disorders that develop in patients who have undergone liver transplantation.- - - - - - - - - - ranking = 3keywords = hybridization (Clic here for more details about this article) |
10/11. Donor origin of posttransplant lymphoproliferative disorder localized to a liver allograft: demonstration by fluorescence in situ hybridization.SETTING: Posttransplant lymphoproliferative disorders in solid organ transplantation are mostly of recipient origin. We report an unusual case of posttransplant lymphoproliferative disorder following liver transplantation with localized limited involvement of the solid organ allograft. DESIGN: tissues were obtained at the time of surgery and evaluated by immunohistochemistry, in situ hybridization, and fluorescence in situ hybridization with chromosome X and Y centromeric probes. PATIENT: A 53-year-old Hispanic man with hepatic failure due to hepatitis c virus who underwent orthotopic liver transplant from a female donor and developed posttransplant lymphoma in the transplanted liver. INTERVENTION: Withdrawal of immunosuppression, resection of liver allograft, and second transplant. RESULTS: This posttransplant lymphoproliferative disorder was clearly shown to be derived from Epstein-Barr virus-infected donor lymphoid cells. This was demonstrated by fluorescence in situ hybridization for X and Y chromosomes in paraffin sections in a sex-mismatched transplant. Despite aggressive histology (monoclonal B-cell immunoblastic lymphoma) and lack of response to withdrawal of immunosuppression, the posttransplant lymphoproliferative disorder was successfully managed by repeat liver transplantation without recurrence. CONCLUSION: fluorescence in situ hybridization was used to prove donor derivation in a posttransplant lymphoma of the liver. Allograft-localized donor posttransplant lymphoproliferative disorder may represent a unique category with more favorable prognosis requiring different clinical management from other cases.- - - - - - - - - - ranking = 8keywords = hybridization (Clic here for more details about this article) |
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