We describe S100 protein positive dendritic cells (S100+DCs) in various liver diseases including chronic viral hepatitis B and C (20 cases), liver cirrhosis (3 cases), hepatocellular carcinoma (2 cases), hepatolithiasis (6 cases), primary biliary cirrhosis (PBC) (2 cases), liver allograft rejection (9 cases), bile duct paucity (1 case), and Wilson's disease (1 case). By immunohistochemical analysis, S100+DCs were absent in fetal and normal livers, while they were variably present in inflammatory liver diseases. In chronic hepatitis and active cirrhosis, S100+DCs were most frequently located in periportal area, at lymphoid follicles within the portal tract, and at foci of spotty necrosis within the lobule. Frequency and intensity of S100+DCs were not related to etiologies of liver diseases, but they were correlated with the activity of hepatitis. In PBC, S100+DCs were found between biliary epithelial cells of the septal bile ducts, as well as, the periductal area of the portal tracts. A posttransplantation liver with features of moderate acute rejection revealed many S100+DCs in polymorphous portal infiltrates. In hepatocellular carcinomas, many S100+DCs were scattered between tumor cells. In the case of the Wilson's disease, S100+DCs were not noted. Presence of S100+DCs in various inflammatory liver diseases indicates that they play a central role as antigen presenting cells in immune responses of inflammatory liver diseases.
Allografts ; Antigen-Presenting Cells ; Bile Ducts ; Carcinoma, Hepatocellular ; Dendritic Cells* ; Epithelial Cells ; Fibrosis ; Hepatitis ; Hepatitis B ; Hepatitis, Chronic ; Hepatolenticular Degeneration ; Liver Cirrhosis ; Liver Cirrhosis, Biliary ; Liver Diseases* ; Liver* ; Necrosis

No abstract available.
Chronic Disease ; Hepatitis/*classification/*pathology ; Hepatitis C, Chronic/classification/pathology ; Humans

The incidence of severe hepatitis A virus (HAV) infection has been increasing. However, clinicopathologic features of severe HAV infection that lead to liver transplantation (LT) have not been reported in Korea. We retrieved 16 LT cases with HAV infection during the last 3 years at Asan Medical Center, Seoul, Korea. Fifteen cases progressed to hepatic encephalopathy. Thirteen cases survived with or without complications, and three patients died of sepsis. The explanted liver showed massive or zonal necrosis with moderate to severe cholestasis. The zonal distribution of necrosis was frequently associated with endothelialitis of portal and/or central veins. Degenerative changes of hepatocytes were various in degree and distribution. Viral inclusions were suspected in two cases. Although HAV infection is usually confirmed by serological tests, significant venulitis of central and/or portal veins and viral inclusions, which are rarely observed, can suggest an HAV infection as a cause of massive hepatic necrosis of unknown mechanism.
Cholestasis ; Fluconazole ; Hepatic Encephalopathy ; Hepatitis ; Hepatitis A ; Hepatitis A virus ; Hepatocytes ; Humans ; Incidence ; Korea ; Liver ; Liver Transplantation ; Massive Hepatic Necrosis ; Necrosis ; Portal Vein ; Sepsis ; Serologic Tests ; Veins

BACKGROUND: We summarize our experience in the pathological diagnosis of late complications of liver transplantation (LT) to better understand the causes of late allograft dysfunction in a population mostly composed of patients with hepatitis B virus (HBV) infection. METHODS: We reviewed 361 post-transplant liver biopsies from 174 patients who underwent LT and first presented with liver function abnormalities 3 months post-procedure. The underlying diseases included HBV-associated liver disease (77%), toxic or alcoholic liver disease (10.3%), hepatitis C virus (HCV)-associated liver disease (8.6%), primary biliary cirrhosis (1.2%), primary sclerosing cholangitis (1.2%), and metabolic disease (1.7%). RESULTS: The three most common late complications were acute rejection (32.5%), recurrent disease (19.1%), and biliary complication (17.1%). Patients who underwent LT for HBV infection or for drug- or alcohol-related liver disease had a lower incidence of recurring disease than those who underwent transplantation for HCV infection. During post-transplantation months 3-12, acute rejection was the most common cause of allograft dysfunction and recurring disease was the leading cause for allograft dysfunction (p=0.039). The two primary causes of late allograft dysfunction have overlapping histological features, although acute rejection more frequently showed bile duct damage and vascular endothelialitis than recurring HBV infection, and recurring HBV infection had more frequent lobular activity and piecemeal necrosis. CONCLUSIONS: The causes of late liver allograft dysfunction are closely associated with the original liver diseases and the period after LT. Careful attention is required for differential diagnosis between acute rejection and recurrent HBV.
Bile Ducts ; Biopsy ; Cholangitis, Sclerosing ; Diagnosis, Differential ; Hepacivirus ; Hepatitis B virus ; Humans ; Incidence ; Liver ; Liver Cirrhosis, Biliary ; Liver Diseases ; Liver Diseases, Alcoholic ; Liver Transplantation ; Metabolic Diseases ; Rejection (Psychology) ; Transplantation, Homologous ; Transplants

To investigate the development of the reticular network of the thymus with aging and under pathologic conditions, we performed reticulin stains on the following samples; 5 fetal thymi (22 to 33 weeks of gestational age) and 35 postnatal thymi (less than 1 month to 33 years of age). The latter included 1 hyperplastic thymus, 4 pathologically involuted thymi and 1 physiologically involuted thymus as well as 29 normal thymi. Reticulin fibers were invariably seen along the capsule and interlobular septae of all the thymi. In fetal thymi, reticulin fibers circumscribed only cortical blood vessels and Hassall's corpuscles. Postnatal thymi from the children aged less than 1 month showed discontinuous reticulin fibers along the blood vessels of the corticomedullary junction. With aging, the amount of reticulin fibers increased and formed a "fibroreticular network(FRN)" from the branching point of the interlobular septae along the corticomedullary junction. It completely circumscribed the outer medulla in fully developed thymi. In the hyperplastic thymus, the reticular network retained its original structure. Both pathologically and physiologically involuted thymi revealed irregularly collapsed reticulin fibers. These findings suggest that the reticular network of the thymus consists of FRNs as well as capsule and interlobular septae and matures with aging before involution.
Adult ; Aging/*pathology ; Child ; Child, Preschool ; Female ; Humans ; Hyperplasia ; Infant ; Infant, Newborn ; Pregnancy ; Thymus Gland/cytology/*pathology

BACKGROUND/AIMS: Hepatic angiomyolipoma (AML) is a rare mesenchymal tumor of the liver and demonstrates a marked histologic diversity. HMB-45 is a promising immunomarker for this tumor and especially helpful to diagnosis of some AMLs with unusual morphology. The purpose of this study was to better define the variable histologic feature of hepatic AML. METHODS: Eight hepatic AMLs were examined, and all of that were resection specimens. The diagnosis was confirmed by the presence of HMB-45 positive cells. Median age was 41.5 years old, and mean size of tumor was 8.94 cm. RESULTS: Conventional mixed type was 5 cases which showed myomatous, angiomatous and lipomatous component, and 3 cases were myomatous predominant. Variable patterns including spider web cell morphology, solid sheet-like and trabecular pattern were identified on myomatous component and variable amount and patterns of inflammatory cell infiltration was identified. CONCLUSIONS: With only histologic features, it is difficult to distinguish hepatic AML from other hepatic tumor including hepatocellular carcinoma or inflammatory pseudotumor. A correct diagnosis of hepatic AML is possible by a close histologic examination with immunohistochemical stainings such as HMB-45 which is important to patient's prognosis.
Adult ; Aged ; Angiomyolipoma/metabolism/*pathology/surgery ; Carcinoma, Hepatocellular/metabolism/*pathology/surgery ; Female ; Granuloma, Plasma Cell/metabolism/pathology ; Humans ; Liver Neoplasms/metabolism/*pathology/surgery ; Male ; Melanoma-Specific Antigens/*metabolism ; Middle Aged ; Tomography, X-Ray Computed

Interpretation of late allograft biopsies can be challenging because of overlapping clinicopathological features, regional difference of underlying liver diseases for liver transplantation, and continuous changing of preoperative treatment modalities of native liver diseases. In this review article, the potential causes and histopathological features of late allograft dysfunction are discussed. The causes include recurrence of native liver disease, late-onset acute rejection, chronic rejection, and posttransplant malignancy or hepatitis of unknown etiology. Differential diagnosis between recurrent or late-onset acute rejection and early-stage chronic rejection, either reversible or finally leading to late-stage chronic rejection, is practically difficult; however, clinically, it affects patient treatment. Diagnosis of recurrent hepatitis B virus/hepatitis C virus hepatitis should be made with consideration of both serological evaluation for deoxyribonucleic acid, ribo nucleic acid, or antibodies and histopathological features. Although differentiation of recurrent or de novo autoimmune hepatitis from acute rejection is difficult, patients with autoimmune hepatitis undergo similar treatment. In pediatric patients, evaluation of Epstein-Barr virus-associated changes, which vary from nonspecific hepatitis to post- transplant lymphoproliferative disorder with or without acute rejection, is practically important from the point of treatment. From our 16-year experience in Asan Medical Center, it has become clear that the histopathological diagnosis of late allograft biopsies must be made on the basis of consensus criteria for the common and problematic causes of late complications of liver transplantations proposed by the Banff Working Group, by integration of clinical features and results of key serological tests, and even by consideration of responses to previous treatment.
Antibodies ; Biopsy ; Chungcheongnam-do ; Consensus ; Diagnosis ; Diagnosis, Differential ; DNA ; Graft Rejection ; Hepatitis ; Hepatitis B ; Hepatitis, Autoimmune ; Humans ; Liver Diseases ; Liver Transplantation ; Liver* ; Lymphoproliferative Disorders ; Recurrence ; Serologic Tests ; Transplantation, Homologous* ; Viruses

No abstract available.
Adenoma, Liver Cell/*pathology ; Aged ; Carcinoma, Hepatocellular/*pathology ; Human ; Liver Neoplasms/*pathology ; Male ; Neoplasms, Multiple Primary/*pathology

To characterize thymic epithelial cells of SCID (severe combined immunodeficiency) mice in comparison with those of Balb C mice, we did an immunohistochemical study using cortical and medullary epithelial cell specific monoclonal antibodies (MoAbs), Th-3 and Th-4, as well as gel electrophoresis and immunoblotting. The thymi of SCID mice were composed of epithelial cells and a few lymphocytes. Most epithelial cells were immunostained diffusely with Th-3, which indicated that they might be "cortical-type" epithelial cells. There were a few clusters of stellate cells with dendritic processes which were negative with Th-3 but stained strongly with Th-4. Cortical type epithelial cells and most of the Th-4 reacting cells were strongly immunostained with cytokeratin antibody MNF116. By immunoblotting, cytokeratin polypeptides No. 10 and 18 were detected in both SCID and Balb C mice; however, the relative amounts of each cytokeratin polypeptides were different. With immunohistochemical and immunoblotting results, we conclude; 1) Th-3 and Th-4 are reliable markers for cortical and medullary thymic epithelial cells in SCID mice; 2) disorganization of cells thymic structure is mostly due to maldevelopment of medullary epithelial and T lymphocytes; and 3) the composition of cytokeratin subfamilies of SCID mice thymi may represent a phenotypic marker of the maldevelopment of medullary epithelial cells.
Animals ; Antibodies, Monoclonal ; Electrophoresis, Polyacrylamide Gel ; Epithelium/pathology ; Immunoblotting ; Keratins/analysis ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Severe Combined Immunodeficiency/*pathology ; Thymus Gland/*pathology

Promyelocytic leukemia protein (PML) is a major component of PML nuclear bodies (PML NBs). Fusion of promyelocytic leukemia gene (PML) with retinoic acid receptor alpha gene with the t (15;17) translocation causes disassembly of PML NBs, leading to development of acute promyelocytic leukemia. In contrast, PML overexpression as well as different morphological changes of PML NBs were described in a few solid tumors. In this study, the expression of PML through the multistep hepatocarcinogenesis was analyzed in 95 cases of human hepatocellular carcinomas (HCCs) for comparison along with dysplastic nodules (DNs) and background liver cirrhosis (LC) or chronic hepatitis by immunohistochemistry and immunoblot. In addition, cases of HCCs were further evaluated according to their histologic grade and etiology. The amount of PML as well as the num-ber and size of PML NBs increased gradually through the progression from LC, DNs to HCCs. The overexpression of PML in HCCs was much more closely associated with HBV infection than HCV infection or alcoholic liver disease. The PML expression, however, was not correlated with histologic grade of HCCs. These results suggest that PML is involved in the early stage of multistep hepatocarcinogenesis, and HBV infection may be associated with the overexpression of PML and the morphological alteration of PML NBs.
Carcinoma, Hepatocellular/*chemistry/ultrastructure ; Cell Nucleus/*chemistry ; Human ; Liver/chemistry ; Liver Neoplasms/*chemistry/ultrastructure ; Neoplasm Proteins/*analysis ; Precancerous Conditions/*chemistry/ultrastructure ; Transcription Factors/*analysis ; Tumor Cells, Cultured