Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatocellular carcinoma (HCC) may uncommonly present with distant metastasis in the absence of a documented neoplasm in the liver. The authors herein describe the case of a 60-year-old man with cirrhosis who developed unilateral enlargement of the breast and a subareolar mass. This problem was clinically thought to represent gynecomastia, but a mammary fine-needle aspiration biopsy demonstrated a malignant epithelial neoplasm composed of large granular amphophilic cells. Bile pigment was visualized in the tumor on aspirate smears and cell block preparations; immunostains showed reactivity for cytokeratin and alpha-fetoprotein, but there was no positivity for epithelial membrane antigen, gross cystic disease fluid protein-15, vimentin, estrogen receptors, progesterone receptors, or S100 protein. These results indicated a diagnosis of metastatic HCC, which was subsequently confirmed by computed tomography of the abdomen.
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PMID:Metastatic hepatocellular carcinoma of the breast, simulating gynecomastia: diagnosis by fine-needle aspiration biopsy. 133 27

The histological and immunohistochemical characteristics of the liver in 44 children (28 boys, 16 girls) with extrahepatic biliary atresia at different stages of the clinical course were studied. Thirty-four wedge liver biopsy specimens taken during Kasai operations (25 specimens) and relaparotomy (9 specimens) and 20 hepatectomy explants taken at the time of transplantation were examined. Routine histological stains and monoclonal antibodies against different molecular weight cytokeratins and HLA-DR were used. The histopathological changes and the pattern of cytokeratin expression observed during the course of the disease were suggestive of persistent or recurrent extrahepatic biliary obstruction that occurred despite the Kasai operation and eventually led to cirrhosis and liver failure. Quantitative studies showed a progressive loss of intrahepatic bile ducts over the time course of the disease. This destruction of bile ducts had a geographic anatomical distribution in hepatectomy specimens, and in two livers it occurred predominantly in only one lobe. This geographic distribution of the vanishing bile ducts probably indicates an unpredictable and uneven obliteration of bile ducts in the porta hepatis during portoenterostomy wound healing and scarring.
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PMID:Intrahepatic bile duct loss in biliary atresia despite portoenterostomy: a consequence of ongoing obstruction? 137 80

This is a case report of a 69-year-old woman with sarcomatoid hepatocellular carcinoma (HCC), which was diagnosed clinically as hemangioma. She was first admitted to our university hospital, complaining of general fatigue in December, 1988, and cholelithiasis and liver cirrhosis with hepatic tumor in Segment 8 were diagnosed. The serum AFP level was within normal range, and the tumor was diagnosed as hemangioma radiologically. She underwent only cholecystectomy and was well without any therapy for the liver tumor up until March in 1991 when she was readmitted to our university hospital due to rapidly progressive liver dysfunction. The size of the liver tumor was unchanged. Despite intensive care, she died of hepatic failure due to cirrhosis in a decompensation state. At autopsy, a well defined yellowish white tumor of 3 cm in maximum diameter was seen in the cirrhotic liver. Although the largest part of the tumor revealed necrosis and hyalinization, a sarcomatoid part composed of spindle-shaped cells was noted in the peripheral portion. In addition, some necrotic ghost cells, probably hepatocellular carcinoma, were also noted. Low molecular cytokeratin, which is always found in HCCs, was seen in spindle-shaped sarcomatoid cells. The liver tumor was diagnosed as sarcomatoid HCC from these pathological findings. We report this histologically unusual HCC with an immunohistochemical study.
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PMID:[Sarcomatoid liver carcinoma diagnosed clinically as hemangioma]. 147 Jul 79

Metastasis of hepatoma to the brain is a rare event. Even rarer is massive hemorrhage of the brain associated with metastatic hepatoma. A 57-year-old man had cirrhosis of the liver with hepatocellular carcinoma. The tumor spread to the lungs and left occipital lobe of the brain. The primary and secondary neoplasms were negative in detection of mucin, but were immunohistochemically positive to cytokeratin CAM 5.2 and KC; the finding supported the hepatocellular origin of the tumor. The metastatic tumor formed papillae in the lung and produced massive hemorrhage in the left occipital lobe. This case raised the total number of intracranial metastatic hepatic carcinomas to 34 cases. Five of 34 hepatic carcinomas metastatic to brain, including the current one, were hepatocellular carcinoma that produced massive hemorrhage.
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PMID:Massive cerebral hemorrhage from metastatic hepatocellular carcinoma. 166 19

The existence of facultative stem cells in the liver has been advocated based on observations from models of carcinogenesis in rat liver. Observations of human liver material from cases of fulminant hepatitis have shown the presence of ductular hepatocytes expressing markers of both hepatocytes and bile duct cells. We describe the morphologic features and antigenic expression of a population of ductular hepatocytes identified in a patient with end-stage cirrhosis resulting from hepatitis B infection and secondary biliary cirrhosis. By conventional light microscopy and electron microscopy, ductular hepatocytes were seen to form pseudoductules within periportal areas. Using immunohistochemical methods, these ductular hepatocytes were found to be positive for both the hepatitis B surface antigen and bile duct epithelial cytokeratin, phenotypic markers classically restricted to expression on hepatocytes and bile duct epithelium, respectively. These findings show definitively that ductular hepatocytes are intermediate cells bearing morphologic and phenotypic characteristics of both hepatocytes and bile duct epithelium. The presence of these cells indicates the existence of facultative stem cells in the adult mammalian liver.
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PMID:Characterization of ductular hepatocytes in end-stage cirrhosis. 232

Aggregation and derangement of cytokeratin intermediate filaments are thought to be the key mechanism in the formation of Mallory bodies in alcoholic liver disease (ALD). To study the incidence and patterns of intracellular distribution of aggregated cytokeratin and to determine its utility as a diagnostic marker of ALD, 108 liver biopsy specimens from patients with various liver abnormalities were examined by an avidin--biotin peroxidase complex technique on paraffin section using a monoclonal antibody to cytokeratins (Hybritech). In normal liver (n = 11), only bile duct epithelium was positive. Both bile ducts and hepatocytes were positive in pathologic livers (n = 97). In ALD, 82 per cent of cases (42 of 51) showed cytokeratin positivity versus 15 per cent (seven of 46) in nonalcoholic liver disease (e.g., chronic hepatitis, nonalcoholic cirrhosis, cholestasis, and primary biliary cirrhosis). The highest incidence (100 per cent, 37 of 37) of positivity was obtained in cases with alcoholic hepatitis and cirrhosis compared with only 36 per cent (five of 14) in alcoholic fatty liver. Mallory bodies were found by the immunoperoxidase method in 71 per cent of cases (30 of 42) versus in 40 per cent (17 cases) by hematoxylin--eosin stain. In alcoholic fatty liver and alcoholic hepatitis, centrilobular hepatocytes showed cytokeratin positivity, whereas such reactivity was seen predominantly at the periphery of the regenerative nodules in alcoholic cirrhosis. A rare periportal hepatocyte was positive in the nonalcoholic group. These findings suggest that the differential distribution patterns of aggregated cytokeratin may be helpful in differentiating alcoholic from nonalcoholic liver diseases.
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PMID:Distribution patterns of cytokeratin antigen determinants in alcoholic and nonalcoholic liver diseases. 243 6

Liver cirrhosis was induced in male Wistar rats by subcutaneous injection (1 ml of 30 g/l) of an aqueous solution of thioacetamide. Using the indirect immunoperoxidase technique, high molecular weight keratins were localized in bile ducts and ductules. Low molecular weight cytokeratins were present in regenerating hepatocytes in active cirrhosis; bile ducts were unstained. These results suggest that cytokeratin staining may be useful in distinguishing bile duct epithelium and hepatocytes in hepatobiliary diseases. Anticollagen type III antibody stained hepatocytes and thin connective tissue fibres, while anticollagen type I antibody stained thicker fibres and some sinusoidal cells but not hepatocytes. Collagens were usually undetectable in normal liver cells. It is suggested, therefore, that hepatocytes may play a major role in collagen type III production which precedes the deposition of collagen type I. By contrast, collagen type I may be produced by fibroblasts and some cells along sinusoids (e.g. perisinusoidal fat-storing cells) after liver injury.
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PMID:Differential immunohistochemical localization of cytokeratins and collagen types I and III in experimentally-induced cirrhosis. 247 87

In the present study, the frequency and the distribution pattern of immunoreactive hepatocytic cytokeratin (CK) inclusions was investigated using the monoclonal antibody (MAb) CAM 5.2 detecting CKs 8, 18 and 19. The CK antigenicity of the inclusions was confirmed on frozen sections with MAbs for the CKs 7, 8, 17, 18 and 19. The frequency of hepatocytic CK aggregates was compared to the presence of non-alcoholic and alcoholic liver disease (ALD) as well as to the average all-year daily ethanol intake of 195 consecutive males subjected to medico-legal autopsy. Hepatocytic CK inclusions were infrequent in patients with normal liver histology, portal fibrosis and/or portal inflammation. In ALD, however, inclusions were observed in 35.6% of patients with fatty liver, in 63.2% of patients with alcoholic hepatitis, in 30.8% of patients with bridging fibrosis and in 60.0% of patients with liver cirrhosis. In all specimens studied, the inclusions were reactive only for CKs 8 and 18, CKs 7, 17, and 19 being unreactive. The frequency of inclusion bodies increased, paralleling increasing average all-year daily alcohol consumption. Compared to non-drinkers, a daily intake of between 40 and 80 g of absolute alcohol was associated with a statistically significantly (relative risk, RR = 6.6) increased risk of formation of aggregates. Similarly, daily consumption exceeding 80 g was related to increased (RR = 6.0) frequency of CK aggregates. The frequency of full-blown "classical" Mallory bodies (MBs) was, however, increased (RR = 8.9) only in patients with a daily intake exceeding 160 g.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokeratin inclusions in alcoholic liver disease and their relation to the amount of alcohol intake. 753 31

The histologic significance of various changes in the bile ductal structures as observed by cytokeratin immunoperoxidase assay was studied in 122 patients with alcoholic liver disease (ALD) as a part of a large Veterans Administration Cooperative Study on alcoholic hepatitis. Four types of morphologic changes in the biliary structures were observed: 1) proliferation of interlobular bile ducts in the portal tracts; 2) marginal bile ductular proliferation at the periphery of the portal tracts; 3) appearance of bile duct type cells ("oval cells") in the liver parenchyma; and 4) metaplasia of bile duct epithelium to cells resembling hepatocytes. These bile ductal changes correlated strongly with liver fibrosis (p = 0.0003; 0.0003; 0.05; 0.0035, for 1, 2, 3, and 4, respectively), cirrhosis (p < 0.0001 for all four parameters), portal inflammation (p < 0.0001 for 1, 2, and 4; p = 0.0024 for "oval cells"), and with overall histologic severity scores (p < 0.0001; p = 0.0001; p = 0.0017; p = 0.0005, respectively). However, these changes did not correlate significantly with fatty change, parenchymal degeneration and necrosis, cellular infiltrate or Kupffer cell hyperplasia, suggesting that they are probably not the direct consequences of liver cell necrosis. Periportal piecemeal necrosis correlated significantly with both portal bile duct (p = 0.0041) and marginal (p = 0.0078) bile ductular proliferation. Among all these changes, only marginal bile ductular proliferation correlated significantly with Mallory bodies present both in the hepatocytes (p = 0.05) and the bile ducts (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bile duct changes in alcoholic liver disease. The Veterans Administration Cooperative Study Group. 768 Nov 37

We clinicopathologically studied 23 surgically resected cases of combined hepatocellular and cholangiocarcinoma (HCC-CC). The frequency of this cancer in our subjects, who had primary liver cancer and who underwent hepatectomy, was 6.3%. The mean age of patients was 64.0 years old and the male: female ratio was 1.9:1. Serum alpha-fetoprotein was positive in 70% of cases and its levels were relatively low (< or = 1000 ng/mL) in most cases. The positive rate of serum carcinoembryonic antigen was 18% and its levels were also low. In regard to hepatitis virus markers, 17% of the 20 combined HCC-CC cases were positive to HBs antigen and 70% were positive to the HCV antibody. Of the 23 combined HCC-CC cases, 9 cases (39%) were associated with liver cirrhosis. Tumours were classified macroscopically into a separated type (HCC and CC are clearly separated 17%), a HCC-predominant type (resembles HCC 49%), and a CC-predominant type (resembles CC 34%). The separated and HCC-predominant types were associated with liver cirrhosis in 50 and 55% of cases, respectively. These cases with liver cirrhosis presented the features of HCC more apparently, while those without liver cirrhosis presented the features of CC. Histologically, all cases were classified into either Type I (HCC and CC were clearly distinguished; 17%), Type II (HCC and CC were contiguous and shared transitional features; 66%), and Type III (cancer cells were able to be evaluated as either HCC or CC and were considered to be an intermediate type; 17%). Immunohistological stains for cytokeratin were useful to distinguish HCC and CC. Specifically, CC was positive to cytokeratin 7 and 19. The tumour, in which HCC and CC were almost indistinguishable, such as Type III), indicates the presence of intermediate tumour cells that can differentiate either to HCC or CC.
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PMID:A clinicopathological study on combined hepatocellular and cholangiocarcinoma. 887 74


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